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Hideki Katagiri

Section

Graduate School of Medicine

Job title

Professor

Degree

博士（医学）（東京大学）

researchmap

https://researchmap.jp/read0095300

J-GLOBAL ID

200901034157566954

Research History 11

2025/04 - Present

Tohoku University
2025/04 - Present

東北大学大学院医学系研究科　研究科長特別顧問
2020/04 - Present

東北大学大学院医学系研究科　創生応用医学研究センター　センター長
2013/05 - Present

東北大学大学院医学系研究科　糖尿病代謝・内分泌内科学分野　教授
2013/04 - 2025/04

Tohoku University Hospital　Department of Diabetes, Metabolism and Endocrinology
2010/04 - 2020/03

東北大学大学院医学系研究科代謝疾患医学コアセンター　センター長
2003/01 - 2015/10

東北大学大学院医学系研究科附属創生応用医学研究センター
2001/12 - 2002/12

東北大学病院
2001/09 - 2001/11

東北大学病院
1990/07 - 2001/08

東京大学医学部附属病院　医員非常勤医員
2025/04 -

Tohoku University

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Education 1

The University of Tokyo　Faculty of Medicine　Faculty of Medicine

- 1987/03/31

Committee Memberships 14

日本内科学会　監事

2025/04 - Present
日本肥満学会　理事

2021/10 - Present
日本糖尿病学会東北支部　支部長

2014/05 - Present
日本糖尿病学会　理事

2014/05 - Present
日本内分泌学会　評議員

2012/04 - Present
日本肥満症治療学会　理事

2011/11 - Present
日本糖尿病・肥満動物学会　評議員

2009/02 - Present
日本糖尿病学会　評議員

2003/05 - Present
日本内科学会　理事

2023/04 - 2025/04
日本内科学会　評議員

2013/04 - 2025/04
日本肥満学会　監事

2017/11 - 2021/10
日本内科学会東北支部　支部長

2019/01 - 2021/01
日本動脈硬化学会　評議員

2012/01 -
日本肥満学会　評議員

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Professional Memberships 9

日本糖尿病学会

1989/12 - Present
日本内科学会

1988/05 - Present
アメリカ糖尿病学会
日本肥満症治療学会
日本動脈硬化学会
日本肥満学会
日本分子生物学会
日本内分泌学会
日本糖尿病・肥満動物学会

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Research Interests 7

脂肪肝
遺伝子治療
再生医学
臓器間相互作用
メタボリックシンドローム
肥満
糖尿病、肥満、メタボリックシンドローム、臓器間相互作用、再生医学、遺伝子治療、脂肪肝

Research Areas 1

Life sciences / Metabolism and endocrinology /

Awards 9

日本肥満学会学会賞

2024/10　日本肥満学会
日本糖尿病学会賞ハーゲドーン賞

2020/05　日本糖尿病学会
文部科学大臣表彰科学技術賞（研究部門）

2014/05　文部科学省
日本医師会研究助成費賞

2007/11/01　日本医師会
日本内分泌学会研究奨励賞

2007/06/14　日本内分泌学会
日本糖尿病学会賞リリー賞

2007/05　日本糖尿病学会
日本学術振興会賞

2007/03/02　日本学術振興会
日本内科学会奨励賞

1994/04/14　日本内科学会
第９回日本内科学会研究奨励賞受賞

1994/04　日本内科学会

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Papers 279

Colonic inflammation triggers β cell proliferation during obesity development via a liver-to-pancreas interorgan mechanism Peer-reviewed

Haremaru Kubo, Junta Imai, Tomohito Izumi, Masato Kohata, Yohei Kawana, Akira Endo, Hiroto Sugawara, Junro Seike, Takahiro Horiuchi, Hiroshi Komamura, Toshihiro Sato, Shinichiro Hosaka, Yoichiro Asai, Shinjiro Kodama, Kei Takahashi, Keizo Kaneko, Hideki Katagiri

JCI Insight　10　(9)　e183864-e183864　2025/05/08
Publisher: American Society for Clinical Investigation
DOI： 10.1172/jci.insight.183864 　

eISSN： 2379-3708
Carnitine Deficiency Caused by Salcaprozic Acid Sodium Contained in Oral Semaglutide in a Patient with Multiple Acyl-CoA Dehydrogenase Deficiency Peer-reviewed

Yasuko Mikami-Saito, Masamitsu Maekawa, Masahiro Watanabe, Shinichiro Hosaka, Kei Takahashi, Eriko Totsune, Natsuko Arai-Ichinoi, Atsuo Kikuchi, Shigeo Kure, Hideki Katagiri, Yoichi Wada

International Journal of Molecular Sciences　26　(7)　2962-2962　2025/03/25
Publisher: MDPI AG
DOI： 10.3390/ijms26072962 　

eISSN： 1422-0067

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Carnitine plays an essential role in maintaining energy homeostasis and metabolic flexibility. Various medications, such as pivalate-conjugated antibiotics, valproic acid, and anticancer agents, can induce carnitine deficiency, inhibit the utilization of fatty acid, and contribute to the development of hypoglycemia. No studies have linked oral semaglutide to carnitine deficiency. Herein, we report the case of a 34-year-old male patient with multiple acyl-CoA dehydrogenase deficiency who developed carnitine deficiency attributable to salcaprozic acid sodium (SNAC) in oral semaglutide. The patient was diagnosed with type 2 diabetes mellitus at 32 years of age and was treated with semaglutide injections. Hypoglycemic symptoms appeared after switching to oral semaglutide, and the mean levels of blood-free carnitine significantly decreased. Liquid chromatography–tandem mass spectrometry analysis revealed a peak corresponding to the SNAC–carnitine complex (m/z 423.24) in the urine exclusively during the oral administration of semaglutide. The MS/MS spectra at m/z 423.24 contained peaks consistent with those of the SNAC and carnitine product ions. Our results suggest that through complexation with carnitine, SNAC may induce carnitine deficiency. Healthcare providers should monitor for carnitine deficiency when administering SNAC-containing medications to at-risk individuals. Furthermore, this case can raise more significant concerns about the potential impact of pharmaceutical excipients like SNAC on metabolic pathways.
Role of radiologists in the diagnosis and management of adrenal disorders Peer-reviewed

Sota Oguro, Hiromitsu Tannai, Hideki Ota, Kazumasa Seiji, Hiroki Kamada, Yoshitaka Toyama, Kei Omata, Yuta Tezuka, Yoshikiyo Ono, Fumitoshi Satoh, Sadayoshi Ito, Tetsuhiro Tanaka, Hideki Katagiri, Kei Takase

Endocrine Journal　72　(2)　131-148　2025/02/03
Publisher: Japan Endocrine Society
DOI： 10.1507/endocrj.ej24-0156 　

ISSN： 0918-8959

eISSN： 1348-4540
Rspo3-mediated metabolic liver zonation regulates systemic glucose metabolism and body mass in mice Peer-reviewed

Kenji Uno, Takuya Uchino, Takashi Suzuki, Yohei Sayama, Naoki Edo, Kiyoko Uno-Eder, Koji Morita, Toshio Ishikawa, Miho Koizumi, Hiroaki Honda, Hideki Katagiri, Kazuhisa Tsukamoto

PLOS Biology　23　(1)　e3002955-e3002955　2025/01/24
Publisher: Public Library of Science (PLoS)
DOI： 10.1371/journal.pbio.3002955 　

eISSN： 1545-7885

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The unique architecture of the liver consists of hepatic lobules, dividing the hepatic features of metabolism into 2 distinct zones, namely the pericentral and periportal zones, the spatial characteristics of which are broadly defined as metabolic zonation. R-spondin3 (Rspo3), a bioactive protein promoting the Wnt signaling pathway, regulates metabolic features especially around hepatic central veins. However, the functional impact of hepatic metabolic zonation, regulated by the Rspo3/Wnt signaling pathway, on whole-body metabolism homeostasis remains poorly understood. In this study, we analyze the local functions of Rspo3 in the liver and the remote actions of hepatic Rspo3 on other organs of the body by using murine models. Rspo3 expression analysis shows that Rspo3 expression patterns are spatiotemporally controlled in the murine liver such that it locates in the pericentral zones and converges after feeding, and the dynamics of these processes are disturbed in obesity. We find that viral-mediated induction of Rspo3 in hepatic tissue of obesity improves insulin resistance and prevents body weight gain by restoring attenuated organ insulin sensitivities, reducing adipose tissue enlargement and reversing overstimulated adaptive thermogenesis. Denervation of the hepatic vagus suppresses these remote effects, derived from hepatic Rspo3 induction, toward adipose tissues and skeletal muscle, suggesting that signals are transduced via the neuronal communication consisting of afferent vagal and efferent sympathetic nerves. Furthermore, the non-neuronal inter-organ communication up-regulating muscle lipid utilization is partially responsible for the ameliorations of both fatty liver development and reduced skeletal muscle quality in obesity. In contrast, hepatic Rspo3 suppression through Cre-LoxP-mediated recombination system exacerbates diabetes due to glucose intolerance and insulin resistance, promotes fatty liver development and decreases skeletal muscle quality, resulting in obesity. Taken together, our study results reveal that modulation of hepatic Rspo3 contributes to maintaining systemic glucose metabolism and body composition via a newly identified inter-organ communication mechanism.
Machine learning-based reproducible prediction of type 2 diabetes subtypes Peer-reviewed

Hayato Tanabe, Masahiro Sato, Akimitsu Miyake, Yoshinori Shimajiri, Takafumi Ojima, Akira Narita, Haruka Saito, Kenichi Tanaka, Hiroaki Masuzaki, Junichiro J. Kazama, Hideki Katagiri, Gen Tamiya, Eiryo Kawakami, Michio Shimabukuro

Diabetologia　67　(11)　2446-2458　2024/11
Publisher: Springer Science and Business Media LLC
DOI： 10.1007/s00125-024-06248-8 　

ISSN： 0012-186X

eISSN： 1432-0428

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Abstract Aims/hypothesis Clustering-based subclassification of type 2 diabetes, which reflects pathophysiology and genetic predisposition, is a promising approach for providing personalised and effective therapeutic strategies. Ahlqvist’s classification is currently the most vigorously validated method because of its superior ability to predict diabetes complications but it does not have strong consistency over time and requires HOMA2 indices, which are not routinely available in clinical practice and standard cohort studies. We developed a machine learning (ML) model to classify individuals with type 2 diabetes into Ahlqvist’s subtypes consistently over time. Methods Cohort 1 dataset comprised 619 Japanese individuals with type 2 diabetes who were divided into training and test sets for ML models in a 7:3 ratio. Cohort 2 dataset, comprising 597 individuals with type 2 diabetes, was used for external validation. Participants were pre-labelled (T2D_kmeans) by unsupervised k-means clustering based on Ahlqvist’s variables (age at diagnosis, BMI, HbA_1c, HOMA2-B and HOMA2-IR) to four subtypes: severe insulin-deficient diabetes (SIDD), severe insulin-resistant diabetes (SIRD), mild obesity-related diabetes (MOD) and mild age-related diabetes (MARD). We adopted 15 variables for a multiclass classification random forest (RF) algorithm to predict type 2 diabetes subtypes (T2D_RF15). The proximity matrix computed by RF was visualised using a uniform manifold approximation and projection. Finally, we used a putative subset with missing insulin-related variables to test the predictive performance of the validation cohort, consistency of subtypes over time and prediction ability of diabetes complications. Results T2D_RF15 demonstrated a 94% accuracy for predicting T2D_kmeans type 2 diabetes subtypes (AUCs ≥0.99 and F1 score [an indicator calculated by harmonic mean from precision and recall] ≥0.9) and retained the predictive performance in the external validation cohort (86.3%). T2D_RF15 showed an accuracy of 82.9% for detecting T2D_kmeans, also in a putative subset with missing insulin-related variables, when used with an imputation algorithm. In Kaplan–Meier analysis, the diabetes clusters of T2D_RF15 demonstrated distinct accumulation risks of diabetic retinopathy in SIDD and that of chronic kidney disease in SIRD during a median observation period of 11.6 (4.5–18.3) years, similarly to the subtypes using T2D_kmeans. The predictive accuracy was improved after excluding individuals with low predictive probability, who were categorised as an ‘undecidable’ cluster. T2D_RF15, after excluding undecidable individuals, showed higher consistency (100% for SIDD, 68.6% for SIRD, 94.4% for MOD and 97.9% for MARD) than T2D_kmeans. Conclusions/interpretation The new ML model for predicting Ahlqvist’s subtypes of type 2 diabetes has great potential for application in clinical practice and cohort studies because it can classify individuals with missing HOMA2 indices and predict glycaemic control, diabetic complications and treatment outcomes with long-term consistency by using readily available variables. Future studies are needed to assess whether our approach is applicable to research and/or clinical practice in multiethnic populations. Graphical Abstract
Inter-Organ Communication Involved in Brown Adipose Tissue Thermogenesis

Kei Takahashi, Tetsuya Yamada, Hideki Katagiri

Advances in Experimental Medicine and Biology　161-175　2024/09/18
Publisher: Springer Nature Singapore
DOI： 10.1007/978-981-97-4584-5_11 　

ISSN： 0065-2598

eISSN： 2214-8019
A multicenter, open‐label, single‐arm trial of the long‐term safety of empagliflozin treatment for refractory diabetes mellitus with insulin resistance (<scp>EMPIRE</scp>‐02) Peer-reviewed

Yushi Hirota, Yasumasa Kakei, Junta Imai, Hideki Katagiri, Ken Ebihara, Jun Wada, Junichi Suzuki, Tatsuhiko Urakami, Takashi Omori, Wataru Ogawa

Journal of Diabetes Investigation　15　(9)　1211-1219　2024/09
Publisher: Wiley
DOI： 10.1111/jdi.14226 　

ISSN： 2040-1116

eISSN： 2040-1124

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ABSTRACT Aims/Introduction Insulin resistance syndrome and lipoatrophic diabetes are rare conditions characterized by the development of treatment‐refractory diabetes with severe insulin resistance. We recently conducted a 24 week, multicenter, single‐arm trial (EMPIRE‐01) that demonstrated a certain level of effectiveness and safety of empagliflozin for these conditions. To evaluate treatment safety over a longer period, we have now performed an additional 28 week trial (EMPIRE‐02) that followed on from EMPIRE‐01. Materials and Methods The primary and secondary outcomes were safety and efficacy evaluations, respectively. All eight subjects of the EMPIRE‐01 trial participated in EMPIRE‐02. Results Twenty adverse events (AEs) were recorded among five individuals during the combined 52 week treatment period of both trials. Whereas one case of chronic hepatitis B was moderate in severity, all other AEs were mild. There were thus no serious AEs or events necessitating discontinuation or suspension of treatment or a reduction in drug dose. Whereas ketoacidosis or marked increases in serum ketone body levels were not observed, the mean body mass of the subjects was decreased slightly after completion of EMPIRE‐02. The improvement in mean values of glycemic parameters observed in EMPIRE‐01 was not sustained in EMPIRE‐02, mostly because of one individual whose parameters deteriorated markedly, likely as a result of nonadherence to diet therapy. The improvement in glycemic parameters was sustained during EMPIRE‐02 after exclusion of this subject from analysis. Conclusions Empagliflozin demonstrated a certain level of safety and efficacy for the treatment of insulin resistance syndrome and lipoatrophic diabetes over 52 weeks, confirming its potential as a therapeutic option.
Investigating the cut-off values of captopril challenge test for primary aldosteronism using the novel chemiluminescent enzyme immunoassay method: a retrospective cohort study Peer-reviewed

Yuta Tezuka, Kei Omata, Yoshikiyo Ono, Kengo Kambara, Hiroki Kamada, Sota Oguro, Yuto Yamazaki, Celso E. Gomez-Sanchez, Akihiro Ito, Hironobu Sasano, Kei Takase, Tetsuhiro Tanaka, Hideki Katagiri, Fumitoshi Satoh

Hypertension Research　47　(5)　1362-1371　2024/05
Publisher: Springer Science and Business Media LLC
DOI： 10.1038/s41440-024-01594-x 　

ISSN： 0916-9636

eISSN： 1348-4214

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Abstract The measurement evolution enabled more accurate evaluation of aldosterone production in hypertensive patients. However, the cut-off values for novel assays have been not sufficiently validated. The present study was undertaken to validate the novel chemiluminescent enzyme immunoassay for aldosterone in conjunction with other methods. Moreover, we also aimed to establish a new cut-off value for primary aldosteronism in the captopril challenge test using the novel assay. First, we collected 390 plasma samples, in which aldosterone levels measured using liquid chromatography-mass spectrometry ranged between 0.18 and 1346 ng/dL. The novel chemiluminescent enzyme immunoassay showed identical correlation of plasma aldosterone with liquid chromatography-mass spectrometry, in contrast to conventional radioimmunoassay. Further, we enrolled 299 and 39 patients with primary aldosteronism and essential hypertension, respectively. Plasma aldosterone concentrations measured using the novel assay were lower than those measured by radioimmunoassay, which resulted in decreased aldosterone-to-renin ratios. Subsequently, positive results of the captopril challenge test based on radioimmunoassay turned into “negative” based on the novel assay in 45% patients with primary aldosteronism, using the conventional cut-off value (aldosterone-to-renin activity ratio > 20 ng/dL per ng/mL/h). Receiver operating characteristic curve analysis demonstrated that aldosterone-to-renin activity ratios > 8.2 ng/dL per ng/mL/h in the novel assay was compatible with the conventional diagnosis (sensitivity, 0.874; specificity, 0.980). Our study indicates the great measurement accuracy of the novel chemiluminescent enzyme immunoassay for aldosterone, and the importance of measurement-adjusted cut-offs in the diagnosis of primary aldosteronism.
Screening Cutoff Values for the Detection of Aldosterone-Producing Adenoma by LC-MS/MS and a Novel Noncompetitive CLEIA Peer-reviewed

Yoshikiyo Ono, Yuta Tezuka, Kei Omata, Ryo Morimoto, Yuto Yamazaki, Sota Oguro, Kei Takase, Akihiro Ito, Tatsunari Yoshimi, Satoshi Kojima, Sadayoshi Ito, Hironobu Sasano, Takashi Suzuki, Tetsuhiro Tanaka, Hideki Katagiri, Fumitoshi Satoh

Journal of the Endocrine Society　8　(6)　2024/04/20
Publisher: The Endocrine Society
DOI： 10.1210/jendso/bvae080 　

eISSN： 2472-1972

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Abstract Context Detecting patients with surgically curable aldosterone-producing adenoma (APA) among hypertensive individuals is clinically pivotal. Liquid chromatography–tandem mass spectrometry (LC-MS/MS) is the ideal method of measuring plasma aldosterone concentration (PAC) because of the inaccuracy of conventional chemiluminescent enzyme immunoassay (CLEIA). However, LC-MS/MS is expensive and requires expertise. We have developed a novel noncompetitive CLEIA (NC-CLEIA) for measuring PAC in 30 minutes. Objective This work aimed to validate NC-CLEIA PAC measurements by comparing them with LC-MS/MS measurements and determining screening cutoffs for both measurements detecting APA. Methods We retrospectively measured PAC using LC-MS/MS and NC-CLEIA in 133 patients with APA, 100 with bilateral hyperaldosteronism, and 111 with essential hypertension to explore the accuracy of NC-CLEIA PAC measurements by comparing with LC-MS/MS measurements and determined the cutoffs for detecting APA. Results Passing-Bablok analysis revealed that the values by NC-CLEIA (the regression slope, intercept, and correlation coefficient were 0.962, −0.043, and 0.994, respectively) were significantly correlated and equivalent to those by LC-MS/MS. Bland-Altman plot analysis of NC-CLEIA and LC-MS/MS also demonstrated smaller systemic errors (a bias of −0.348 ng/dL with limits of agreement of −4.390 and 3.694 within a 95% CI) in NC-CLEIA than LC-MS/MS. The receiver operating characteristic analysis demonstrated that cutoff values for aldosterone/renin activity ratio obtained by LC-MS/MS and NC-CLEIA were 31.2 and 31.5 (ng/dL per ng/mL/hour), with a sensitivity of 91.0% and 90.2% and specificity of 75.4% and 76.8%, respectively, to differentiate APA from non-APA. Conclusion This newly developed NC-CLEIA for measuring PAC could serve as a clinically reliable alternative to LC-MS/MS.
A Multicenter, Open-Label, Single-Arm Trial of the Efficacy and Safety of Empagliflozin Treatment for Refractory Diabetes Mellitus with Insulin Resistance (EMPIRE-01) Peer-reviewed

Yushi Hirota, Yasumasa Kakei, Junta Imai, Hideki Katagiri, Ken Ebihara, Jun Wada, Junichi Suzuki, Tatsuhiko Urakami, Takashi Omori, Wataru Ogawa

Diabetes Therapy　15　(2)　533-545　2024/02
Publisher: Springer Science and Business Media LLC
DOI： 10.1007/s13300-023-01526-x 　

ISSN： 1869-6953

eISSN： 1869-6961
Effects of empagliflozin on progression of chronic kidney disease: a prespecified secondary analysis from the empa-kidney trial Peer-reviewed

EMPA-KIDNEY Collaborative Group

The Lancet Diabetes & Endocrinology　12　(1)　39-50　2024/01
Publisher: Elsevier BV
DOI： 10.1016/s2213-8587(23)00321-2 　

ISSN： 2213-8587
Impact of primary kidney disease on the effects of empagliflozin in patients with chronic kidney disease: secondary analyses of the EMPA-KIDNEY trial Peer-reviewed

EMPA-KIDNEY Collaborative Group

The Lancet Diabetes & Endocrinology　12　(1)　51-60　2024/01
Publisher: Elsevier BV
DOI： 10.1016/s2213-8587(23)00322-4 　

ISSN： 2213-8587
Stealthy progression of type 2 diabetes mellitus due to impaired ketone production in an adult patient with multiple acyl-CoA dehydrogenase deficiency. International-journal Peer-reviewed

Nodoka Ikeda, Yoichi Wada, Tomohito Izumi, Yuichiro Munakata, Hideki Katagiri, Shigeo Kure

Molecular genetics and metabolism reports　38　101061-101061　2024/01

DOI： 10.1016/j.ymgmr.2024.101061 　

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BACKGROUND: Multiple acyl-CoA dehydrogenase deficiency (MADD) is an inherited metabolic disorder caused by biallelic pathogenic variants in genes related to the flavoprotein complex. Dysfunction of the complex leads to impaired fatty acid oxidation and ketone body production which can cause hypoketotic hypoglycemia with prolonged fasting. Patients with fatty acid oxidation disorders (FAODs) such as MADD are treated primarily with a dietary regimen consisting of high-carbohydrate foods and avoidance of prolonged fasting. However, information on the long-term sequelae associated with this diet have not been accumulated. In general, high-carbohydrate diets can induce diseases such as type 2 diabetes mellitus (T2DM), although few patients with both MADD and T2DM have been reported. CASE: We present the case of a 32-year-old man with MADD who was on a high-carbohydrate diet for >30 years and exhibited symptoms resembling diabetic ketoacidosis. He presented with polydipsia, polyuria, and weight loss with a decrease in body mass index from 31 to 25 kg/m2 over 2 months. Laboratory tests revealed a HbA1c level of 13.9%; however, the patient did not show metabolic acidosis but only mild ketosis. DISCUSSION/CONCLUSION: This report emphasizes the potential association between long-term adherence to high-carbohydrate dietary therapy and T2DM development. Moreover, this case underscores the difficulty of detecting diabetic ketosis in patients with FAODs such as MADD due to their inability to produce ketone bodies. These findings warrant further research of the long-term complications associated with this diet as well as warning of the potential progression of diabetes in patients with FAODs such as MADD.
Pituitary gland agouti‐related peptide cells: Novel player controlling glucose metabolism Peer-reviewed

Kei Takahashi, Hideki Katagiri

Journal of Diabetes Investigation　15　(1)　67-69　2024/01
Publisher: Wiley
DOI： 10.1111/jdi.14098 　

ISSN： 2040-1116

eISSN： 2040-1124
Inter-organ communication involved in metabolic regulation at the whole-body level Peer-reviewed

Hideki Katagiri

Inflammation and Regeneration　43　(1)　60-60　2023/12
Publisher: Springer Science and Business Media LLC
DOI： 10.1186/s41232-023-00306-1 　

eISSN： 1880-8190

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Abstract Metabolism in each organ of multi-organ organisms, including humans, is regulated in a coordinated manner to dynamically maintain whole-body homeostasis. Metabolic information exchange among organs/tissues, i.e., inter-organ communication, which is necessary for this purpose, has been a subject of ongoing research. In particular, it has become clear that metabolism of energy, glucose, lipids, and amino acids is dynamically regulated at the whole-body level mediated by the nervous system, including afferent, central, and efferent nerves. These findings imply that the central nervous system obtains metabolic information from peripheral organs at all times and sends signals selectively to peripheral organs/tissues to maintain metabolic homeostasis, and that the liver plays an important role in sensing and transmitting information on the metabolic status of the body. Furthermore, the utilization of these endogenous mechanisms is expected to lead to the development of novel preventive/curative therapies for metabolic diseases such as diabetes and obesity. (This is a summarized version of the subject matter presented at Symposium 7 presented at the 43rd Annual Meeting of the Japanese Society of Inflammation and Regeneration.)
Optogenetic stimulation of vagal nerves for enhanced glucose-stimulated insulin secretion and β cell proliferation. International-journal Peer-reviewed

Yohei Kawana, Junta Imai, Yosuke M Morizawa, Yoko Ikoma, Masato Kohata, Hiroshi Komamura, Toshihiro Sato, Tomohito Izumi, Junpei Yamamoto, Akira Endo, Hiroto Sugawara, Haremaru Kubo, Shinichiro Hosaka, Yuichiro Munakata, Yoichiro Asai, Shinjiro Kodama, Kei Takahashi, Keizo Kaneko, Shojiro Sawada, Tetsuya Yamada, Akira Ito, Kuniyasu Niizuma, Teiji Tominaga, Akihiro Yamanaka, Ko Matsui, Hideki Katagiri

Nature biomedical engineering　2023/11/09

DOI： 10.1038/s41551-023-01113-2 　

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The enhancement of insulin secretion and of the proliferation of pancreatic β cells are promising therapeutic options for diabetes. Signals from the vagal nerve regulate both processes, yet the effectiveness of stimulating the nerve is unclear, owing to a lack of techniques for doing it so selectively and prolongedly. Here we report two optogenetic methods for vagal-nerve stimulation that led to enhanced glucose-stimulated insulin secretion and to β cell proliferation in mice expressing choline acetyltransferase-channelrhodopsin 2. One method involves subdiaphragmatic implantation of an optical fibre for the photostimulation of cholinergic neurons expressing a blue-light-sensitive opsin. The other method, which suppressed streptozotocin-induced hyperglycaemia in the mice, involves the selective activation of vagal fibres by placing blue-light-emitting lanthanide microparticles in the pancreatic ducts of opsin-expressing mice, followed by near-infrared illumination. The two methods show that signals from the vagal nerve, especially from nerve fibres innervating the pancreas, are sufficient to regulate insulin secretion and β cell proliferation.
A newly identified compound activating UCP1 inhibits obesity and its related metabolic disorders Peer-reviewed

Ken Onodera, Yutaka Hasegawa, Nozomi Yokota, Shukuko Tamura, Hirofumi Kinno, Iwao Takahashi, Hiraku Chiba, Hirotatsu Kojima, Hideki Katagiri, Koji Nata, Yasushi Ishigaki

Obesity　32　(2)　324-338　2023/11
Publisher: Wiley
DOI： 10.1002/oby.23948 　

ISSN： 1930-7381

eISSN： 1930-739X

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Abstract Objective Promoting thermogenesis in adipose tissue has been a promising strategy against obesity and related metabolic complications. We aimed to identify compounds that promote thermogenesis in adipocytes and to elucidate their functions and roles in metabolism. Methods To identify compounds that directly promote thermogenesis from a structurally diverse set of 4800 compounds, we utilized a cell‐based platform for high‐throughput screening that induces uncoupling protein 1 (Ucp1) expression in adipocytes. Results We identified one candidate compound that activates UCP1. Additional characterization of this compound revealed that it induced cellular thermogenesis in adipocytes with negligible cytotoxicity. In a subsequent diet‐induced obesity model, mice treated with this compound exhibited a slower rate of weight gain, improved insulin sensitivity, and increased energy expenditure. Mechanistic studies have revealed that this compound increases mitochondrial biogenesis by elevating maximal respiration, which is partly mediated by the protein kinase A (PKA)‐p38 mitogen‐activated protein kinase (MAPK) signaling pathway. A further comprehensive genetic analysis of adipocytes treated with these compounds identified two novel UCP1‐dependent thermogenic genes, potassium voltage‐gated channel subfamily C member 2 (Kcnc2) and predicted gene 5627 (Gm5627). Conclusions The identified compound can serve as a potential therapeutic drug for the treatment of obesity and its related metabolic disorders. Furthermore, our newly clarified thermogenic genes play an important role in UCP1‐dependent thermogenesis in adipocytes.
Phagocytosis by macrophages promotes pancreatic β cell mass reduction after parturition in mice Peer-reviewed

Akira Endo, Junta Imai, Tomohito Izumi, Yohei Kawana, Hiroto Sugawara, Masato Kohata, Junro Seike, Haremaru Kubo, Hiroshi Komamura, Toshihiro Sato, Yoichiro Asai, Shinichiro Hosaka, Shinjiro Kodama, Kei Takahashi, Keizo Kaneko, Hideki Katagiri

Developmental Cell　58　(19)　1819-1829　2023/09
Publisher: Elsevier BV
DOI： 10.1016/j.devcel.2023.08.002 　

ISSN： 1534-5807
A case of fulminant type 1 diabetes and protein C deficiency complicated by deep vein thrombosis Peer-reviewed

Masato Kohata, Shinjiro Kodama, Nobuhiro Yaoita, Shinichiro Hosaka, Kei Takahashi, Keizo Kaneko, Junta Imai, Satoshi Yasuda, Hideki Katagiri

Journal of Diabetes Investigation　2023/06/15
Publisher: Wiley
DOI： 10.1111/jdi.14020 　

ISSN： 2040-1116

eISSN： 2040-1124
A highly sensitive strategy for monitoring real-time proliferation of targeted cell types in vivo Peer-reviewed

Hiroto Sugawara, Junta Imai, Junpei Yamamoto, Tomohito Izumi, Yohei Kawana, Akira Endo, Masato Kohata, Junro Seike, Haremaru Kubo, Hiroshi Komamura, Yuichiro Munakata, Yoichiro Asai, Shinichiro Hosaka, Shojiro Sawada, Shinjiro Kodama, Kei Takahashi, Keizo Kaneko, Hideki Katagiri

Nature Communications　14　(1)　2023/06/14
Publisher: Springer Science and Business Media LLC
DOI： 10.1038/s41467-023-38897-5 　

eISSN： 2041-1723

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Abstract Cell proliferation processes play pivotal roles in timely adaptation to many biological situations. Herein, we establish a highly sensitive and simple strategy by which time-series showing the proliferation of a targeted cell type can be quantitatively monitored in vivo in the same individuals. We generate mice expressing a secreted type of luciferase only in cells producing Cre under the control of the Ki67 promoter. Crossing these with tissue-specific Cre-expressing mice allows us to monitor the proliferation time course of pancreatic β-cells, which are few in number and weakly proliferative, by measuring plasma luciferase activity. Physiological time courses, during obesity development, pregnancy and juvenile growth, as well as diurnal variation, of β-cell proliferation, are clearly detected. Moreover, this strategy can be utilized for highly sensitive ex vivo screening for proliferative factors for targeted cells. Thus, these technologies may contribute to advancements in broad areas of biological and medical research.
Impact of COVID‐19 pandemic on behavioral changes and glycemic control and a survey of telemedicine in patients with diabetes: A multicenter retrospective observational study Peer-reviewed

Ryotaro Bouchi, Takehiro Sugiyama, Atsushi Goto, Mitsuru Ohsugi, Narihito Yoshioka, Hideki Katagiri, Tomoya Mita, Yushi Hirota, Hiroshi Ikegami, Munehide Matsuhisa, Eiichi Araki, Hiroki Yokoyama, Masae Minami, Katsuya Yamazaki, Hideaki Jinnouchi, Hiroki Ikeda, Hitomi Fujii, Miyuki Nogawa, Masahiro Kaneshige, Kengo Miyo, Kohjiro Ueki

Journal of Diabetes Investigation　14　(8)　994-1004　2023/05
Publisher: Wiley
DOI： 10.1111/jdi.14027 　

ISSN： 2040-1116

eISSN： 2040-1124

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ABSTRACT Aims/Introduction To investigate whether the COVID‐19 pandemic affected behavioral changes and glycemic control in patients with diabetes and to conduct a survey of telemedicine during the pandemic. Materials and Methods In this retrospective study, a total of 2,348 patients were included from 15 medical facilities. Patients were surveyed about their lifestyle changes and attitudes toward telemedicine. Hemoglobin A1c (HbA1c) levels were compared among before (from June 1 to August 31, 2019) and in the first (from June 1 to August 31, 2020) and in the second (from June 1 to August 31, 2021) year of the pandemic. A survey of physician attitudes toward telemedicine was also conducted. Results The HbA1c levels were comparable between 2019 (7.27 ± 0.97%), 2020 (7.28 ± 0.92%), and 2021 (7.25 ± 0.94%) without statistical difference between each of those 3 years. Prescriptions for diabetes medications increased during the period. The frequency of eating out was drastically reduced (51.7% in 2019; 30.1% in 2020), and physical activity decreased during the pandemic (48.1% in 2019; 41.4% in 2020; 43.3% in 2021). Both patients and physicians cited increased convenience and reduced risk of infection as their expectations for telemedicine, while the lack of physician–patient interaction and the impossibility of consultation and examination were cited as sources of concern. Conclusions Our data suggest that glycemic control did not deteriorate during the COVID‐19 pandemic with appropriate intensification of diabetes treatment in patients with diabetes who continued to attend specialized diabetes care facilities, and that patients and physicians shared the same expectations and concerns about telemedicine.
Inter-organ insulin-leptin signal crosstalk from the liver enhances survival during food shortages Peer-reviewed

Kei Takahashi, Tetsuya Yamada, Shinichiro Hosaka, Keizo Kaneko, Yoichiro Asai, Yuichiro Munakata, Junro Seike, Takahiro Horiuchi, Shinjiro Kodama, Tomohito Izumi, Shojiro Sawada, Kyoko Hoshikawa, Jun Inoue, Atsushi Masamune, Yoshiyuki Ueno, Junta Imai, Hideki Katagiri

Cell Reports　42　(5)　112415-112415　2023/05
Publisher: Elsevier BV
DOI： 10.1016/j.celrep.2023.112415 　

ISSN： 2211-1247
Ketone bodies: A double‐edged sword for mammalian life span Peer-reviewed

Issei Tomita, Hiroaki Tsuruta, Mako Yasuda‐Yamahara, Kosuke Yamahara, Shogo Kuwagata, Yuki Tanaka‐Sasaki, Masami Chin‐Kanasaki, Yukihiro Fujita, Eiichiro Nishi, Hideki Katagiri, Hiroshi Maegawa, Shinji Kume

Aging Cell　22　(6)　e13833-e13833　2023/04
Publisher: Wiley
DOI： 10.1111/acel.13833 　

ISSN： 1474-9718

eISSN： 1474-9726

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Abstract Accumulating evidence suggests health benefits of ketone bodies, and especially for longevity. However, the precise role of endogenous ketogenesis in mammalian life span, and the safety and efficacy of the long‐term exogenous supplementation of ketone bodies remain unclear. In the present study, we show that a deficiency in endogenous ketogenesis, induced by whole‐body Hmgcs2 deletion, shortens life span in mice, and that this is prevented by daily ketone body supplementation using a diet containing 1,3‐butanediol, a precursor of β‐hydroxybutyrate. Furthermore, feeding the 1,3‐butanediol‐containing diet from early in life increases midlife mortality in normal mice, but in aged mice it extends life span and prevents the high mortality associated with atherosclerosis in ApoE‐deficient mice. By contrast, an ad libitum low‐carbohydrate ketogenic diet markedly increases mortality. In conclusion, endogenous ketogenesis affects mammalian survival, and ketone body supplementation may represent a double‐edged sword with respect to survival, depending on the method of administration and health status.
Insulin allergy manifesting soon after COVID-19 vaccination (BNT162b2). Peer-reviewed

Hiroshi Komamura, Yohei Kawana, Junta Imai, Hideki Katagiri

Journal of diabetes investigation　14　(3)　498-499　2022/12/23

DOI： 10.1111/jdi.13969 　

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We experienced a case with insulin allergy which manifested soon after COVID-19 vaccination.
Insulin-like growth factor-1 levels are associated with high comorbidity of metabolic disorders in obese subjects; a Japanese single-center, retrospective-study International-journal Peer-reviewed

Haremaru Kubo, Shojiro Sawada, Michihiro Satoh, Yoichiro Asai, Shinjiro Kodama, Toshihiro Sato, Seitaro Tomiyama, Junro Seike, Kei Takahashi, Keizo Kaneko, Junta Imai, Hideki Katagiri

Scientific Reports　12　(1)　20130-20130　2022/11/22
Publisher: Springer Science and Business Media LLC
DOI： 10.1038/s41598-022-23521-1 　

eISSN： 2045-2322

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Abstract Insulin like growth factor-1 (IGF-1) plays important roles in metabolic functions, especially in adulthood. Additionally, obese subjects are reportedly predisposed to having low absolute IGF-1 levels. However, the prevalence and clinical characteristics of obese subjects with low IGF-1 levels are unknown. We examined 64 obese subjects with a body mass index (BMI) ≥ 35 kg/m², with no history of endocrinological disorders, receiving inpatient care. IGF-1 levels were interpreted based on the IGF-1 standard deviation score (SDS) clinically used and standardized by age and sex (low IGF-1 group; ≤ − 2.0 SDS and standard IGF-1 group; − 2.0 < and < + 2.0 SDS). Notably, 26.6% of the subjects had low IGF-1. Body fat mass and percentage, but not BMI, were significantly higher in the low than in the standard IGF-1 group. Furthermore, natural log-transformed high-sensitivity C-reactive protein, and the frequencies of dyslipidemia and hyperuricemia were higher in the low IGF-1 group. Moreover, among the subjects without diabetes, fasting glucose levels were significantly higher in the low IGF-1 group. Stepwise variable selection procedure revealed body fat percentage to be a parameter most strongly associated with low IGF-1. Thus, low IGF-1 levels may be an important marker of adiposity-associated metabolic disorders in obese patients.
Roles of FoxM1‐driven basal β‐cell proliferation in maintenance of β‐cell mass and glucose tolerance during adulthood Peer-reviewed

Masato Kohata, Junta Imai, Tomohito Izumi, Junpei Yamamoto, Yohei Kawana, Akira Endo, Hiroto Sugawara, Junro Seike, Haremaru Kubo, Hiroshi Komamura, Toshihiro Sato, Shinichiro Hosaka, Yuichiro Munakata, Yoichiro Asai, Shinjiro Kodama, Kei Takahashi, Keizo Kaneko, Hideki Katagiri

Journal of Diabetes Investigation　13　(10)　1666-1676　2022/10
Publisher: Wiley
DOI： 10.1111/jdi.13846 　

ISSN： 2040-1116

eISSN： 2040-1124

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AIMS/INTRODUCTION: Whether basal β-cell proliferation during adulthood is involved in maintaining sufficient β-cell mass, and if so, the molecular mechanism(s) underlying basal β-cell proliferation remain unclear. FoxM1 is a critical transcription factor which is known to play roles in 'adaptive' β-cell proliferation, which facilitates rapid increases in β-cell mass in response to increased insulin demands. Therefore, herein we focused on the roles of β-cell FoxM1 in 'basal' β-cell proliferation under normal conditions and in the maintenance of sufficient β-cell mass as well as glucose homeostasis during adulthood. MATERIALS AND METHODS: FoxM1 deficiency was induced specifically in β-cells of 8-week-old mice, followed by analyzing its short- (2 weeks) and long- (10 months) term effects on β-cell proliferation, β-cell mass, and glucose tolerance. RESULTS: FoxM1 deficiency suppressed β-cell proliferation at both ages, indicating critical roles of FoxM1 in basal β-cell proliferation throughout adulthood. While short-term FoxM1 deficiency affected neither β-cell mass nor glucose tolerance, long-term FoxM1 deficiency suppressed β-cell mass increases with impaired insulin secretion, thereby worsening glucose tolerance. In contrast, the insulin secretory function was not impaired in islets isolated from mice subjected to long-term β-cell FoxM1 deficiency. Therefore, β-cell mass reduction is the primary cause of impaired insulin secretion and deterioration of glucose tolerance due to long-term β-cell FoxM1 deficiency. CONCLUSIONS: Basal low-level proliferation of β-cells during adulthood is important for maintaining sufficient β-cell mass and good glucose tolerance and β-cell FoxM1 underlies this mechanism. Preserving β-cell FoxM1 activity may prevent the impairment of glucose tolerance with advancing age.
Two cases with fulminant type 1 diabetes that developed long after cessation of immune checkpoint inhibitor treatment Peer-reviewed

Satoko Hatayama, Shinjiro Kodama, Yohei Kawana, Sonoko Otake, Daiki Sato, Takahiro Horiuchi, Kei Takahashi, Keizo Kaneko, Junta Imai, Hideki Katagiri

Journal of Diabetes Investigation　13　(8)　1458-1460　2022/08
Publisher: Wiley
DOI： 10.1111/jdi.13807 　

ISSN： 2040-1116

eISSN： 2040-1124

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Various immune-related adverse events (irAEs), including fulminant type 1 diabetes (FT1D), are known to be associated with immune checkpoint inhibitors (ICIs). We experienced two lung adenocarcinoma cases who developed fulminant type 1 diabetes long after discontinuation of ICI therapies. One, a 74-year-old male, received nivolumab and developed fulminant type 1 diabetes 44 days after the last infusion. The other, an 85-year-old male, received atezolizumab and developed fulminant type 1 diabetes 171 days after the last infusion. Clinical ICI treatment guidelines recommend laboratory tests during ICI treatments but the necessity of tests in patients whose ICI therapy has been discontinued is not clearly described. These cases indicate that blood glucose monitoring should be continued at least for several months, and that patients should be informed of the possibility of fulminant type 1 diabetes after ICI discontinuation, because fulminant type 1 diabetes progresses rapidly and can be life-threatening if not promptly recognized.
Association of home and office systolic and diastolic hypertension with glucose metabolism in a general population: the Ohasama study. International-journal Peer-reviewed

Yukako Tatsumi, Michihiro Satoh, Kei Asayama, Takahisa Murakami, Takuo Hirose, Azusa Hara, Megumi Tsubota-Utsugi, Ryusuke Inoue, Masahiro Kikuya, Kyoko Nomura, Hirohito Metoki, Atsushi Hozawa, Hideki Katagiri, Yutaka Imai, Takayoshi Ohkubo

Journal of hypertension　40　(7)　1336-1343　2022/07/01

DOI： 10.1097/HJH.0000000000003145 　

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OBJECTIVE: This study was performed to investigate the association of hypertension subtypes with glucose metabolism among the Japanese general population. METHODS: The study involved 646 residents (mean age: 62.4 years) without treatment for hypertension or a history of diabetes from Ohasama, a rural Japanese community, who underwent an oral glucose tolerance test. Hypertension subtypes [normotension, isolated systolic hypertension (ISH), isolated diastolic hypertension (IDH), and systolic and diastolic hypertension (SDH)] were defined on the basis of home and office SBP and DBP (HBP and OBP, respectively). The estimated means of blood glucose related indices among the groups were compared by analysis of covariance adjusted for possible confounding factors. RESULTS: Blood glucose related indices were not different among the morning HBP-defined hypertension subtypes. Participants with evening HBP-defined ISH had a significantly higher estimated mean BG at 120 min, higher homeostasis model assessment-insulin resistance (HOMA-IR) and lower Matsuda-DeFronzo index than participants with NT (all P < 0.021). Participants with OBP-defined SDH had a significantly higher estimated mean fasting blood glucose; blood glucose at 30, 60 and 120 min; and HOMA-IR and a lower Matsuda-DeFronzo index than participants with NT (all P < 0.0025). CONCLUSION: The blood glucose related indices were different among hypertension subtypes. Participants with evening HBP-defined ISH and OBP-defined SDH had higher blood glucose levels and insulin resistance than participants with correspondingly defined normotension, while those with morning HBP did not. These findings suggest the importance of measuring evening HBP and office blood pressure for early detection of coexisting hypertension and diabetes.
Type 1 Diabetes Mellitus Associated with Nivolumab after Second SARS-CoV-2 Vaccination, Japan International-journal Peer-reviewed

Toshihiro Sato, Shinjiro Kodama, Keizo Kaneko, Junta Imai, Hideki Katagiri

Emerging Infectious Diseases　28　(7)　1518-1520　2022/07
Publisher: Centers for Disease Control and Prevention (CDC)
DOI： 10.3201/eid2807.220127 　

ISSN： 1080-6040

eISSN： 1080-6059

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Recently, along with increasing use of immune checkpoint inhibitors such as nivolumab, the incidence of immune-related adverse events, including type 1 diabetes mellitus, has become a serious problem. We report a patient who had immune checkpoint inhibitor‒associated type 1 diabetes mellitus that developed after a second mRNA-based SARS-CoV-2 vaccination.
New classification and diagnostic criteria for insulin resistance syndrome. Peer-reviewed

Wataru Ogawa, Eiichi Araki, Yasushi Ishigaki, Yushi Hirota, Hiroshi Maegawa, Toshimasa Yamauchi, Tohru Yorifuji, Hideki Katagiri

Diabetology international　13　(2)　337-343　2022/04

DOI： 10.1007/s13340-022-00570-5 　

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This report of a working group established by the Japan Diabetes Society proposes a new classification and diagnostic criteria for insulin resistance syndrome. Insulin resistance syndrome is defined as a condition characterized by severe attenuation of insulin action due to functional impairment of the insulin receptor or its downstream signaling molecules. This syndrome is classified into two types: genetic insulin resistance syndrome, caused by gene abnormalities, and type B insulin resistance syndrome, caused by autoantibodies to the insulin receptor. Genetic insulin resistance syndrome includes type A insulin resistance as well as Donohue and Rabson-Mendenhall syndromes, all of which are caused by abnormalities of the insulin receptor gene; conditions such as SHORT syndrome caused by abnormalities of PIK3R1, which encodes a regulatory subunit of phosphatidylinositol 3-kinase; conditions caused by abnormalities of AKT2, TBC1D4, or PRKCE; and conditions in which a causative gene has not yet been identified. Type B insulin resistance syndrome is characterized by severe impairment of insulin action due to the presence of insulin receptor autoantibodies. Cases in which hypoglycemia alone is induced by autoantibodies that stimulate insulin receptor were not included in Type B insulin resistance syndrome.
New classification and diagnostic criteria for insulin resistance syndrome. Peer-reviewed

Wataru Ogawa, Eiichi Araki, Yasushi Ishigaki, Yushi Hirota, Hiroshi Maegawa, Toshimasa Yamauchi, Tohru Yorifuji, Hideki Katagiri

Endocrine journal　69　(2)　107-113　2022/02/28

DOI： 10.1507/endocrj.EJ21-0725 　

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This report of a working group established by the Japan Diabetes Society proposes a new classification and diagnostic criteria for insulin resistance syndrome. Insulin resistance syndrome is defined as a condition characterized by severe attenuation of insulin action due to functional impairment of the insulin receptor or its downstream signaling molecules. This syndrome is classified into two types: genetic insulin resistance syndrome, caused by gene abnormalities, and type B insulin resistance syndrome, caused by autoantibodies to the insulin receptor. Genetic insulin resistance syndrome includes type A insulin resistance as well as Donohue and Rabson-Mendenhall syndromes, all of which are caused by abnormalities of the insulin receptor gene; conditions such as SHORT syndrome caused by abnormalities of PIK3R1, which encodes a regulatory subunit of phosphatidylinositol 3-kinase; conditions caused by abnormalities of AKT2, TBC1D4, or PRKCE; and conditions in which a causative gene has not yet been identified. Type B insulin resistance syndrome is characterized by severe impairment of insulin action due to the presence of insulin receptor autoantibodies. Cases in which hypoglycemia alone is induced by autoantibodies that stimulate insulin receptor were not included in Type B insulin resistance syndrome.
Regulation of systemic metabolism by the autonomic nervous system consisting of afferent and efferent innervation International-journal Peer-reviewed

Junta Imai, Hideki Katagiri

International Immunology　34　(2)　67-79　2022/01/22
Publisher: Oxford University Press (OUP)
DOI： 10.1093/intimm/dxab023 　

eISSN： 1460-2377

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<title>Abstract</title> Autonomic nerves, sympathetic and parasympathetic, innervate organs and modulate their functions. It has become evident that afferent and efferent signals of the autonomic nervous system play important roles in regulating systemic metabolism, thereby maintaining homeostasis at the whole-body level. Vagal afferent nerves receive signals, such as nutrients and hormones, from the peripheral organs/tissues including the gastrointestinal tract and adipose tissue then transmit these signals to the hypothalamus, thereby regulating feeding behavior. In addition to roles in controlling appetite, areas in the hypothalamus serve as regulatory centers of both sympathetic and parasympathetic efferent fibers. These efferent innervations regulate the functions of peripheral organs/tissues, such as pancreatic islets, adipose tissues and the liver, which play roles in metabolic regulation. Furthermore, recent evidence has unraveled the metabolic regulatory systems governed by autonomic nerve circuits. In these systems, afferent nerves transmit metabolic information from peripheral organs to the central nervous system (CNS) and the CNS thereby regulates the organ functions through the efferent fibers of autonomic nerves. Thus, the autonomic nervous system regulates the homeostasis of systemic metabolism, and both afferent and efferent fibers play critical roles in its regulation. In addition, several lines of evidence demonstrate the roles of the autonomic nervous system in regulating and dysregulating the immune system. This review introduces variety of neuron-mediated inter-organ cross-talk systems and organizes the current knowledge of autonomic control/coordination of systemic metabolism, focusing especially on a liver–brain–pancreatic β-cell autonomic nerve circuit, as well as highlighting the potential importance of connections with the neuronal and immune systems.
The return of individual genomic results to research participants: design and pilot study of Tohoku Medical Megabank Project International-journal Peer-reviewed

Hiroshi Kawame, Akimune Fukushima, Nobuo Fuse, Fuji Nagami, Yoichi Suzuki, Mika Sakurai-Yageta, Jun Yasuda, Yumi Yamaguchi-Kabata, Kengo Kinoshita, Soichi Ogishima, Takako Takai, Shinichi Kuriyama, Atsushi Hozawa, Naoki Nakaya, Tomohiro Nakamura, Naoko Minegishi, Junichi Sugawara, Kichiya Suzuki, Hiroaki Tomita, Akira Uruno, Tomoko Kobayashi, Yayoi Aizawa, Tomoharu Tokutomi, Kayono Yamamoto, Kinuko Ohneda, Shigeo Kure, Yoko Aoki, Hideki Katagiri, Yasushi Ishigaki, Shojiro Sawada, Makoto Sasaki, Masayuki Yamamoto

Journal of Human Genetics　67　(1)　9-17　2022/01
Publisher: Springer Science and Business Media LLC
DOI： 10.1038/s10038-021-00952-8 　

ISSN： 1434-5161

eISSN： 1435-232X

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Certain large genome cohort studies attempt to return the individual genomic results to the participants; however, the implementation process and psychosocial impacts remain largely unknown. The Tohoku Medical Megabank Project has conducted large genome cohort studies of general residents. To implement the disclosure of individual genomic results, we extracted the potential challenges and obstacles. Major challenges include the determination of genes/disorders based on the current medical system in Japan, the storage of results, prevention of misunderstanding, and collaboration of medical professionals. To overcome these challenges, we plan to conduct multilayer pilot studies, which deal with different disorders/genes. We finally chose familial hypercholesterolemia (FH) as a target disease for the first pilot study. Of the 665 eligible candidates, 33.5% were interested in the pilot study and provided consent after an educational "genetics workshop" on the basic genetics and medical facts of FH. The genetics professionals disclosed the results to the participants. All positive participants were referred to medical care, and a serial questionnaire revealed no significant psychosocial distress after the disclosure. Return of genomic results to research participants was implemented using a well-prepared protocol. To further elucidate the impact of different disorders, we will perform multilayer pilot studies with different disorders, including actionable pharmacogenomics and hereditary tumor syndromes.
Dual-specificity phosphatase 8: A gatekeeper in hypothalamic control of glucose metabolism in males. Peer-reviewed

Keizo Kaneko, Hideki Katagiri

Journal of diabetes investigation　12　(7)　1138-1140　2021/07

DOI： 10.1111/jdi.13561 　
Intrahepatic distribution of nerve fibers and alterations due to fibrosis in diseased liver International-journal

Kei Mizuno, Hiroaki Haga, Kazuo Okumoto, Kyoko Hoshikawa, Tomohiro Katsumi, Taketo Nishina, Takafumi Saito, Hideki Katagiri, Yoshiyuki Ueno

PLOS ONE　16　(4)　e0249556-e0249556　2021/04/14
Publisher: Public Library of Science (PLoS)
DOI： 10.1371/journal.pone.0249556 　

eISSN： 1932-6203

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Autonomic nerve fibers in the liver are distributed along the portal tract, being involved in the regulation of blood flow, bile secretion and hepatic metabolism, thus contributing to systemic homeostasis. The present study investigated changes in hepatic nerve fibers in liver biopsy specimens from patients with normal liver, viral hepatitis and non-alcoholic steatohepatitis, in relation to clinical background. The areal ratio of nerve fibers to the total portal area was automatically calculated for each sample. The nerve fiber areal ratios (NFAR) for total nerve fibers and sympathetic nerve fibers were significantly lower in liver affected by chronic hepatitis, particularly viral hepatitis, and this was also the case for advanced liver fibrosis. However, the degree of inflammatory activity did not affect NFAR for either whole nerves or sympathetic nerves. Comparison of samples obtained before and after antiviral treatment for HCV demonstrated recovery of NFAR along with improvement of liver fibrosis.
The Authors' Reply to "Additional Bacteriological Examinations Might be Required for the Correct Identification of Staphylococcus warneri". Peer-reviewed

Junpei Yamamoto, Hideki Katagiri

Internal medicine (Tokyo, Japan)　60　(5)　823-823　2021/03/01

DOI： 10.2169/internalmedicine.6014-20 　
Long-term safety and efficacy of alogliptin, a DPP-4 inhibitor, in patients with type 2 diabetes: a 3-year prospective, controlled, observational study (J-BRAND Registry) International-journal

Kohjiro Ueki, Yukio Tanizawa, Jiro Nakamura, Yuichiro Yamada, Nobuya Inagaki, Hirotaka Watada, Iichiro Shimomura, Rimei Nishimura, Hideaki Miyoshi, Atsuko Abiko, Hideki Katagiri, Michio Hayashi, Akira Shimada, Keiko Naruse, Shimpei Fujimoto, Masazumi Fujiwara, Kenichi Shikata, Yosuke Okada, Eiichi Araki, Tsutomu Yamazaki, Takashi Kadowaki

BMJ Open Diabetes Research & Care　9　(1)　e001787-e001787　2021/01
Publisher: BMJ
DOI： 10.1136/bmjdrc-2020-001787 　

eISSN： 2052-4897

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<sec><title>Introduction</title>Given an increasing use of dipeptidyl peptidase-4 (DPP-4) inhibitors to treat patients with type 2 diabetes mellitus in the real-world setting, we conducted a prospective observational study (Japan-based Clinical Research Network for Diabetes Registry: J-BRAND Registry) to elucidate the safety and efficacy profile of long-term usage of alogliptin. </sec><sec><title>Research design and methods</title>We registered 5969 patients from April 2012 through September 2014, who started receiving alogliptin (group A) or other classes of oral hypoglycemic agents (OHAs; group B), and were followed for 3 years at 239 sites nationwide. Safety was the primary outcome. Symptomatic hypoglycemia, pancreatitis, skin disorders of non-extrinsic origin, severe infections, and cancer were collected as major adverse events (AEs). Efficacy assessment was the secondary outcome and included changes in hemoglobin A1c (HbA1c), fasting blood glucose, fasting insulin and urinary albumin. </sec><sec><title>Results</title>Of the registered, 5150 (group A: 3395 and group B: 1755) and 5096 (3358 and 1738) were included for safety and efficacy analysis, respectively. Group A patients mostly (>90%) continued to use alogliptin. In group B, biguanides were the primary agents, while DPP-4 inhibitors were added in up to ~36% of patients. The overall incidence of AEs was similar between the two groups (42.7% vs 42.2%). Kaplan-Meier analysis revealed the incidence of cancer was significantly higher in group A than in group B (7.4% vs 4.8%, p=0.040), while no significant incidence difference was observed in the individual cancer. Multivariate Cox regression analysis revealed that the imbalanced patient distribution (more elderly patients in group A than in group B), but not alogliptin usage per se, contributed to cancer development. The incidence of other major AE categories was with no between-group difference. Between-group difference was not detected, either, in the incidence of microvascular and macrovascular complications. HbA1c and fasting glucose decreased significantly at the 0.5-year visit and nearly plateaued thereafter in both groups. </sec><sec><title>Conclusions</title>Alogliptin as a representative of DPP-4 inhibitors was safe and durably efficacious when used alone or with other OHAs for patients with type 2 diabetes in the real world setting. </sec>
Continuous glucose monitoring in patients with remission of type 2 diabetes after laparoscopic sleeve gastrectomy without or with duodenojejunal bypass. International-journal Peer-reviewed

Shojiro Sawada, Shinjiro Kodama, Satoko Tsuchiya, Satoko Kurosawa, Akira Endo, Hiroto Sugawara, Shinichiro Hosaka, Yohei Kawana, Yoichiro Asai, Junpei Yamamoto, Yuichiro Munakata, Tomohito Izumi, Kei Takahashi, Keizo Kaneko, Junta Imai, Hirofumi Imoto, Naoki Tanaka, Takeshi Naitoh, Yasushi Ishigaki, Hideki Katagiri

Clinical obesity　10　(6)　e12409　2020/12

DOI： 10.1111/cob.12409 　

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Bariatric surgery is associated with a high remission rate of type 2 diabetes mellitus. However, it is unclear whether patients showing remission of diabetes actually have normal blood glucose levels throughout the day. We therefore performed continuous glucose monitoring (CGM) in 15 ambulatory patients showing remission of diabetes after laparoscopic sleeve gastrectomy (LSG) without or with duodenojejunal bypass (DJB) at the time of diabetic remission (12.9 ± 1.8 months after bariatric surgery). The definition of remission of diabetes was based on the American Diabetes Association criteria. The mean, SD, and coefficient of variation (CV) of glucose calculated from CGM were 6.2 ± 0.6 mmol/L, 1.5 ± 0.4 mmol/L, and 23.7 ± 6.2%, respectively. These values were higher than those of healthy participants without diabetes previously reported. The percentages of time spent above 10.0 mmol/L and below 3.9 mmol/L were 2.6 (IQR 0-5.0)% and 0 (IQR 0-8.0)%, respectively. Thus, patients with remission of diabetes after LSG or LSG/DJB still had substantial periods of hyperglycemia and hypoglycemia throughout the day. Therefore, we must manage patients with diabetes carefully, even after apparent remission of type 2 diabetes in response to bariatric surgery.
Diabetic Muscle Infarction with High Fever. International-journal Peer-reviewed

Keizo Kaneko, Shojiro Sawada, Sonoko Otake, Akira Endo, Junta Imai, Shigehito Miyagi, Takashi Kamei, Hideki Katagiri

The American journal of medicine　133　(10)　e594-e595　2020/10

DOI： 10.1016/j.amjmed.2020.03.021 　
Extraordinarily long-inactive solitary fibrous tumor transformed to produce big insulin-like growth factor-2, leading to hypoglycemia and rapid liposarcoma growth: a case report. International-journal Peer-reviewed

Keizo Kaneko, Shojiro Sawada, Chihiro Satake, Keiichi Kondo, Tomohito Izumi, Mamiko Tanaka, Junta Imai, Tetsuya Yamada, Hiroki Katsushima, Fumiyoshi Fujishima, Hideki Katagiri

BMC endocrine disorders　20　(1)　148-148　2020/09/29

DOI： 10.1186/s12902-020-00624-2 　

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BACKGROUND: A high-molecular-weight form of insulin-like growth factor-2 (IGF-2), known as "big" IGF-2, is occasionally produced by various tumor types, leading to hypoglycemia. Although solitary fibrous tumor (SFT) is a rare mesenchymal neoplasm, it has been estimated that 4-6% of SFT patients develop hypoglycemia due to circulating big IGF-2. The mean time elapsed from tumor detection until the onset of hypoglycemia is reportedly less than one year (8.5 ± 1.9 months). CASE PRESENTATION: A 68-year-old man was hospitalized for exacerbation of recurring hypoglycemic episodes. He had been diagnosed with an SFT 17 years before the onset of hypoglycemia, and the SFT had already been very large at that time. The tumor, which was non-resectable and refractory to chemotherapies, had slowly increased in size since the initial diagnosis. Half a year before the hypoglycemic episodes manifested, another tumor, adjacent to the left kidney, was newly identified. Fluorodeoxyglucose positron emission tomography-computed tomography scanning, revealed the left peri-renal tumor to show much higher fluorodeoxyglucose uptake than the preexisting SFT, suggesting that it was unlikely to be a metastasis from the SFT. Abundant serum big IGF-2 was detected by western immunoblot analysis, indicating it to be the cause of the hypoglycemia. Since the 17 years between SFT detection and the onset of IGF-2-induced hypoglycemia was an extremely long period as compared with those in previous reports, we initially suspected that the new, peri-renal tumor had produced big IGF-2, but transcatheter arterial embolization of its feeding arteries did not suppress hypoglycemia. Notably, by measuring the tumor volume doubling time, the peri-renal tumor growth was shown to be markedly accelerated in parallel with exacerbation of the hypoglycemia. The patient died of heart failure 21 months after the onset of hypoglycemia. Unexpectedly, autopsy revealed that big IGF-2 had been produced only by the preexisting SFT, not the peri-renal tumor, and that the peri-renal tumor was a dedifferentiated liposarcoma. CONCLUSIONS: We should keep in mind that even a long-inactive SFT can undergo transformation to produce big IGF-2, which then acts on both insulin and IGF-1 receptors, possibly leading to both hypoglycemia and the development/growth of another tumor, respectively.
Native Valve Endocarditis due to Staphylococcus warneri Developing in a Patient with Type 1 Diabetes. Peer-reviewed

Junpei Yamamoto, Akira Endo, Hiroto Sugawara, Tomohito Izumi, Kenji Takahashi, Saori Yamamoto, Masatoshi Akiyama, Osamu Adachi, Keizo Kaneko, Shojiro Sawada, Junta Imai, Yoshikatsu Saiki, Hiroaki Shimokawa, Hideki Katagiri

Internal medicine (Tokyo, Japan)　59　(18)　2269-2274　2020/09/15

DOI： 10.2169/internalmedicine.4661-20 　

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A 59-year-old man with type 1 diabetes presented with heart failure. Echocardiography showed large vegetations on the mitral and aortic valves. Blood bacterial culture was positive for Staphylococcus warneri, a coagulase-negative staphylococcus (CoNS) family member. He was diagnosed with native valve endocarditis (NVE) induced by the resident bacteria and ultimately underwent double valve replacement. Retrospectively, slight laboratory data abnormalities and weight loss beginning four months before may have been signs of NVE. He had no history of immunosuppressive therapies or medical device implantation. Thus, CoNS can cause NVE after a long asymptomatic course in patients with poorly controlled diabetes.
Vascular resistance of carotid and vertebral arteries is associated with retinal microcirculation measured by laser speckle flowgraphy in patients with type 2 diabetes mellitus. International-journal Peer-reviewed

Shojiro Sawada, Satoko Tsuchiya, Shinjiro Kodama, Satoko Kurosawa, Akira Endo, Hiroto Sugawara, Shinichiro Hosaka, Yohei Kawana, Yoichiro Asai, Junpei Yamamoto, Yuichiro Munakata, Tomohito Izumi, Kei Takahashi, Keizo Kaneko, Junta Imai, Azusa Ito, Masayuki Yasuda, Hiroshi Kunikata, Toru Nakazawa, Hideki Katagiri

Diabetes research and clinical practice　165　108240-108240　2020/07

DOI： 10.1016/j.diabres.2020.108240 　

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AIMS: Evaluation of the retinal microcirculation is key to understanding retinal vasculopathies, such as diabetic retinopathy. Laser speckle flowgraphy (LSFG) has recently enabled us to directly evaluate the vascular resistance in both retinal vessels and capillaries, non-invasively. We therefore assessed whether retinal vessel blood flow and/or the capillary microcirculation are associated with blood flow in the cervical arteries in diabetic patients without severe retinopathy. METHODS: We enrolled 110 type 2 diabetes patients, with no or mild non-proliferative diabetic retinopathy, in this prospective cross-sectional study. We measured the resistivity indices (RIs) of the retinal vessel and capillaries by LSFG and those of cervical arteries by Doppler ultrasonography, followed by analyzing associations. RESULTS: The RIs of not only the carotid but also vertebral arteries were associated with those of retinal vessel blood flow and the retinal capillary microcirculation. Multiple regression analyses revealed these associations to be independent of other explanatory variables including age and diabetes duration. CONCLUSIONS: We obtained novel and direct evidence demonstrating a close association between the retinal microcirculation and cervical artery hemodynamics in diabetic patients. These findings suggest shared mechanisms to underlie micro- and macro-angiopathies. Thus, high vascular resistance of cervical arteries may be a risk of developing retinopathy.
Inhibition of Plasminogen Activator Inhibitor-1 Activation Suppresses High Fat Diet-Induced Weight Gain via Alleviation of Hypothalamic Leptin Resistance. International-journal Peer-reviewed

Shinichiro Hosaka, Tetsuya Yamada, Kei Takahashi, Takashi Dan, Keizo Kaneko, Shinjiro Kodama, Yoichiro Asai, Yuichiro Munakata, Akira Endo, Hiroto Sugawara, Yohei Kawana, Junpei Yamamoto, Tomohito Izumi, Shojiro Sawada, Junta Imai, Toshio Miyata, Hideki Katagiri

Frontiers in pharmacology　11　943-943　2020/06/24
Publisher: Frontiers Media SA
DOI： 10.3389/fphar.2020.00943 　

eISSN： 1663-9812

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Leptin resistance is an important mechanism underlying the development and maintenance of obesity and is thus regarded as a promising target of obesity treatment. Plasminogen activator inhibitor 1 (PAI-1), a physiological inhibitor of tissue-type and urokinase-type plasminogen activators, is produced at high levels in adipose tissue, especially in states of obesity, and is considered to primarily be involved in thrombosis. PAI-1 may also have roles in inter-organ tissue communications regulating body weight, because PAI-1 knockout mice reportedly exhibit resistance to high fat diet (HFD)-induced obesity. However, the role of PAI-1 in body weight regulation and the underlying mechanisms have not been fully elucidated. We herein studied how PAI-1 affects systemic energy metabolism. We examined body weight and food intake of PAI-1 knockout mice fed normal chow or HFD. We also examined the effects of pharmacological inhibition of PAI-1 activity by a small molecular weight compound, TM5441, on body weight, leptin sensitivities, and expressions of thermogenesis-related genes in brown adipose tissue (BAT) of HFD-fed wild type (WT) mice. Neither body weight gain nor food intake was reduced in PAI-1 KO mice under chow fed conditions. On the other hand, under HFD feeding conditions, food intake was decreased in PAI-1 KO as compared with WT mice (HFD-WT mice 3.98 ± 0.08 g/day vs HFD-KO mice 3.73 ± 0.07 g/day, P = 0.021), leading to an eventual significant suppression of weight gain (HFD-WT mice 40.3 ± 1.68 g vs HFD-KO mice 34.6 ± 1.84 g, P = 0.039). Additionally, TM5441 treatment of WT mice pre-fed the HFD resulted in a marked suppression of body weight gain in a PAI-1-dependent manner (HFD-WT-Control mice 37.6 ± 1.07 g vs HFD-WT-TM5441 mice 33.8 ± 0.97 g, P = 0.017). TM5441 treatment alleviated HFD-induced systemic and hypothalamic leptin resistance, before suppression of weight gain was evident. Moreover, improved leptin sensitivity in response to TM5441 treatment was accompanied by increased expressions of thermogenesis-related genes such as uncoupling protein 1 in BAT (HFD-WT-Control mice 1.00 ± 0.07 vs HFD-WT-TM5441 mice 1.32 ± 0.05, P = 0.002). These results suggest that PAI-1 plays a causative role in body weight gain under HFD-fed conditions by inducing hypothalamic leptin resistance. Furthermore, they indicate that pharmacological inhibition of PAI-1 activity is a potential strategy for alleviating diet-induced leptin resistance in obese subjects.
Dose-response, efficacy, and safety of oral semaglutide monotherapy in Japanese patients with type 2 diabetes (PIONEER 9): a 52-week, phase 2/3a, randomised, controlled trial. International-journal Peer-reviewed

Yuichiro Yamada, Hideki Katagiri, Yoshiyuki Hamamoto, Srikanth Deenadayalan, Andrea Navarria, Keiji Nishijima, Yutaka Seino

The lancet. Diabetes & endocrinology　8　(5)　377-391　2020/05

DOI： 10.1016/S2213-8587(20)30075-9 　

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BACKGROUND: Given the unique phenotype of type 2 diabetes in Japanese patients, novel therapies such as oral semaglutide require evaluation in this population. PIONEER 9 aimed to assess the dose-response of oral semaglutide and to compare the efficacy and safety of oral semaglutide with placebo and a subcutaneous GLP-1 receptor agonist in a Japanese population. METHODS: PIONEER 9 was a 52-week, phase 2/3a, randomised, controlled trial done at 16 sites (clinics and university hospitals) in Japan. Japanese patients aged 20 years or older with uncontrolled type 2 diabetes managed by diet or exercise or with oral glucose-lowering drug monotherapy (washed out) were randomly assigned (1:1:1:1:1) to receive double-blind once-daily oral semaglutide (3 mg, 7 mg, or 14 mg) or placebo, or open-label subcutaneous once-daily liraglutide 0·9 mg. The primary endpoint was change in HbA1c from baseline to week 26 with the trial product (primary) estimand (which assumes all patients remained on trial product without rescue medication use) in all randomly assigned patients. This trial is registered with ClinicalTrials.gov, NCT03018028. FINDINGS: Between Jan 10, and July 11, 2017, 243 patients were randomly assigned to oral semaglutide 3 mg (n=49), 7 mg (n=49), or 14 mg (n=48), or placebo (n=49), or to liraglutide 0·9 mg (n=48). Changes in HbA1c from baseline (mean 8·2%) to week 26 were dose-dependent with oral semaglutide (mean change -1·1% [SE 0·1] for oral semaglutide 3 mg, -1·5% [0·1] for 7 mg, and -1·7% [0·1] for 14 mg), -0·1% (0·1) with placebo, and -1·4% (0·1) with liraglutide 0·9 mg. Estimated treatment differences for change in HbA1c compared with placebo were -1·1 percentage points (95% CI -1·4 to -0·8; p<0·0001) for oral semaglutide 3 mg, -1·5 percentage points (-1·7 to -1·2; p<0·0001) for oral semaglutide 7 mg, and -1·7 percentage points (-2·0 to -1·4; p<0·0001) for oral semaglutide 14 mg. Estimated treatment differences for change in HbA1c compared with liraglutide 0·9 mg were 0·3 percentage points (95% CI -0·0 to 0·6; p=0·0799) for oral semaglutide 3 mg, -0·1 percentage points (-0·4 to 0·2; p=0·3942) for oral semaglutide 7 mg, and -0·3 percentage points (-0·6 to -0·0; p=0·0272) for oral semaglutide 14 mg. Gastrointestinal events, predominantly of mild or moderate severity, were the most frequently reported class of adverse event with oral semaglutide: constipation was most common, occurring in five to six (10-13%) patients with oral semaglutide, three (6%) with placebo, and nine (19%) with liraglutide 0·9 mg. INTERPRETATION: This study showed that oral semaglutide provides significant reductions in HbA1c compared with placebo in a dose-dependent manner in Japanese patients with type 2 diabetes, and has a safety profile consistent with that of GLP-1 receptor agonists. FUNDING: Novo Nordisk.
Clinical characteristics of insulin resistance syndromes: A nationwide survey in Japan. Peer-reviewed

Takehito Takeuchi, Yasushi Ishigaki, Yushi Hirota, Yutaka Hasegawa, Tohru Yorifuji, Hiroko Kadowaki, Takashi Akamizu, Wataru Ogawa, Hideki Katagiri

Journal of diabetes investigation　11　(3)　603-616　2020/05

DOI： 10.1111/jdi.13171 　

ISSN： 2040-1116

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AIMS/INTRODUCTION: Insulin resistance syndrome (IRS) of type A or B is triggered by gene abnormalities of or autoantibodies to the insulin receptor, respectively. Rabson-Mendenhall/Donohue syndrome is also caused by defects of the insulin receptor gene (INSR), but is more serious than type A IRS. Here, we carried out a nationwide survey of these syndromes in Japan. MATERIALS AND METHODS: We sent questionnaires to a total of 1,957 academic councilors or responsible individuals at certified facilities of the Japan Diabetes Society, as well as at the department pediatrics or neonatology in medical centers with >300 beds. RESULTS: We received 904 responses with information on 23, 30 and 10 cases of type A or B IRS and Rabson-Mendenhall/Donohue syndrome, respectively. Eight cases with type A IRS-like clinical features, but without an abnormality of INSR, were tentatively designated type X IRS, with five of these cases testing positive for PIK3R1 mutations. Fasting serum insulin levels at diagnosis (mean ± standard deviation) were 132.0 ± 112.4, 1122.1 ± 3292.5, 2895.5 ± 3181.5 and 145.0 ± 141.4 μU/mL for type A IRS, type B IRS, Rabson-Mendenhall/Donohue syndrome and type X IRS, respectively. Type A and type X IRS, as well as Rabson-Mendenhall/Donohue syndrome were associated with low birthweight. Type B IRS was diagnosed most frequently in older individuals, and was often associated with concurrent autoimmune conditions and hypoglycemia. CONCLUSIONS: Information yielded by this first nationwide survey should provide epidemiological insight into these rare conditions and inform better healthcare for affected patients.
Laparoscopic Sleeve Gastrectomy on Severe Obesity after Intracranial Germinoma Treatment: A Case Report. Peer-reviewed

Masahiro Nezu, Masataka Kudo, Yoshikiyo Ono, Yuta Tezuka, Ryo Morimoto, Shojiro Sawada, Hirofumi Imoto, Takeshi Naitoh, Hideki Katagiri, Sadayoshi Ito, Fumitoshi Satoh

The Tohoku journal of experimental medicine　249　(3)　223-229　2019/11

DOI： 10.1620/tjem.249.223 　

ISSN： 0040-8727

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Hypothalamic obesity is a clinical syndrome characterized by severe and refractory obesity that is caused by hypothalamic function impairment. Recently, bariatric surgery has been attempted for patients with hypothalamic obesity after craniopharyngioma, but experiences have not yet been accumulated in other hypothalamic disorders. Here, we report the case of a 39-year-old male patient with panhypopituitarism who received laparoscopic sleeve gastrectomy (LSG) after intracranial germinoma treatment. The patient was diagnosed with intracranial germinoma at age 15 and achieved complete remission after radiotherapy (total 50 Gy). He was obese during diagnosis [body mass index (BMI), 29.2 kg/m2], and his obesity gradually worsened after the intracranial germinoma treatment, and LSG was considered when his BMI was 48.6 kg/m2. After 1 month of hospitalized diet-exercise program, LSG was performed. After LSG, his BMI gradually decreased and reached 38.8 kg/m2 on the day of discharge (6 weeks after the surgery). Five months after LSG, his insulin resistance improved, but insulin hypersecretion remained. Fifteen months after the surgery, his BMI was 31.2 kg/m2, with marked decrease in visceral and subcutaneous fat areas (from 393.8 cm2 and 168.2 cm2 before the surgery to 111.5 cm2 and 56.3 cm2, respectively.). To our knowledge, this is the first case of LSG for hypothalamic obesity after intracranial germinoma treatment. Although the pathophysiology of hypothalamic obesity is different from that of primary obesity, LSG could be a successful therapeutic choice for patients with hypothalamic obesity after the intracranial germinoma treatment.
Diabetes Care Providers' Manual for Disaster Diabetes Care. Peer-reviewed

Jo Satoh, Koichi Yokono, Rie Ando, Toshinari Asakura, Kazuhiko Hanzawa, Yasushi Ishigaki, Takashi Kadowaki, Masato Kasuga, Hideki Katagiri, Yasuhisa Kato, Koreyuki Kurosawa, Masanobu Miura, Jiro Nakamura, Koichi Nishitsuka, Susumu Ogawa, Tomoko Okamoto, Sadanori Sakuma, Shigeru Sakurai, Hiroaki Satoh, Hidetoshi Shimauchi, Hiroaki Shimokawa, Wataru Shoji, Takashi Sugiyama, Akira Suwabe, Masahiro Tachi, Kazuma Takahashi, Susumu Takahashi, Yasuo Terayama, Hiroaki Tomita, Yoko Tsuchiya, Hironori Waki, Tsuyoshi Watanabe, Kazuaki Yahata, Hidetoshi Yamashita

Journal of diabetes investigation　10　(4)　1118-1142　2019/07

DOI： 10.1111/jdi.13053 　

ISSN： 2040-1116

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To ensure that experiences and lessons learned from the unprecedented 2011 Great East Japan Earthquake are used to improve future disaster planning, the Japan Diabetes Society (JDS) launched the "Research and Survey Committee for Establishing Disaster Diabetes Care Systems Based on Relevant Findings from the Great East Japan Earthquake" under the supervision of the Chairman of the JDS. The Committee conducted a questionnaire survey among patients with diabetes, physicians, disaster medical assistance teams (DMATs), nurses, pharmacists, and nutritionists in disaster areas about the events they saw happening, the situations they found difficult to handle, and the needs that they felt required to be met during the 2011 Great East Japan Earthquake. A total of 3,481 completed questionnaires were received. Based on these and other experiences and lessons reported following the 2011 Great East Japan Earthquake and the 2004 Niigata-Chuetsu Earthquakes, the current "Manual for Disaster Diabetes Care" has been developed by the members of the Committee and other invited authors from relevant specialties. To our knowledge, the current Manual is the world's first to focus on emergency diabetes care, with this digest English version translated from the Japanese original. It is sincerely hoped that patients with diabetes and healthcare providers around the world will find this manual helpful in promoting disaster preparedness and implementing disaster relief.
Diabetes care providers' manual for disaster diabetes care. Peer-reviewed

Jo Satoh, Koichi Yokono, Rie Ando, Toshinari Asakura, Kazuhiko Hanzawa, Yasushi Ishigaki, Takashi Kadowaki, Masato Kasuga, Hideki Katagiri, Yasuhisa Kato, Koreyuki Kurosawa, Masanobu Miura, Jiro Nakamura, Koichi Nishitsuka, Susumu Ogawa, Tomoko Okamoto, Sadanori Sakuma, Shigeru Sakurai, Hiroaki Satoh, Hidetoshi Shimauchi, Hiroaki Shimokawa, Wataru Shoji, Takashi Sugiyama, Akira Suwabe, Masahiro Tachi, Kazuma Takahashi, Susumu Takahashi, Yasuo Terayama, Hiroaki Tomita, Yoko Tsuchiya, Hironori Waki, Tsuyoshi Watanabe, Kazuaki Yahata, Hidetoshi Yamashita

Diabetology international　10　(3)　153-179　2019/07

DOI： 10.1007/s13340-019-00397-7 　

ISSN： 2190-1678

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To ensure that experiences and lessons learned from the unprecedented 2011 Great East Japan Earthquake are used to improve future disaster planning, the Japan Diabetes Society (JDS) launched the "Research and Survey Committee for Establishing Disaster Diabetes Care Systems Based on Relevant Findings from the Great East Japan Earthquake" under the supervision of the Chairman of the JDS. The Committee conducted a questionnaire survey among patients with diabetes, physicians, disaster medical assistance teams (DMATs), nurses, pharmacists, and nutritionists in disaster areas about the events they saw happening, the situations they found difficult to handle, and the needs that they felt required to be met during the 2011 Great East Japan Earthquake. A total of 3,481 completed questionnaires were received. Based on these and other experiences and lessons reported following the 2011 Great East Japan Earthquake and the 2004 Niigata-Chuetsu Earthquakes, the current "Manual for Disaster Diabetes Care" has been developed by the members of the Committee and other invited authors from relevant specialties. To our knowledge, the current Manual is the world's first to focus on emergency diabetes care, with this digest English version translated from the Japanese original. It is sincerely hoped that patients with diabetes and healthcare providers around the world will find this manual helpful in promoting disaster preparedness and implementing disaster relief.
Branched chain amino acids are associated with the heterogeneity of the area of lipid droplets in hepatocytes of patients with non-alcoholic fatty liver disease. International-journal Peer-reviewed

Kakazu E, Sano A, Morosawa T, Inoue J, Ninomiya M, Iwata T, Nakamura T, Takai S, Sawada S, Katagiri H, Shimosegawa T, Masamune A

Hepatology research : the official journal of the Japan Society of Hepatology　49　(8)　860-871　2019/04

DOI： 10.1111/hepr.13346 　

ISSN： 1386-6346

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AIM: Macrovesicular steatosis around the central vein (zone 3) is one of the pathological features of non-alcoholic fatty liver disease or steatohepatitis (NAFLD/NASH). The aim of this study is to elucidate precisely the association between the area of lipid droplets (LDs) and the plasma metabolic parameters in patients with NAFLD/NASH. METHODS: Eighty patients with NAFLD/NASH diagnosed by needle biopsy were enrolled. The LDs around zone 3 were counted automatically by image processing software, the total area of LDs (TLDs), the maximum area of LDs (MAXLDs), the average area of LDs (AVELDs) and the heterogeneity by the coefficient of variation (CV [%]) were quantified. The correlations between these values and plasma metabolic parameters were analyzed. We evaluated the association between branched chain amino acids (BCAAs) and the heterogeneity of LDs in hepatocytes in vitro and in vivo. RESULTS: The MAXLDs was significantly correlated with more metabolic parameters than AVELDs and TLDs. The level of BCAAs was independently associated with the CV among the metabolic parameters. In early stage NAFLD, aspartate and alanine aminotransferase were significantly higher in the high CV group than in the low CV group. The high concentration of BCAAs increased the CV of LDs in hepatocytes accompanied by the expression of phosphor-p70 S6 kinase and sterol regulatory element-binding protein 1 in vitro. A high BCAA diet induced high heterogeneity of LDs around zone 3 in ob/ob mice. CONCLUSIONS: The levels of BCAAs were associated with the LD heterogeneity of hepatocytes around zone 3 in patients with NAFLD/NASH.
Prolyl Isomerase Pin1 Suppresses Thermogenic Programs in Adipocytes by Promoting Degradation of Transcriptional Co-activator PRDM16. International-journal Peer-reviewed

Yusuke Nakatsu, Yasuka Matsunaga, Takeshi Yamamotoya, Koji Ueda, Masa-Ki Inoue, Yu Mizuno, Mikako Nakanishi, Tomomi Sano, Yosuke Yamawaki, Akifumi Kushiyama, Hideyuki Sakoda, Midori Fujishiro, Akihide Ryo, Hiraku Ono, Tohru Minamino, Shin-Ichiro Takahashi, Haruya Ohno, Masayasu Yoneda, Kei Takahashi, Hisamitsu Ishihara, Hideki Katagiri, Fusanori Nishimura, Takashi Kanematsu, Tetsuya Yamada, Tomoichiro Asano

Cell reports　26　(12)　3221-3230　2019/03/19

DOI： 10.1016/j.celrep.2019.02.066 　

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Non-shivering thermogenesis in adipocytes provides defense against low temperatures and obesity development, but the underlying regulatory mechanism remains to be fully clarified. Based on both markedly increased Pin1 expression in states of excess nutrition and resistance to obesity development in Pin1 null mice, we speculated that adipocyte Pin1 may play a role in thermogenic programs. Adipose-specific Pin1 knockout (adPin1 KO) mice showed enhanced transcription of thermogenic genes and tolerance to hypothermia when exposed to cold. In addition, adPin1 KO mice were resistant to high-fat diet-induced obesity and glucose intolerance. A series of experiments revealed that Pin1 binds to PRDM16 and thereby promotes its degradation through the ubiquitin-proteasome system. Consistent with these results, Pin1 deletion in differentiated adipocytes showed enhancement of thermogenic programs in response to the β3 agonist CL316243 through the upregulation of PRDM16 proteins. These observations indicate that Pin1 is a negative regulator of non-shivering thermogenesis.
Liver Transplantation for Homozygous Familial Hypercholesterolemia. Peer-reviewed

Ishigaki Y, Kawagishi N, Hasegawa Y, Sawada S, Katagiri H, Satomi S, Oikawa S

Journal of atherosclerosis and thrombosis　26　(2)　121-127　2019/02

DOI： 10.5551/jat.RV17029 　

ISSN： 1340-3478
Eruptive xanthomas in a patient with soft-drink diabetic ketosis and apolipoprotein E4/2. Peer-reviewed

Tsuchiya S, Sawada S, Takeda K, Takahashi K, Nakajima T, Kohata M, Kurosawa S, Satake C, Imai J, Kikuchi K, Aiba S, Katagiri H

Endocrine journal　66　(1)　107-114　2019/01

DOI： 10.1507/endocrj.EJ18-0356 　

ISSN： 0918-8959
Enhancement of postprandial endogenous insulin secretion rather than exogenous insulin injection ameliorated insulin antibody-induced unstable diabetes: a case report. Peer-reviewed

Kaneko K, Satake C, Izumi T, Tanaka M, Yamamoto J, Asai Y, Sawada S, Imai J, Yamada T, Katagiri H

BMC endocrine disorders　19　(1)　5　2019/01

DOI： 10.1186/s12902-018-0326-3 　
The Relationship between Carotid Intima-Media Thickness and Ocular Circulation in Type-2 Diabetes. International-journal Peer-reviewed

Kohei Ichinohasama, Hiroshi Kunikata, Azusa Ito, Masayuki Yasuda, Shojiro Sawada, Keiichi Kondo, Chihiro Satake, Hideki Katagiri, Toru Nakazawa

Journal of ophthalmology　2019　3421305-3421305　2019

DOI： 10.1155/2019/3421305 　

ISSN： 2090-004X

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Purpose: To compare clinical findings, including ocular blood flow and intima-media thickness (IMT) of the carotid artery, in mild nonproliferative diabetic retinopathy (NPDR) and no diabetic retinopathy (NDR) patients, and to determine risk factors contributing to mild NPDR. Methods: In 129 subjects (129 eyes) with type-2 diabetes patients and mild NPDR or NDR, standard statistical techniques were used to determine associations between clinical findings, including diabetes duration, blood levels of creatinine and hemoglobin A1c (HbA1c), central macular thickness (CMT; measured with optical coherence tomography), mean blur rate (MBR; measured with laser speckle flowgraphy), and ultrasound-measured carotid IMT. Results: Diabetes duration, IMT, and CMT were significantly higher in the mild NPDR patients than the NDR patients (P=0.004, P=0.004, and P=0.003, respectively), while conversely, MBR in the overall optic nerve head (MBR-A) was lower in the mild NPDR patients. Furthermore, a logistic regression analysis showed that diabetes duration (OR, 1.11; P=0.006), diastolic blood pressure (OR, 0.93; P=0.025), heart rate (OR, 1.07; P=0.004), IMT (OR, 8.65; P=0.005), and CMT (OR, 1.03; P=0.007) were independent contributing factors to mild NPDR. Spearman's rank correlation test also showed that IMT was negatively correlated with MBR-A (P=0.011). Conclusions: Increased IMT showed a close association with ocular ischemia in patients with type-2 diabetes and contributed to the presence of mild NPDR. These findings suggest that IMT may be an early biomarker of mild NPDR.
Glial Fatty Acid-Binding Protein 7 (FABP7) Regulates Neuronal Leptin Sensitivity in the Hypothalamic Arcuate Nucleus. International-journal Peer-reviewed

Yuki Yasumoto, Hirofumi Miyazaki, Masaki Ogata, Yoshiteru Kagawa, Yui Yamamoto, Ariful Islam, Tetsuya Yamada, Hideki Katagiri, Yuji Owada

Molecular neurobiology　55　(12)　9016-9028　2018/12

DOI： 10.1007/s12035-018-1033-9 　

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The hypothalamus is involved in the regulation of food intake and energy homeostasis. The arcuate nucleus (ARC) and median eminence (ME) are the primary hypothalamic sites that sense leptin and nutrients in the blood, thereby mediating food intake. Recently, studies demonstrating a role for non-neuronal cell types, including astrocytes and tanycytes, in these regulatory processes have begun to emerge. However, the molecular mechanisms involved in these activities remain largely unknown. In this study, we examined in detail the localization of fatty acid-binding protein 7 (FABP7) in the hypothalamic ARC and sought to determine its role in the hypothalamus. We performed a phenotypic analysis of diet-induced FABP7 knockout (KO) obese mice and of FABP7 KO mice treated with a single leptin injection. Immunohistochemistry revealed that FABP7+ cells are NG2+ or GFAP+ in the ARC and ME. In mice fed a high-fat diet, weight gain and food intake were lower in FABP7 KO mice than in wild-type (WT) mice. FABP7 KO mice also had lower food intake and weight gain after a single injection of leptin, and we consistently confirmed that the number of pSTAT3+ cells in the ARC indicated that the leptin-induced activation of neurons was significantly more frequent in FABP7 KO mice than in WT mice. In FABP7 KO mice-derived primary astrocyte cultures, the level of ERK phosphorylation was lower after leptin treatment. Collectively, these results indicate that in hypothalamic astrocytes, FABP7 might be involved in sensing neuronal leptin via glia-mediated mechanisms and plays a pivotal role in controlling systemic energy homeostasis.
Vagus-macrophage-hepatocyte link promotes post-injury liver regeneration and whole-body survival through hepatic FoxM1 activation. International-journal Peer-reviewed

Izumi T, Imai J, Yamamoto J, Kawana Y, Endo A, Sugawara H, Kohata M, Asai Y, Takahashi K, Kodama S, Kaneko K, Gao J, Uno K, Sawada S, Kalinichenko VV, Ishigaki Y, Yamada T, Katagiri H

Nature communications　9　(1)　5300-5300　2018/12

DOI： 10.1038/s41467-018-07747-0 　

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The liver possesses a high regenerative capacity. Liver regeneration is a compensatory response overcoming disturbances of whole-body homeostasis provoked by organ defects. Here we show that a vagus-macrophage-hepatocyte link regulates acute liver regeneration after liver injury and that this system is critical for promoting survival. Hepatic Foxm1 is rapidly upregulated after partial hepatectomy (PHx). Hepatic branch vagotomy (HV) suppresses this upregulation and hepatocyte proliferation, thereby increasing mortality. In addition, hepatic FoxM1 supplementation in vagotomized mice reverses the suppression of liver regeneration and blocks the increase in post-PHx mortality. Hepatic macrophage depletion suppresses both post-PHx Foxm1 upregulation and remnant liver regeneration, and increases mortality. Hepatic Il-6 rises rapidly after PHx and this is suppressed by HV, muscarinic blockade or resident macrophage depletion. Furthermore, IL-6 neutralization suppresses post-PHx Foxm1 upregulation and remnant liver regeneration. Collectively, vagal signal-mediated IL-6 production in hepatic macrophages upregulates hepatocyte FoxM1, leading to liver regeneration and assures survival.
Deficient ganglioside synthesis restores responsiveness to leptin and melanocortin signaling in obese KKAy mice. International-journal Peer-reviewed

Kei-Ichiro Inamori, Hideki Ito, Yumi Tamura, Takahiro Nitta, Xiaohua Yang, Wataru Nihei, Fumi Shishido, Susumu Imazu, Sohei Tsukita, Tetsuya Yamada, Hideki Katagiri, Jin-Ichi Inokuchi

Journal of lipid research　59　(8)　1472-1481　2018/08

DOI： 10.1194/jlr.M085753 　

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GM3, a precursor for synthesis of a- and b-series gangliosides, is elevated in adipocytes of obese model animals and in sera of obese human patients with type 2 diabetes and/or dyslipidemia. GM3 synthase (GM3S)-KO C57BL/6 mice display enhanced insulin sensitivity and reduced development of high-fat diet-induced insulin resistance. However, the pathophysiological roles of GM3 and related gangliosides in the central control of feeding and metabolism remain unclear. We found that a mouse model (KKAy GM3S KO) generated by KO of the GM3S gene in the yellow obese strain, KKAy, displayed significant amelioration of obese phenotype. Whereas KKAy mice were hyperphagic and developed severe obesity, KKAy GM3S KO mice had significantly lower body weight and food intake, and greater glucose and insulin tolerance. The hypothalamic response to intraperitoneal administration of leptin was greatly reduced in KKAy mice, but was retained in KKAy GM3S KO mice. In studies of a cultured mouse hypothalamic neuronal cell line, enhanced leptin-dependent phosphorylation of ERK was observed in GM3S-deficient cells. Furthermore, KKAy GM3S KO mice did show altered coat color, suggesting that GM3S is also involved in melanocortin signaling. Our findings, taken together, indicate that GM3-related gangliosides play key roles in leptin and melanocortin signaling.
Selective insulin resistance with differential expressions of IRS-1 and IRS-2 in human NAFLD livers Peer-reviewed

Midori Honma, Shojiro Sawada, Yoshiyuki Ueno, Keigo Murakami, Tetsuya Yamada, Junhong Gao, Shinjiro Kodama, Tomohito Izumi, Kei Takahashi, Sohei Tsukita, Kenji Uno, Junta Imai, Eiji Kakazu, Yasuteru Kondo, Kei Mizuno, Naoki Kawagishi, Tooru Shimosegawa, Hideki Katagiri

International Journal of Obesity　1-12　2018/05/01
Publisher: Nature Publishing Group
DOI： 10.1038/s41366-018-0062-9 　

ISSN： 1476-5497 0307-0565
Serum cystatin C level is associated with carotid arterial wall elasticity in subjects with type 2 diabetes mellitus: A potential marker of early-stage atherosclerosis Peer-reviewed

Rei Kaneko, Shojiro Sawada, Ai Tokita, Rieko Honkura, Noriko Tamura, Shinjiro Kodama, Tomohito Izumi, Kei Takahashi, Kenji Uno, Junta Imai, Tetsuya Yamada, Yukiya Miyachi, Hideyuki Hasegawa, Hiroshi Kanai, Yasushi Ishigaki, Hideki Katagiri

Diabetes Research and Clinical Practice　139　43-51　2018/05/01
Publisher: Elsevier Ireland Ltd
DOI： 10.1016/j.diabres.2018.02.003 　

ISSN： 1872-8227 0168-8227

eISSN： 1872-8227
Myriad mysteries of glucose homeostasis Peer-reviewed

Hideki Katagiri

Diabetology International　9　(1)　46-47　2018/02/01
Publisher: Springer Tokyo
DOI： 10.1007/s13340-018-0343-5 　

ISSN： 2190-1686 2190-1678
The Relationship between Peripheral Nerve Conduction Velocity and Ophthalmological Findings in Type 2 Diabetes Patients with Early Diabetic Retinopathy. International-journal Peer-reviewed

Azusa Ito, Hiroshi Kunikata, Masayuki Yasuda, Shojiro Sawada, Keiichi Kondo, Chihiro Satake, Kazuki Hashimoto, Naoko Aizawa, Hideki Katagiri, Toru Nakazawa

Journal of ophthalmology　2018　2439691-2439691　2018

DOI： 10.1155/2018/2439691 　

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Purpose: Nerve conduction velocity (NCV) is an indicator of neuronal damage in the distal segment of the peripheral nerves. Here, we determined the association between NCV and other systemic and ocular clinical findings, in type 2 diabetes patients with early diabetic retinopathy (DR). Methods: This study included 42 eyes of 42 type 2 diabetes patients (median age: 54 years) with no DR or with mild nonproliferative DR. Standard statistical techniques were used to determine associations between clinical findings. Results: Sural sensory conduction velocity (SCV) and tibial motor conduction velocity (MCV) were significantly lower in mild nonproliferative DR patients than patients with no DR (P = 0.008 and P = 0.01, resp.). Furthermore, logistic regression analyses revealed that sural SCV and tibial MCV were independent factors contributing to the presence of mild nonproliferative DR (OR 0.83, P = 0.012 and OR 0.69 P = 0.02, resp.). Tibial MCV was correlated with choroidal thickness (CT) (P = 0.01), and a multiple regression analysis revealed that age, tibial MCV, and carotid intima-media thickness were independent associating factors with CT (P = 0.035, P = 0.015, and P = 0.008, resp.). Conclusions: Our findings suggest that reduced NCV may be closely associated with early DR in type 2 diabetes patients. Thus, reduced nerve conduction is a potential early biomarker of DR.
Selective insulin resistance with differential expressions of IRS-1 and IRS-2 in human NAFLD livers Peer-reviewed

Honma M, Sawada S, Ueno Y, Murakami K, Yamada T, Gao J, Kodama S, Izumi T, Takahashi K, Tsukita S, Uno K, Imai J, Kakazu E, Kondo Y, Mizuno K, Kawagishi N, Shimosegawa T, Katagiri H

Int J Obes (Lond)　42　(9)　1544-1555　2018

DOI： 10.1038/s41366-018-0062-9. 　
Olfactory receptors are expressed in pancreatic β-cells and promote glucose-stimulated insulin secretion. Peer-reviewed

Munakata Y, Yamada T, Imai J, Takahashi K, Tsukita S, Shirai Y, Kodama S, Asai Y, Sugisawa T, Chiba Y, Kaneko K, Uno K, Sawada S, Hatakeyama H, Kanzaki M, Miyazaki J-I, Oka Y, Katagiri H

Sci Rep　8　(1)　1499-1499　2018

DOI： 10.1038/s41598-018-19765-5. 　
Neuronal signals regulate obesity induced beta-cell proliferation by FoxM1 dependent mechanism Peer-reviewed

Junpei Yamamoto, Junta Imai, Tomohito Izumi, Hironori Takahashi, Yohei Kawana, Kei Takahashi, Shinjiro Kodama, Keizo Kaneko, Junhong Gao, Kenji Uno, Shojiro Sawada, Tomoichiro Asano, Vladimir V. Kalinichenko, Etsuo A. Susaki, Makoto Kanzaki, Hiroki R. Ueda, Yasushi Ishigaki, Tetsuya Yamada, Hideki Katagiri

NATURE COMMUNICATIONS　8　(1)　1930-1930　2017/12

DOI： 10.1038/s41467-017-01869-7 　

ISSN： 2041-1723
Severely impaired activity of lipoprotein lipase Arg243His is partially ameliorated by emulsifying phospholipids in invitro triolein hydrolysis analysis Peer-reviewed

Takashi Yamaguchi, Takeyoshi Murano, Ichiro Tatsuno, Nobuyuki Hiruta, Toru Suzuki, Shojiro Sawada, Hideki Katagiri, Kohji Shirai, Wolfgang J. Schneider, Hideaki Bujo

ANNALS OF CLINICAL BIOCHEMISTRY　54　(6)　712-715　2017/11

DOI： 10.1177/0004563217693258 　

ISSN： 0004-5632

eISSN： 1758-1001
Effects of the Activation of Three Major Hepatic Akt Substrates on Glucose Metabolism in Male Mice Peer-reviewed

Gota Sakai, Ikuo Inoue, Tokuko Suzuki, Takashi Sumita, Kouichi Inukai, Shigehiro Katayama, Takuya Awata, Tetsuya Yamada, Tomoichiro Asano, Hideki Katagiri, Mitsuhiko Noda, Akira Shimada, Hiraku Ono

ENDOCRINOLOGY　158　(8)　2659-2671　2017/08

DOI： 10.1210/en.2016-1969 　

ISSN： 0013-7227

eISSN： 1945-7170
Common Hepatic Branch of Vagus Nerve-Dependent Expression of Immediate Early Genes in the Mouse Brain by Intraportal L-Arginine: Comparison with Cholecystokinin-8 Peer-reviewed

Daisuke Yamada, Peter Koppensteiner, Saori Odagiri, Megumi Eguchi, Shun Yamaguchi, Tetsuya Yamada, Hideki Katagiri, Keiji Wada, Masayuki Sekiguchi

FRONTIERS IN NEUROSCIENCE　11　366-366　2017/06

DOI： 10.3389/fnins.2017.00366 　

ISSN： 1662-453X
Activation of the Hypoxia Inducible Factor 1 alpha Subunit Pathway in Steatotic Liver Contributes to Formation of Cholesterol Gallstones Peer-reviewed

Yoichiro Asai, Tetsuya Yamada, Sohei Tsukita, Kei Takahashi, Masamitsu Maekawa, Midori Honma, Masanori Ikeda, Keigo Murakami, Yuichiro Munakata, Yuta Shirai, Shinjiro Kodama, Takashi Sugisawa, Yumiko Chiba, Yasuteru Kondo, Keizo Kaneko, Kenji Uno, Shojiro Sawada, Junta Imai, Yasuhiro Nakamura, Hiroaki Yamaguchi, Kozo Tanaka, Hironobu Sasano, Nariyasu Mano, Yoshiyuki Ueno, Tooru Shimosegawa, Hideki Katagiri

GASTROENTEROLOGY　152　(6)　1521-+　2017/05

DOI： 10.1053/j.gastro.2017.01.001 　

ISSN： 0016-5085

eISSN： 1528-0012
Metforimin directly binds the alarmin HMGB1 and inhibits its proinflammatory activity Peer-reviewed

Horiuchi T, Sakata N, Narumi Y, Kimura T, Hayashi T, Nagano K, Liu K, Nishibori M, Tsukita S, Yamada T, Katagiri H, Shirakawa R, Horiuchi H

J Biol Chem　292　(20)　8436-8446　2017/03/19

DOI： 10.1074/jbc.M116.769380. 　
Sodium-Glucose Cotransporter 2 Inhibitor Improves Complications of Lipodystrophy: A Case Report Peer-reviewed

Yohei Kawana, Junta Imai, Shojiro Sawada, Tetsuya Yamada, Hideki Katagiri

ANNALS OF INTERNAL MEDICINE　166　(6)　450-451　2017/03

DOI： 10.7326/L16-0372 　

ISSN： 0003-4819

eISSN： 1539-3704
MicroRNAs 106b and 222 Improve Hyperglycemia in a Mouse Model of Insulin-Deficient Diabetes via Pancreatic beta-Cell Proliferation Peer-reviewed

Sohei Tsukita, Tetsuya Yamada, Kei Takahashi, Yuichiro Munakata, Shinichiro Hosaka, Hironobu Takahashi, Junhong Gao, Yuta Shirai, Shinjiro Kodama, Yoichiro Asai, Takashi Sugisawa, Yumiko Chiba, Keizo Kaneko, Kenji Uno, Shojiro Sawada, Junta Imai, Hideki Katagiri

EBIOMEDICINE　15　163-172　2017/02

DOI： 10.1016/j.ebiom.2016.12.002 　

ISSN： 2352-3964
ER Stress Protein CHOP Mediates Insulin Resistance by Modulating Adipose Tissue Macrophage Polarity Peer-reviewed

Toru Suzuki, Junhong Gao, Yasushi Ishigaki, Keiichi Kondo, Shojiro Sawada, Tomohito Izumi, Kenji Uno, Keizo Kaneko, Sohei Tsukita, Kei Takahashi, Atsuko Asao, Naoto Ishii, Junta Imai, Tetsuya Yamada, Seiichi Oyadomari, Hideki Katagiri

CELL REPORTS　18　(8)　2045-2057　2017/02

DOI： 10.1016/j.celrep.2017.01.076 　

ISSN： 2211-1247
Knockout of Vasohibin-1 Gene in Mice Results in Healthy Longevity with Reduced Expression of Insulin Receptor, Insulin Receptor Substrate 1, and Insulin Receptor Substrate 2 in Their White Adipose Tissue

Eichi Takeda, Yasuhiro Suzuki, Tetsuya Yamada, Hideki Katagiri, Yasufumi Sato

Journal of Aging Research　2017　1-11　2017
Publisher: Hindawi Limited
DOI： 10.1155/2017/9851380 　

ISSN： 2090-2204

eISSN： 2090-2212
A case of idiopathic type 1 diabetes with subsequent recovery of endogenous insulin secretion despite initial diagnosis of fulminant type 1 diabetes Peer-reviewed

Keizo Kaneko, Chihiro Satake, Junpei Yamamoto, Hironori Takahashi, Shojiro Sawada, Junta Imai, Tetsuya Yamada, Hideki Katagiri

ENDOCRINE JOURNAL　64　(3)　369-374　2017

DOI： 10.1507/endocrj.EJ16-0245. 　

ISSN： 0918-8959

eISSN： 1348-4540
The relationship between advanced glycation end products and ocular circulation in type 2 diabetes Peer-reviewed

Kazuki Hashimoto, Hiroshi Kunikata, Masayuki Yasuda, Azusa Ito, Naoko Aizawa, Shojiro Sawada, Keiichi Kondo, Chihiro Satake, Yoshimasa Takano, Koji M. Nishiguchi, Hideki Katagiri, Toru Nakazawa

JOURNAL OF DIABETES AND ITS COMPLICATIONS　30　(7)　1371-1377　2016/09

DOI： 10.1016/j.jdiacomp.2016.04.024 　

ISSN： 1056-8727

eISSN： 1873-460X
Dapagliflozin, a Sodium-Glucose Co-Transporter 2 Inhibitor, Acutely Reduces Energy Expenditure in BAT via Neural Signals in Mice Peer-reviewed

Yumiko Chiba, Tetsuya Yamada, Sohei Tsukita, Kei Takahashi, Yuichiro Munakata, Yuta Shirai, Shinjiro Kodama, Yoichiro Asai, Takashi Sugisawa, Kenji Uno, Shojiro Sawada, Junta Imai, Kazuhiro Nakamura, Hideki Katagiri

PLOS ONE　11　(3)　e0150756-e0150756　2016/03

DOI： 10.1371/journal.pone.0150756 　

ISSN： 1932-6203
強化インスリン療法を持続性エキセナチドへ変更し、CGMで観察したPrader-Willi症候群の1例

木幡将人, 児玉慎二郎, 大方香菜子, 穂坂真一郎, 高橋広延, 金子礼, 宇野健司, 澤田正二郎, 今井淳太, 山田哲也, 片桐秀樹

糖尿病　59　(2)　133-133　2016/02
Publisher: (一社)日本糖尿病学会
ISSN： 0021-437X

eISSN： 1881-588X
術前CT、MRI検査にて局在診断が困難であったインスリノーマの1例

穂坂真一郎, 児玉慎二郎, 大方香菜子, 金子礼, 高橋広延, 木幡将人, 澤田正二郎, 今井淳太, 山田哲也, 片桐秀樹

糖尿病　59　(2)　143-143　2016/02
Publisher: (一社)日本糖尿病学会
ISSN： 0021-437X

eISSN： 1881-588X
Maternal Dietary Imbalance between Omega-6 and Omega-3 Polyunsaturated Fatty Acids Impairs Neocortical Development via Epoxy Metabolites Peer-reviewed

Nobuyuki Sakayori, Takako Kikkawa, Hisanori Tokuda, Emiko Kiryu, Kaichi Yoshizaki, Hiroshi Kawashima, Tetsuya Yamada, Hiroyuki Arai, Jing X. Kang, Hideki Katagiri, Hiroshi Shibata, Sheila M. Innis, Makoto Arita, Noriko Osumi

STEM CELLS　34　(2)　470-482　2016/02

DOI： 10.1002/stem.2246 　

ISSN： 1066-5099

eISSN： 1549-4918
Lipoprotein Lipase Deficiency (R243H) in a Type 2 Diabetes Patient with Multiple Arterial Aneurysms Peer-reviewed

Toru Suzuki, Shojiro Sawada, Yasushi Ishigaki, Sohei Tsukita, Shinjiro Kodama, Takashi Sugisawa, Junta Imai, Tetsuya Yamada, Takashi Yamaguchi, Takeyoshi Murano, Hideki Katagiri

INTERNAL MEDICINE　55　(9)　1131-1136　2016

DOI： 10.2169/internalmedicine.55.5239 　

ISSN： 0918-2918

eISSN： 1349-7235
Genome-wide approaches for BACH1 target genes in mouse embryonic fibroblasts revealed BACH1-Pparg pathway in adipogenesis. Peer-reviewed

Matsumoto M, Kondo K, Shiraki T, Brydun A, Funayama R, Nakayama K, Yaegashi N, Katagiri H, Igarashi K

Genes Cells　21　(6)　553-567　2016/01

DOI： 10.1111/gtc.12365. 　
Involvement of resistin-like molecule beta in the development of methionine-choline deficient diet-induced non-alcoholic steatohepatitis in mice Peer-reviewed

Hirofumi Okubo, Akifumi Kushiyama, Hideyuki Sakoda, Yusuke Nakatsu, Masaki Iizuka, Naoyuki Taki, Midori Fujishiro, Toshiaki Fukushima, Hideaki Kamata, Akiko Nagamachi, Toshiya Inaba, Fusanori Nishimura, Hideki Katagiri, Takashi Asahara, Yasuto Yoshida, Osamu Chonan, Jeffery Encinas, Tomoichiro Asano

SCIENTIFIC REPORTS　6　20157-20157　2016/01

DOI： 10.1038/srep20157 　

ISSN： 2045-2322
Prolyl Isomerase Pin1 Negatively Regulates AMP-activated Protein Kinase (AMPK) by Associating with the CBS Domain in the gamma Subunit Peer-reviewed

Yusuke Nakatsu, Misaki Iwashita, Hideyuki Sakoda, Hiraku Ono, Kengo Nagata, Yasuka Matsunaga, Toshiaki Fukushima, Midori Fujishiro, Akifumi Kushiyama, Hideaki Kamata, Shin-Ichiro Takahashi, Hideki Katagiri, Hiroaki Honda, Hiroshi Kiyonari, Takafumi Uchida, Tomichiro Asano

JOURNAL OF BIOLOGICAL CHEMISTRY　290　(40)　24255-24266　2015/10

DOI： 10.1074/jbc.M115.658559 　

ISSN： 0021-9258

eISSN： 1083-351X
Impacts of the Great East Japan Earthquake on diabetic patients Peer-reviewed

Mamiko Tanaka, Junta Imai, Michihiro Satoh, Takanao Hashimoto, Tomohito Izumi, Shojiro Sawada, Kenji Uno, Yutaka Hasegawa, Keizo Kaneko, Tetsuya Yamada, Yasushi Ishigaki, Yutaka Imai, Hideki Katagiri

JOURNAL OF DIABETES INVESTIGATION　6　(5)　577-586　2015/09

DOI： 10.1111/jdi.12336 　

ISSN： 2040-1116

eISSN： 2040-1124
A hepatic amino acid/mTOR/S6K-dependent signalling pathway modulates systemic lipid metabolism via neuronal signals Peer-reviewed

Kenji Uno, Tetsuya Yamada, Yasushi Ishigaki, Junta Imai, Yutaka Hasegawa, Shojiro Sawada, Keizo Kaneko, Hiraku Ono, Tomoichiro Asano, Yoshitomo Oka, Hideki Katagiri

NATURE COMMUNICATIONS　6　7940-7940　2015/08

DOI： 10.1038/ncomms8940 　

ISSN： 2041-1723
Neuronal Signals from the Hepatic Amino Acid/mTOR/S6K Pathway Regulates Systemic Lipid Metabolism Peer-reviewed

Kenji Uno, Hideki Katagiri

DIABETES　64　A507-A507　2015/06

ISSN： 0012-1797

eISSN： 1939-327X
Identification of Pathogenic Cardiac CD11c(+) Macrophages in Nod1-Mediated Acute Coronary Arteritis Peer-reviewed

Yoshitomo Motomura, Shunsuke Kanno, Kenichi Asano, Masato Tanaka, Yutaka Hasegawa, Hideki Katagiri, Takashi Saito, Hiromitsu Hara, Hisanori Nishio, Toshiro Hara, Sho Yamasaki

ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY　35　(6)　1423-1433　2015/06

DOI： 10.1161/ATVBAHA.114.304846 　

ISSN： 1079-5642

eISSN： 1524-4636
Rho-Kinase Inhibition Ameliorates Metabolic Disorders through Activation of AMPK Pathway in Mice Peer-reviewed

Kazuki Noda, Sota Nakajima, Shigeo Godo, Hiroki Saito, Shohei Ikeda, Toru Shimizu, Budbazar Enkhjargal, Yoshihiro Fukumoto, Sohei Tsukita, Tetsuya Yamada, Hideki Katagiri, Hiroaki Shimokawa

PLOS ONE　9　(11)　e110446-e110446　2014/11

DOI： 10.1371/journal.pone.0110446 　

ISSN： 1932-6203
Glycemic Control in Diabetic Patients With Impaired Endogenous Insulin Secretory Capacity Is Vulnerable After a Natural Disaster: Study of Great East Japan Earthquake Peer-reviewed

Mamiko Tanaka, Junta Imai, Michihiro Satoh, Takanao Hashimoto, Tomohito Izumi, Shojiro Sawada, Kenji Uno, Yutaka Hasegawa, Keizo Kaneko, Tetsuya Yamada, Yasushi Ishigaki, Yutaka Imai, Hideki Katagiri

DIABETES CARE　37　(10)　E212-E213　2014/10

DOI： 10.2337/dc14-1479 　

ISSN： 0149-5992

eISSN： 1935-5548
Mediobasal hypothalamic PTEN modulates hepatic insulin resistance independently of food intake in rats Peer-reviewed

Takashi Sumita, Hiraku Ono, Tokuko Suzuki, Gota Sakai, Kouichi Inukai, Hideki Katagiri, Tomoichiro Asano, Shigehiro Katayama, Takuya Awata

AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM　307　(1)　E47-E60　2014/07

DOI： 10.1152/ajpendo.00361.2013 　

ISSN： 0193-1849

eISSN： 1522-1555
Insulin-Mimicking Bioactivities of Acylated Inositol Glycans in Several Mouse Models of Diabetes with or without Obesity Peer-reviewed

Susumu Suzuki, Chitose Suzuki, Yoshinori Hinokio, Yasushi Ishigaki, Hideki Katagiri, Makoto Kanzaki, Viatcheslav N. Azev, Nilanjana Chakraborty, Marc d'Alarcao

PLOS ONE　9　(6)　e100466-e100466　2014/06

DOI： 10.1371/journal.pone.0100466 　

ISSN： 1932-6203
Simultaneous Copy Number Losses within Multiple Subtelomeric Regions in Early-Onset Type2 Diabetes Mellitus Peer-reviewed

Shinjiro Kodama, Tetsuya Yamada, Junta Imai, Shojiro Sawada, Kei Takahashi, Sohei Tsukita, Keizo Kaneko, Kenji Uno, Yasushi Ishigaki, Yoshitomo Oka, Hideki Katagiri

PLOS ONE　9　(4)　e88602-e88602　2014/04

DOI： 10.1371/journal.pone.0088602 　

ISSN： 1932-6203
Type B insulin resistance syndrome as an H. Pylori-associated autoimmune disease. Peer-reviewed

Imai J, Yamada T, Satoh J, Katagiri H

J Endocrinol Diabetes Obes　2　(2)　1026-1026　2014
Elevation of HDL-C in Response to Statin Treatment is Involved in the Regression of Carotid Atherosclerosis Peer-reviewed

Yasushi Ishigaki, Suminori Kono, Hideki Katagiri, Yoshitomo Oka, Shinichi Oikawa

JOURNAL OF ATHEROSCLEROSIS AND THROMBOSIS　21　(10)　1055-1065　2014

ISSN： 1340-3478

eISSN： 1880-3873
Glycogen shortage during fasting triggers liver-brain-adipose neurocircuitry to facilitate fat utilization (vol 4, pg 2316, 2013) Peer-reviewed

Yoshihiko Izumida, Naoya Yahagi, Yoshinori Takeuchi, Makiko Nishi, Akito Shikama, Ayako Takarada, Yukari Masuda, Midori Kubota, Takashi Matsuzaka, Yoshimi Nakagawa, Yoko Iizuka, Keiji Itaka, Kazunori Kataoka, Seiji Shioda, Akira Niijima, Tetsuya Yamada, Hideki Katagiri, Ryozo Nagai, Nobuhiro Yamada, Takashi Kadowaki, Hitoshi Shimano

NATURE COMMUNICATIONS　4　(2316)　---　2013/12

DOI： 10.1038/ncomms3930 　

ISSN： 2041-1723
Bach1 deficiency protects pancreatic beta-cells from oxidative stress injury Peer-reviewed

Keiichi Kondo, Yasushi Ishigaki, Junhong Gao, Tetsuya Yamada, Junta Imai, Shojiro Sawada, Akihiko Muto, Yoshitomo Oka, Kazuhiko Igarashi, Hideki Katagiri

AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM　305　(5)　E641-E648　2013/09

DOI： 10.1152/ajpendo.00120.2013 　

ISSN： 0193-1849
Glycogen shortage during fasting triggers liver-brain-adipose neurocircuitry to facilitate fat utilization Peer-reviewed

Yoshihiko Izumida, Naoya Yahagi, Yoshinori Takeuchi, Makiko Nishi, Akito Shikama, Ayako Takarada, Yukari Masuda, Midori Kubota, Takashi Matsuzaka, Yoshimi Nakagawa, Yoko Iizuka, Keiji Itaka, Kazunori Kataoka, Seiji Shioda, Akira Niijima, Tetsuya Yamada, Hideki Katagiri, Ryozo Nagai, Nobuhiro Yamada, Takashi Kadowaki, Hitoshi Shimano

NATURE COMMUNICATIONS　4　2013/08

DOI： 10.1038/ncomms3316 　

ISSN： 2041-1723
Resistin-Like Molecule Is Abundantly Expressed in Foam Cells and Is Involved in Atherosclerosis Development Peer-reviewed

Akifumi Kushiyama, Hideyuki Sakoda, Naohide Oue, Masamichi Okubo, Yusuke Nakatsu, Haruya Ono, Toshiaki Fukushima, Hideaki Kamata, Fusanori Nishimura, Takako Kikuchi, Midori Fujishiro, Koichi Nishiyama, Hiroyuki Aburatani, Sakura Kushiyama, Masaki Iizuka, Naoyuki Taki, Jeffrey Encinas, Kazuhiro Sentani, Narumi Ogonuki, Atsuo Ogura, Shoji Kawazu, Wataru Yasui, Yukihito Higashi, Hiroki Kurihara, Hideki Katagiri, Tomoichiro Asano

ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY　33　(8)　1986-1993　2013/08

DOI： 10.1161/ATVBAHA.113.301546 　

ISSN： 1079-5642

eISSN： 1524-4636
Cognitive dysfunction associated with anti-glutamic acid decarboxylase autoimmunity: a case-control study Peer-reviewed

Masahito Takagi, Yasushi Ishigaki, Kenji Uno, Shojiro Sawada, Junta Imai, Keizo Kaneko, Yutaka Hasegawa, Tetsuya Yamada, Ai Tokita, Kazumi Iseki, Shigenori Kanno, Yoshiyuki Nishio, Hideki Katagiri, Etsuro Mori

BMC NEUROLOGY　13　(76)　---　2013/07

DOI： 10.1186/1471-2377-13-76 　

ISSN： 1471-2377
Par14 Protein Associates with Insulin Receptor Substrate 1 (IRS-1), Thereby Enhancing Insulin-induced IRS-1 Phosphorylation and Metabolic Actions International-journal

Jun Zhang, Yusuke Nakatsu, Takanori Shinjo, Ying Guo, Hideyuki Sakoda, Takeshi Yamamotoya, Yuichiro Otani, Hirofumi Okubo, Akifumi Kushiyama, Midori Fujishiro, Toshiaki Fukushima, Yoshihiro Tsuchiya, Hideaki Kamata, Misaki Iwashita, Fusanori Nishimura, Hideki Katagiri, Shin-ichiro Takahashi, Hiroki Kurihara, Takafumi Uchida, Tomoichiro Asano

Journal of Biological Chemistry　288　(28)　20692-20701　2013/07
Publisher: Elsevier BV
DOI： 10.1074/jbc.m113.485730 　

ISSN： 0021-9258
Integrator complex plays an essential role in adipose differentiation Peer-reviewed

Yuichiro Otani, Yusuke Nakatsu, Hideyuki Sakoda, Toshiaki Fukushima, Midori Fujishiro, Akifumi Kushiyama, Hirofumi Okubo, Yoshihiro Tsuchiya, Haruya Ohno, Shin-Ichiro Takahashi, Fusanori Nishimura, Hideaki Kamata, Hideki Katagiri, Tomoichiro Asano

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS　434　(2)　197-202　2013/05

DOI： 10.1016/j.bbrc.2013.03.029 　

ISSN： 0006-291X
Identification of a novel interorgan mechanism favoring energy storage in overnutrition. Peer-reviewed

Yamada T, Tsukita S, Katagiri H

Adipocyte　2　(4)　281-284　2013
Clinical experiences in the treatment of pancreatic arteriovenous malformation by total pancreatectomy with islet autotransplantation. Peer-reviewed

Sakata N, Goto M, Motoi F, Hayashi H, Nakagawa K, Mizuma M, Yamaya H, Hasegawa Y, Yamaguchi S, Sawada S, Ottomo S, Okada T, Fukase K, Yoshida H, Ito T, Hirota M, Ishigaki Y, Sekiguchi S, Rikiyama T, Katayose Y, Fujimori K, Egawa S, Shimosegawa T, Katagiri H, Satomi S, Unno M

Transplantaton　96　(5)　e38-e40　2013
Importance of endothelial NF-kappa B signalling in vascular remodelling and aortic aneurysm formation Peer-reviewed

Tokuo Saito, Yutaka Hasegawa, Yasushi Ishigaki, Tetsuya Yamada, Junhong Gao, Junta Imai, Kenji Uno, Keizo Kaneko, Takehide Ogihara, Tatsuo Shimosawa, Tomoichiro Asano, Toshiro Fujita, Yoshitomo Oka, Hideki Katagiri

CARDIOVASCULAR RESEARCH　97　(1)　106-114　2013/01

DOI： 10.1093/cvr/cvs298 　

ISSN： 0008-6363
Chronic mild stress alters circadian expressions of molecular clock genes in the liver. Peer-reviewed

Takahashi K, Yamada T, Tsukita S, Kaneko K, Shirai Y, Munakata Y, Ishigaki Y, Imai J, Uno K, Hasegawa Y, Sawada S, Oka Y, Katagiri H

Am J Physiol Endocrinol Metab　304　(3)　E301-E309　2013
Hepatic Glucokinase Modulates Obesity Predisposition by Regulating BAT Thermogenesis via Neural Signals Peer-reviewed

Sohei Tsukita, Tetsuya Yamada, Kenji Uno, Kei Takahashi, Keizo Kaneko, Yasushi Ishigaki, Junta Imai, Yutaka Hasegawa, Shojiro Sawada, Hisamitsu Ishihara, Yoshitomo Oka, Hideki Katagiri

CELL METABOLISM　16　(6)　825-832　2012/12

DOI： 10.1016/j.cmet.2012.11.006 　

ISSN： 1550-4131
Role of Pin1 Protein in the Pathogenesis of Nonalcoholic Steatohepatitis in a Rodent Model Peer-reviewed

Yusuke Nakatsu, Yuichiro Otani, Hideyuki Sakoda, Jun Zhang, Ying Guo, Hirofumi Okubo, Akifumi Kushiyama, Midori Fujishiro, Takako Kikuch, Toshiaki Fukushima, Haruya Ohno, Yoshihiro Tsuchiya, Hideaki Kamata, Akiko Nagamachi, Toshiya Inaba, Fusanori Nishimura, Hideki Katagiri, Shin-ichiro Takahashi, Hiroki Kurihara, Takafumi Uchida, Tomoichiro Asano

JOURNAL OF BIOLOGICAL CHEMISTRY　287　(53)　44526-44535　2012/12

DOI： 10.1074/jbc.M112.397133 　

ISSN： 0021-9258

eISSN： 1083-351X
Intracellular and Extracellular ATP Coordinately Regulate the Inverse Correlation between Osteoclast Survival and Bone Resorption Peer-reviewed

Tsuyoshi Miyazaki, Mitsuyasu Iwasawa, Tomoki Nakashima, Shuuichi Mori, Kazuhiro Shigemoto, Hiroaki Nakamura, Hideki Katagiri, Hiroshi Takayanagi, Sakae Tanaka

JOURNAL OF BIOLOGICAL CHEMISTRY　287　(45)　37808-37823　2012/11

DOI： 10.1074/jbc.M112.385369 　

ISSN： 0021-9258

eISSN： 1083-351X
Brain-Derived Neurotrophic Factor Protects Against Cardiac Dysfunction After Myocardial Infarction via a Central Nervous System-Mediated Pathway Peer-reviewed

Sho Okada, Masataka Yokoyama, Haruhiro Toko, Kaoru Tateno, Junji Moriya, Ippei Shimizu, Aika Nojima, Takashi Ito, Yohko Yoshida, Yoshio Kobayashi, Hideki Katagiri, Tohru Minamino, Issei Komuro

ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY　32　(8)　1902-1909　2012/08

DOI： 10.1161/ATVBAHA.112.248930 　

ISSN： 1079-5642
Atf6 alpha-null mice are glucose intolerant due to pancreatic beta-cell failure on a high-fat diet but partially resistant to diet-induced insulin resistance Peer-reviewed

Masahiro Usui, Suguru Yamaguchi, Yasuhiro Tanji, Ryu Tominaga, Yasushi Ishigaki, Manabu Fukumoto, Hideki Katagiri, Kazutoshi Mori, Yoshitomo Oka, Hisamitsu Ishihara

METABOLISM-CLINICAL AND EXPERIMENTAL　61　(8)　1118-1128　2012/08

DOI： 10.1016/j.metabol.2012.01.004 　

ISSN： 0026-0495
LST8 level controls basal p70 S6 kinase and Akt phosphorylations, and mTORC1 and mTORC2 negatively regulate each other by competing for association with LST8 Peer-reviewed

Takako Kikuchi, Jun Zhang, Hideyuki Sakoda, Yuko Koketsu, Midori Fujishiro, Akifumi Kushiyama, Yusuke Nakatsu, Hideaki Kamata, Ken Inoki, Shin-Ichiro Takahashi, Hiroki Kurihara, Katagiri Hideki, Yoshitomo Oka, Tomoichiro Asano

Obesity Research and Clinical Practice　6　(3)　e215-e224　2012/07

DOI： 10.1016/j.orcp.2011.10.002 　

ISSN： 1871-403X 1878-0318

eISSN： 1878-0318
Hepatic Glucokinase Negatively Regulates BAT Thermogenesis via a Neural Pathway Peer-reviewed

Tsukita Sohei, Yamada Tetsuya, Uno Kenji, Oka Yoshitomo, Katagiri Hideki

DIABETES　61　A66　2012/06/01

ISSN： 0012-1797
Hepatic DEPTOR Expression Improves Systemic Insulin Resistance Peer-reviewed

Chiba Yumiko, Uno Kenji, Katagiri Hideki

DIABETES　61　A455　2012/06/01

ISSN： 0012-1797
[Regulation of pancreatic beta-cells by inter-organ networks]. Peer-reviewed

Imai J, Katagiri H

Nihon rinsho. Japanese journal of clinical medicine　70 Suppl 3　109-112　2012/05

ISSN： 0047-1852
Hepatic peroxisome proliferator-activated receptor-gamma-fat-specific protein 27 pathway contributes to obesity-related hypertension via afferent vagal signals Peer-reviewed

Kenji Uno, Tetsuya Yamada, Yasushi Ishigaki, Junta Imai, Yutaka Hasegawa, Junhong Gao, Keizo Kaneko, Kimihiko Matsusue, Tomomi Yamazaki, Yoshitomo Oka, Hideki Katagiri

EUROPEAN HEART JOURNAL　33　(10)　1279-1289　2012/05

DOI： 10.1093/eurheartj/ehr265 　

ISSN： 0195-668X
Blockade of the Nuclear Factor-kappa B Pathway in the Endothelium Prevents Insulin Resistance and Prolongs Life Spans Peer-reviewed

Yutaka Hasegawa, Tokuo Saito, Takehide Ogihara, Yasushi Ishigaki, Tetsuya Yamada, Junta Imai, Kenji Uno, Junhong Gao, Keizo Kaneko, Tatsuo Shimosawa, Tomoichiro Asano, Toshiro Fujita, Yoshitomo Oka, Hideki Katagiri

CIRCULATION　125　(9)　1122-U140　2012/03

DOI： 10.1161/CIRCULATIONAHA.111.054346 　

ISSN： 0009-7322
Role of Pin1 protein in the pathogenesis of nonalcoholic steatohepatitis in a rodent model. Peer-reviewed

Nakatsu Y, Otani Y, Sakoda H, Zhang J, Guo Y, Okubo H, Kushiyama A, Fujishiro M, Kikuch T, Fukushima T, Ohno H, Tsuchiya Y, Kamata H, Nagamachi A, Inaba T, Nishimura F, Katagiri H, Takahashi S, Kurihara H, Uchida T, Asano T.

Journal of Biological Chemistry　287(53): 44526-44535　A466-A466　2012

ISSN： 0012-1797

eISSN： 1939-327X
A Case of Slowly Progressive Type 1 Diabetes with Insulin Independence Maintained for 10 Years with alpha-glucosidase Inhibitor Monotherapy Peer-reviewed

Yuichiro Munakata, Tetsuya Yamada, Kazuma Takahashi, Sohei Tsukita, Kei Takahashi, Shojiro Sawada, Junta Imai, Yasushi Ishigaki, Yoshitomo Oka, Hideki Katagiri

INTERNAL MEDICINE　51　(24)　3391-3394　2012

DOI： 10.2169/internalmedicine.51.8123 　

ISSN： 0918-2918
Recurrent hypoglycemia during pregnancies in a woman with multiple autoantibodies including anti-insulin receptor antibody and anti-platelet antibody, whose serum lowered murine blood glucose levels and phosphorylated insulin receptor of CHO-IR cells Peer-reviewed

Makiko Toshihiro, Hideki Katagiri, Koujiro Kataoka, Akimune Fukushima, Toshie Segawa, Takuya Fujiwara, Isao Hikichi, Noriko Takebe, Jo Satoh

ENDOCRINE JOURNAL　58　(12)　1037-1043　2011/12

DOI： 10.1507/endocrj.EJ11-0145 　

ISSN： 0918-8959
Involvement of Endoplasmic Stress Protein C/EBP Homologous Protein in Arteriosclerosis Acceleration With Augmented Biological Stress Responses Peer-reviewed

Junhong Gao, Yasushi Ishigaki, Tetsuya Yamada, Keiichi Kondo, Suguru Yamaguchi, Junta Imai, Kenji Uno, Yutaka Hasegawa, Shojiro Sawada, Hisamitsu Ishihara, Seiichi Oyadomari, Masataka Mori, Yoshitomo Oka, Hideki Katagiri

CIRCULATION　124　(7)　830-U183　2011/08

DOI： 10.1161/CIRCULATIONAHA.110.014050 　

ISSN： 0009-7322

eISSN： 1524-4539
Peptidyl-prolyl Cis/Trans Isomerase NIMA-interacting 1 Associates with Insulin Receptor Substrate-1 and Enhances Insulin Actions and Adipogenesis Peer-reviewed

Yusuke Nakatsu, Hideyuki Sakoda, Akifumi Kushiyama, Jun Zhang, Hiraku Ono, Midori Fujishiro, Takako Kikuchi, Toshiaki Fukushima, Masayasu Yoneda, Haruya Ohno, Nanao Horike, Machi Kanna, Yoshihiro Tsuchiya, Hideaki Kamata, Fusanori Nishimura, Toshiaki Isobe, Takehide Ogihara, Hideki Katagiri, Yoshitomo Oka, Shin-ichiro Takahashi, Hiroki Kurihara, Takafumi Uchida, Tomoichiro Asano

JOURNAL OF BIOLOGICAL CHEMISTRY　286　(23)　20812-20822　2011/06

DOI： 10.1074/jbc.M110.206904 　

ISSN： 0021-9258

eISSN： 1083-351X
Increased Systemic Glucose Tolerance with Increased Muscle Glucose Uptake in Transgenic Mice Overexpressing RXR gamma in Skeletal Muscle Peer-reviewed

Satoshi Sugita, Yasutomi Kamei, Fumiko Akaike, Takayoshi Suganami, Sayaka Kanai, Maki Hattori, Yasuko Manabe, Nobuharu Fujii, Takako Takai-Igarashi, Miki Tadaishi, Jun-ichiro Oka, Hiroyuki Aburatani, Tetsuya Yamada, Hideki Katagiri, Saori Kakehi, Yoshifumi Tamura, Hideo Kubo, Kenichi Nishida, Shinji Miura, Osamu Ezaki, Yoshihiro Ogawa

PLOS ONE　6　(5)　e20467-e20467　2011/05

DOI： 10.1371/journal.pone.0020467 　

ISSN： 1932-6203
4F2hc stabilizes GLUT1 protein and increases glucose transport activity Peer-reviewed

Haruya Ohno, Yusuke Nakatsu, Hideyuki Sakoda, Akifumi Kushiyama, Hiraku Ono, Midori Fujishiro, Yuichiro Otani, Hirofumi Okubo, Masayasu Yoneda, Toshiaki Fukushima, Yoshihiro Tsuchiya, Hideaki Kamata, Fusanori Nishimura, Hiroki Kurihara, Hideki Katagiri, Yoshitomo Oka, Tomoichiro Asano

AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY　300　(5)　C1047-C1054　2011/05

DOI： 10.1152/ajpcell.00416.2010 　

ISSN： 0363-6143
Interleukin-6 Enhances Glucose-Stimulated Insulin Secretion From Pancreatic beta-Cells Potential Involvement of the PLC-IP3-Dependent Pathway Peer-reviewed

Toshinobu Suzuki, Junta Imai, Tetsuya Yamada, Yasushi Ishigaki, Keizo Kaneko, Kenji Uno, Yutaka Hasegawa, Hisamitsu Ishihara, Yoshitomo Oka, Hideki Katagiri

DIABETES　60　(2)　537-547　2011/02

DOI： 10.2337/db10-0796 　

ISSN： 0012-1797
Fbxw7 regulates lipid metabolism and cell fate decisions in the mouse liver Peer-reviewed

Ichiro Onoyama, Atsushi Suzuki, Akinobu Matsumoto, Kengo Tomita, Hideki Katagiri, Yuichi Oike, Keiko Nakayama, Keiichi I. Nakayama

JOURNAL OF CLINICAL INVESTIGATION　121　(1)　342-354　2011/01

DOI： 10.1172/JCI40725 　

ISSN： 0021-9738
Frequent Loss of Genome Gap Region in 4p16.3 Subtelomere in Early-Onset Type 2 Diabetes Mellitus Peer-reviewed

Hirohito Kudo, Mitsuru Emi, Yasushi Ishigaki, Uiko Tsunoda, Yoshinori Hinokio, Miho Ishii, Hidenori Sato, Tetsuya Yamada, Hideki Katagiri, Yoshitomo Oka

EXPERIMENTAL DIABETES RESEARCH　2011　498460-498460　2011

DOI： 10.1155/2011/498460 　

ISSN： 1687-5214
Pin1 Associates with and Induces Translocation of CRTC2 to the Cytosol, Thereby Suppressing cAMP-responsive Element Transcriptional Activity Peer-reviewed

Yusuke Nakatsu, Hideyuki Sakoda, Akifumi Kushiyama, Hiraku Ono, Midori Fujishiro, Nanao Horike, Masayasu Yoneda, Haruya Ohno, Yoshihiro Tsuchiya, Hideaki Kamata, Hidetoshi Tahara, Toshiaki Isobe, Fusanori Nishimura, Hideki Katagiri, Yoshitomo Oka, Toshiaki Fukushima, Shin-Ichiro Takahashi, Hiroki Kurihara, Takafumi Uchida, Tomoichiro Asanoa

JOURNAL OF BIOLOGICAL CHEMISTRY　285　(43)　33018-33027　2010/10

DOI： 10.1074/jbc.M110.137836 　

ISSN： 0021-9258

eISSN： 1083-351X
Metabolic Information Highway: Interorgan Metabolic Communication Via the Autonomic Nervous System. Peer-reviewed

Katagiri H

Systems Biology: The Challenge of Complexity　221-227　2010/10
The JNK pathway modulates expression and phosphorylation of 4E-BP1 in MIN6 pancreatic beta-cells under oxidative stress conditions Peer-reviewed

Ryu Tominaga, Suguru Yamaguchi, Chihiro Satake, Masahiro Usui, Yasuhiro Tanji, Keiichi Kondo, Hideki Katagiri, Yoshitomo Oka, Hisamitsu Ishihara

CELL BIOCHEMISTRY AND FUNCTION　28　(5)　387-393　2010/07

DOI： 10.1002/cbf.1667 　

ISSN： 0263-6484
Increased E4 Activity in Mice Leads to Ubiquitin-containing Aggregates and Degeneration of Hypothalamic Neurons Resulting in Obesity Peer-reviewed

Etsuo Susaki, Chie Kaneko-Oshikawa, Keishi Miyata, Mitsuhisa Tabata, Tetsuya Yamada, Yuichi Oike, Hideki Katagiri, Keiichi I. Nakayama

JOURNAL OF BIOLOGICAL CHEMISTRY　285　(20)　15538-15547　2010/05

DOI： 10.1074/jbc.M110.105841 　

ISSN： 0021-9258
Characterization of a novel murine preadipocyte line, AP-18, isolated from subcutaneous tissue: analysis of adipocyte-related gene expressions Peer-reviewed

Chen Chen, Kazuma Takahashi, Ayumi Yoshida, Yumiko Takizawa, Yan Lee, Masaki Nakui, Hideyuki Doi, Yuji Takebayashi, Manabu Fukumoto, Testuya Yamada, Hideki Katagiri, Yoshitomo Oka, Jo Satoh

CELL BIOLOGY INTERNATIONAL　34　(3)　293-299　2010/03

DOI： 10.1042/CBI20090063 　

ISSN： 1065-6995
Different impacts of saturated and unsaturated free fatty acids on COX-2 expression in C2C12 myotubes Peer-reviewed

Akito Kadotani, Yo Tsuchiya, Hiroyasu Hatakeyama, Hideki Katagiri, Makoto Kanzaki

AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM　297　(6)　E1291-E1303　2009/12

DOI： 10.1152/ajpendo.00293.2009 　

ISSN： 0193-1849

eISSN： 1522-1555
Identification of a Novel Mechanism Regulating β Cell Mass: Neuronal relay from the Liver to Pancreatic β Cells. Peer-reviewed

Imai J Oka, Y, Katagiri H

Islets　1　(1)　75-77　2009/10
Circulating oxidized LDL: A biomarker and a pathogenic factor Peer-reviewed

Yasushi Ishigaki, Yoshitomo Oka, Hideki Katagiri

Current Opinion in Lipidology　20　(5)　363-369　2009/10

DOI： 10.1097/MOL.0b013e32832fa58d 　

ISSN： 0957-9672
Angiopoietin-like Protein 2 Promotes Chronic Adipose Tissue Inflammation and Obesity-Related Systemic Insulin Resistance Peer-reviewed

Mitsuhisa Tabata, Tsuyoshi Kadomatsu, Shigetomo Fukuhara, Keishi Miyata, Yasuhiro Ito, Motoyoshi Endo, Takashi Urano, Hui Juan Zhu, Hiroto Tsukano, Hirokazu Tazume, Koichi Kaikita, Kazuya Miyashita, Takao Iwawaki, Michio Shimabukuro, Kazuhiko Sakaguchi, Takaaki Ito, Naomi Nakagata, Tetsuya Yamada, Hideki Katagiri, Masato Kasuga, Yukio Ando, Hisao Ogawa, Naoki Mochizuki, Hiroshi Itoh, Toshio Suda, Yuichi Oike

CELL METABOLISM　10　(3)　178-188　2009/09

DOI： 10.1016/j.cmet.2009.08.003 　

ISSN： 1550-4131
Carotid arterial elasticity is a sensitive atherosclerosis value reflecting visceral fat accumulation in obese subjects Peer-reviewed

Ai Tokita, Yasushi Ishigaki, Hisashi Okimoto, Hideyuki Hasegawa, Yoshiro Koiwa, Makoto Kato, Hisamitsu Ishihara, Yoshinori Hinokio, Hideki Katagiri, Hiroshi Kanai, Yoshitomo Oka

ATHEROSCLEROSIS　206　(1)　168-172　2009/09

DOI： 10.1016/j.atherosclerosis.2009.01.046 　

ISSN： 0021-9150
Neural relay from the liver induces proliferation of pancreatic beta cells: a path to regenerative medicine using the self-renewal capabilities. Peer-reviewed

Katagiri Hideki, Imai Junta, Oka Yoshitomo

Commun Integr Biol　2　(5)　425-427　2009/09
Eradication of insulin resistance Peer-reviewed

Junta Imai, Tetsuya Yamada, Tokuo Saito, Yasushi Ishigaki, Yoshinori Hinokio, Hidetoshi Kotake, Yoshitomo Oka, Hideki Katagiri

LANCET　374　(9685)　264-264　2009/07

DOI： 10.1016/S0140-6736(09)60872-2 　

ISSN： 0140-6736
Obesity alters circadian expressions of molecular clock genes in the brainstem Peer-reviewed

Keizo Kaneko, Tetsuya Yamada, Sohei Tsukita, Kei Takahashi, Yasushi Ishigaki, Yoshitomo Oka, Hideki Katagiri

BRAIN RESEARCH　1263　58-68　2009/03

DOI： 10.1016/j.brainres.2008.12.071 　

ISSN： 0006-8993
Adiponectin Upregulates Ferritin Heavy Chain in Skeletal Muscle Cells Peer-reviewed

Yuichi Ikegami, Kouichi Inukai, Kenta Imai, Yasushi Sakamoto, Hideki Katagiri, Susumu Kurihara, Takuya Awata, Shigehiro Katayama

DIABETES　58　(1)　61-70　2009/01

DOI： 10.2337/db07-0690 　

ISSN： 0012-1797
Peginterferon (PEG-IFN) Plus Ribavirin Combination Therapy, but neither Interferon nor PGE-IFN Alone, Induced Type 1 Diabetes in a Patient with Chronic Hepatitis C Peer-reviewed

Takehide Ogihara, Hideki Katagiri, Tetsuya Yamada, Hirohito Kudo, Junta Imai, Yasushi Ishigaki, Yoshinori Hinokio, Yoko Yamagiwa, Yoshiyuki Ueno, Tooru Shimosegawa, Yoshitomo Oka

INTERNAL MEDICINE　48　(16)　1387-1390　2009

DOI： 10.2169/internalmedicine.48.2220 　

ISSN： 0918-2918
Molecular Characterization of the Tumor Suppressor Candidate 5 Gene: Regulation by PPAR gamma and Identification of TUSC5 Coding Variants in Lean and Obese Humans Peer-reviewed

Trina A. Knotts, Hyun Woo Lee, Jae Bum Kim, Pieter J. Oort, Ruth McPherson, Robert Dent, Keisuke Tachibana, Takefumi Doi, Songtao Yu, Janardan K. Reddy, Kenji Uno, Hideki Katagiri, Magdalena Pasarica, Steven R. Smith, Dorothy D. Sears, Michel Grino, Sean H. Adams

PPAR RESEARCH　2009　867678-867678　2009

DOI： 10.1155/2009/867678 　

ISSN： 1687-4757
Metabolic Information Highway: Interorgan Metabolic Communication Via the Autonomic Nervous System Peer-reviewed

Hideki Katagiri

SYSTEMS BIOLOGY: THE CHALLENGE OF COMPLEXITY　221-+　2009

DOI： 10.1007/978-4-431-87704-2_23 　
Regulation of pancreatic β cell mass by neuronal signals from the liver. "jointly worked" Peer-reviewed

Imai J, Katagiri H, Yamada T, Ishigaki Y, Suzuki T, Kudo H, Uno K, Hasegawa Y, Gao JH, Kaneko K, Ishihara H, Niijima A, Nakazato M, Asano T, Minokoshi Y, Oka Y

Science,　322　(5905)　1250-1254　2008/11/21

ISSN： 0193-4511
Regulation of Pancreatic beta Cell Mass by Neuronal Signals from the Liver Peer-reviewed

Junta Imai, Hideki Katagiri, Tetsuya Yamada, Yasushi Ishigaki, Toshinobu Suzuki, Hirohito Kudo, Kenji Uno, Yutaka Hasegawa, Junhong Gao, Keizo Kaneko, Hisamitsu Ishihara, Akira Niijima, Masamitsu Nakazato, Tomoichiro Asano, Yasuhiko Minokoshi, Yoshitomo Oka

SCIENCE　322　(5905)　1250-1254　2008/11

DOI： 10.1126/science.1163971 　

ISSN： 0036-8075
Impact of plasma oxidized low-density lipoprotein removal on atherosclerosis Peer-reviewed

Yasushi Ishigaki, Hideki Katagiri, Junhong Gao, Tetsuya Yamada, Junta Imai, Kenji Uno, Yutaka Hasegawa, Keizo Kaneko, Takehide Ogihara, Hisamitsu Ishihara, Yuko Sato, Kenji Takikawa, Norihisa Nishimichi, Haruo Matsuda, Tatsuya Sawamura, Yoshitomo Oka

CIRCULATION　118　(1)　75-83　2008/07

DOI： 10.1161/CIRCULATIONAHA.107.745174 　

ISSN： 0009-7322
Ambient glucose levels qualify the potency of insulin myogenic actions by regulating SIRT1 and FoxO3a in C2C12 myocytes Peer-reviewed

Taku Nedachi, Akito Kadotani, Miyako Ariga, Hideki Katagiri, Makoto Kanzaki

AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM　294　(4)　E668-E678　2008/04

DOI： 10.1152/ajpendo.00640.2007 　

ISSN： 0193-1849

eISSN： 1522-1555
Functional role of sortilin in myogenesis and development of insulin-responsive glucose transport system in C2C12 myocytes Peer-reviewed

Miyako Ariga, Taku Nedachi, Hideki Katagiri, Makoto Kanzaki

JOURNAL OF BIOLOGICAL CHEMISTRY　283　(15)　10208-10220　2008/04

DOI： 10.1074/jbc.M710604200 　

ISSN： 0021-9258
ATF4-mediated induction of 4E-BP1 contributes to pancreatic beta cell survival under endoplasmic reticulum stress Peer-reviewed

Suguru Yamaguchi, Hisamitsu Lshihara, Takahiro Yamada, Akira Tamura, Masahiro Iusui, Ryu Tominaga, Yuichiro Munakata, Chihiro Satake, Hideki Katagiri, Fumi Tashiro, Hiroyuki Aburatani, Kyoko Tsukiyama-Kohara, Jun-ichi Miyazaki, Nahum Sonenberg, Yoshitomo Oka

CELL METABOLISM　7　(3)　269-276　2008/03

DOI： 10.1016/j.cmet.2008.01.008 　

ISSN： 1550-4131
Inter-organ metabolic communication involved in energy homeostasis: potential therapeutic targets for obesity and metabolic syndrome Peer-reviewed

Yamada T, Oka Y, Katagiri H

Pharmacol Ther　117　(1)　188-198　2008
A novel method for evaluating human carotid artery elasticity: Possible detection of early stage atherosclerosis in subjects with type 2 diabetes Peer-reviewed

Hisashi Okimoto, Yasushi Ishigaki, Yoshihiro Koiwa, Yoshinori Hinokio, Takehide Ogihara, Susumu Suzuki, Hideki Katagiri, Takayoshi Ohkubo, Hideyuki Hasegawa, Hiroshi Kanai, Yoshitomo Oka

ATHEROSCLEROSIS　196　(1)　391-397　2008/01

DOI： 10.1016/j.atherosclerosis.2006.11.020 　

ISSN： 0021-9150
Possible relevance of HLA-DRB1 *0403 haplotype in insulin autoimmune syndrome induced by α-lipoic acid, used as a dietary supplement [4] Peer-reviewed

Tetsuya Yamada, Junta Imai, Yasushi Ishigaki, Yoshinori Hinokio, Yoshitomo Oka, Hideki Katagiri

Diabetes Care　30　(12)　e131-e131　2007/12

DOI： 10.2337/dc07-1636 　

ISSN： 0149-5992
Carboxy-terminal modulator protein induces Akt phosphorylation and activation, thereby enhancing antiapoptotic, glycogen synthetic, and glucose uptake pathways Peer-reviewed

Hiraku Ono, Hideyuki Sakoda, Midori Fujishiro, Motonobu Anai, Akifumi Kushiyama, Yasushi Fukushima, Hideki Katagiri, Takehide Ogihara, Yoshitomo Oka, Hideaki Kamata, Nanao Horike, Yasunobu Uchijima, Hiroki Kurihara, Tomoichiro Asano

AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY　293　(5)　C1576-C1585　2007/11

DOI： 10.1152/ajpcell.00570.2006 　

ISSN： 0363-6143
Avenues of communication between the brain and tissues/organs involved in energy homeostasis Peer-reviewed

Tetsuya Yamada, Hideki Katagiri

ENDOCRINE JOURNAL　54　(4)　497-505　2007/08

ISSN： 0918-8959
Bone marrow (BM) transplantation promotes beta-cell regeneration after acute injury through BM cell mobilization Peer-reviewed

Yutaka Hasegawa, Takehide Ogihara, Tetsuya Yamada, Yasushi Ishigaki, Junta Imai, Kenji Uno, Junhong Gao, Keizo Kaneko, Hisamitsu Ishihara, Hironobu Sasano, Hiromitsu Nakauchi, Yoshitomo Oka, Hideki Katagiri

ENDOCRINOLOGY　148　(5)　2006-2015　2007/05

DOI： 10.1210/en.2006-1351 　

ISSN： 0013-7227
Efficient and controlled gene expression in mouse pancreatic islets by arterial delivery of tetracycline-inducible adenoviral vectors Peer-reviewed

Rui Takahashi, Hisamitsu Ishihara, Kazuma Takahashi, Akira Tamura, Suguru Yamaguchi, Takahiro Yamada, Hideki Katagiri, Yoshitomo Oka

JOURNAL OF MOLECULAR ENDOCRINOLOGY　38　(1-2)　127-136　2007/02

DOI： 10.1677/jme.1.02189 　

ISSN： 0952-5041
Involvement of apolipoprotein E in excess fat accumulation and insulin resistance Peer-reviewed

Junhong Gao, Hideki Katagiri, Yasushi Ishigaki, Tetsuya Yamada, Takehide Ogihara, Junta Imai, Kenji Uno, Yutaka Hasegawa, Makoto Kanzaki, Tokuo T. Yamamoto, Shun Ishibashi, Yoshitomo Oka

DIABETES　56　(1)　24-33　2007/01

DOI： 10.2337/db06-0144 　

ISSN： 0012-1797
WFS1 protein modulates the free Ca2+ concentration in the endoplasmic reticulum Peer-reviewed

Daisuke Takei, Hisamitsu Ishihara, Suguru Yamaguchi, Takahiro Yamada, Akira Tamura, Hideki Katagiri, Yoshio Maruyama, Yoshitomo Oka

FEBS LETTERS　580　(24)　5635-5640　2006/10

DOI： 10.1016/j.febslet.2006.09.007 　

ISSN： 0014-5793
[Hypoglycemia associated with hyperinsulinemia in a subject with type 2 diabetes and liver cirrhosis] Peer-reviewed

Tamura Akira, Ishihara Hisamitsu, Suzuki Susumu, Hirai Masashi, Takahashi Rui, Yamaguchi Suguru, Satoh Fumitoshi, Kanno Noriatsu, Katagiri Hideki, Oka Yoshitomo

Nippon Naika Gakkai Zasshi　95　(7)　1371-1374　2006/07/10
Publisher: The Japanese Society of Internal Medicine
DOI： 10.2169/naika.95.1371 　

ISSN： 0021-5384
Cold exposure suppresses serum adiponectin levels through sympathetic nerve activation in mice Peer-reviewed

Junta Imai, Hideki Katagiri, Tetsuya Yamada, Yasushi Ishigaki, Takehide Ogihara, Kenji Uno, Yutaka Hasegawa, Junhong Gao, Hisamitsu Ishihara, Hironobu Sasano, Yoshitomo Oka

OBESITY　14　(7)　1132-1141　2006/07

DOI： 10.1038/oby.2006.130 　

ISSN： 1071-7323
Neuronal pathway from the liver modulates energy expenditure and systemic insulin sensitivity Invited Peer-reviewed

Hideki Katagiri, Kenji Uno, Tetsuya Yamada, Yoshitomo Oka

DIABETES　55　(5780)　A5-A5　2006/06

DOI： 10.1126/science.1126010 　

ISSN： 0012-1797
Neuronal pathway from the liver modulates energy expenditure and systemic insulin sensitivity Peer-reviewed

K Uno, H Katagiri, T Yamada, Y Ishigaki, T Ogihara, J Imai, Y Hasegawa, JH Gao, K Kaneko, H Iwasaki, H Ishihara, H Sasano, K Inukai, H Mizuguchi, T Asano, M Shiota, M Nakazato, Y Oka

SCIENCE　312　(5780)　1656-1659　2006/06

DOI： 10.1126/science.1126010 　

ISSN： 0036-8075
WFS1-deficiency increases endoplasmic reticulum stress, impairs cell cycle progression and triggers the apoptotic pathway specifically in pancreatic beta-cells Peer-reviewed

T Yamada, H Ishihara, A Tamura, R Takahashi, S Yamaguchi, D Takei, A Tokita, C Satake, F Tashiro, H Katagiri, H Aburatani, J Miyazaki, Y Oka

HUMAN MOLECULAR GENETICS　15　(10)　1600-1609　2006/05

DOI： 10.1093/hmg/ddl081 　

ISSN： 0964-6906
Signals from intra-abdominal fat modulate insulin and leptin sensitivity through different mechanisms: Neuronal involvement in food-intake regulation Peer-reviewed

T Yamada, H Katagiri, Y Ishigaki, T Ogihara, J Imai, K Uno, Y Hasegawa, JH Gao, H Ishihara, A Niijima, H Mano, H Aburatani, T Asano, Y Oka

CELL METABOLISM　3　(3)　223-229　2006/03

DOI： 10.1016/j.cmet.2006.02.001 　

ISSN： 1550-4131
Cell type-specific activation of metabolism reveals that beta-cell secretion suppresses glucagon release from alpha-cells in rat pancreatic islets Peer-reviewed

R Takahashi, H Ishihara, A Tamura, S Yamaguchi, T Yamada, D Takei, H Katagiri, H Endou, Y Oka

AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM　290　(2)　E308-E316　2006/02

DOI： 10.1152/ajpendo.00131.2005 　

ISSN： 0193-1849
Resistin-like molecule beta activates MAPKs, suppresses insulin signaling in hepatocytes, and induces diabetes, hyperlipidemia, and fatty liver in transgenic mice on a high fat diet Peer-reviewed

A Kushiyama, N Shojima, T Ogihara, K Inukai, H Sakoda, M Fujishiro, Y Fukushima, M Anai, H Ono, N Horike, AYI Viana, Y Uchijima, K Nishiyama, T Shimosawa, T Fujita, H Katagiri, Y Oka, H Kurihara, T Asano

JOURNAL OF BIOLOGICAL CHEMISTRY　280　(51)　42016-42025　2005/12

DOI： 10.1074/jbc.M503065200 　

ISSN： 0021-9258
Serum concentrations of resistin-like molecules beta and Y are elevated in high-fat-fed and obese db/db mice, with increased production in the intestinal tract and bone marrow Peer-reviewed

N Shojima, T Ogihara, K Inukai, M Fujishiro, H Sakoda, A Kushiyama, H Katagiri, M Anai, H Ono, Y Fukushima, N Horike, A Viana, Y Uchijima, H Kurihara, T Asano

DIABETOLOGIA　48　(5)　984-992　2005/05

DOI： 10.1007/s00125-005-1735-1 　

ISSN： 0012-186X
A novel protein kinase B (PKB)/AKT-binding protein enhances PKB kinase activity and regulates DNA synthesis Peer-reviewed

M Anai, N Shojima, H Katagiri, T Ogihara, H Sakoda, Y Onishi, H Ono, M Fujishiro, Y Fukushima, N Horike, A Viana, M Kikuchi, N Noguchi, S Takahashi, K Takata, Y Oka, Y Uchijima, H Kurihara, T Asano

JOURNAL OF BIOLOGICAL CHEMISTRY　280　(18)　18525-18535　2005/05

DOI： 10.1074/jbc.M500586200 　

ISSN： 0021-9258
Dissipating excess energy stored in the liver is a potential treatment strategy for diabetes associated with obesity Peer-reviewed

Y Ishigaki, H Katagiri, T Yamada, T Ogihara, J Imai, K Uno, Y Hasegawa, J Gao, H Ishihara, T Shimosegawa, H Sakoda, T Asano, Y Oka

DIABETES　54　(2)　322-332　2005/02

DOI： 10.2337/diabetes.54.2.322 　

ISSN： 0012-1797
Secondary sulfonylurea failure: Comparison of period until insulin treatment between diabetic patients treated with gliclazide and glibenclamide Peer-reviewed

Satoh J, Takahashi K, Takizawa Y, Ishihara H, Hirai M, Katagiri H, Hinokio Y, Suzuki S, Tsuji I, Oka Y

Diabetes Res Clin Plact　70　291-297　2005
Constitutively active PDX1 induced efficient insulin production in adult murine liver Peer-reviewed

J Imai, H Katagiri, T Yamada, Y Ishigaki, T Ogihara, K Uno, Y Hasegawa, JH Gao, H Ishihara, H Sasano, H Mizuguchi, T Asano, Y Oka

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS　326　(2)　402-409　2005/01

DOI： 10.1016/j.bbrc.2004.11.047 　

ISSN： 0006-291X
Endoplasmic reticulum stress and N-glycosylation modulate expression of WFS1 protein Peer-reviewed

S Yamaguchi, H Ishihara, A Tamura, T Yamada, R Takahashi, D Takei, H Katagiri, Y Oka

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS　325　(1)　250-256　2004/12

DOI： 10.1016/j.bbrc.2004.10.017 　

ISSN： 0006-291X
Glucose transporter and Na+/glucose cotransporter as molecular targets of anti-diabetic drugs Peer-reviewed

T Asano, T Ogihara, H Katagiri, H Sakoda, H Ono, M Fujishiro, M Anai, H Kurihara, Y Uchijima

CURRENT MEDICINAL CHEMISTRY　11　(20)　2717-2724　2004/10

ISSN： 0929-8673
Disruption of the WFS1 gene in mice causes progressive beta-cell loss and impaired stimulus-secretion coupling in insulin secretion Peer-reviewed

H Ishihara, S Takeda, A Tamura, R Takahashi, S Yamaguchi, D Takei, T Yamada, H Inoue, H Soga, H Katagiri, Y Tanizawa, Y Oka

HUMAN MOLECULAR GENETICS　13　(11)　1159-1170　2004/06

DOI： 10.1093/hmg/ddh125 　

ISSN： 0964-6906
Oxidative stress induces insulin resistance by activating the nuclear factor-kappa B pathway and disrupting normal subcellular distribution of phosphatidylinositol 3-kinase Peer-reviewed

T Ogihara, T Asano, H Katagiri, H Sakoda, M Anai, N Shojima, H Ono, M Fujishiro, A Kushiyama, Y Fukushima, M Kikuchi, N Noguchi, H Aburatani, Y Gotoh, Komuro, I, T Fujita

DIABETOLOGIA　47　(5)　794-805　2004/05

DOI： 10.1007/s00125-004-1391-x 　

ISSN： 0012-186X
Integrin-linked kinase (ILK) regulation of the cell viability in PTEN mutant glioblastoma and in vitro inhibition by the specific COX-2 inhibitor NS-398 Peer-reviewed

S Obara, M Nakata, H Takeshima, H Katagiri, T Asano, Y Oka, Maruyama, I, J Kuratsu

CANCER LETTERS　208　(1)　115-122　2004/05

DOI： 10.1016/j.canlet.2003.11.020 　

ISSN： 0304-3835
ANGPTL3 is increased in both insulin-deficient and -resistant diabetic states Peer-reviewed

K Inukai, Y Nakashima, M Watanabe, S Kurihara, T Awata, H Katagiri, Y Oka, S Katayama

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS　317　(4)　1075-1079　2004/05

DOI： 10.1016/j.bbrc.2004.03.151 　

ISSN： 0006-291X
Overexpression of constitutively activated glutamate dehydrogenase induces insulin secretion through enhanced glutamate oxidation Peer-reviewed

T Anno, S Uehara, H Katagiri, Y Ohta, K Ueda, H Mizuguchi, Y Moriyama, Y Oka, Y Tanizawa

AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM　286　(2)　E280-E285　2004/02

DOI： 10.1152/ajpendo.00380.2003 　

ISSN： 0193-1849
Hepatic akt activation induces marked hypoglycemia, hepatomegaly, and hypertriglyceridemia with sterol regulatory element binding protein involvement Peer-reviewed

H Ono, H Shimano, H Katagiri, N Yahagi, H Sakoda, Y Onishi, M Anai, T Ogihara, M Fujishiro, AYI Viana, Y Fukushima, M Abe, N Shojima, M Kikuchi, N Yamada, Y Oka, T Asano

DIABETES　52　(12)　2905-2913　2003/12

DOI： 10.2337/diabetes.52.12.2905 　

ISSN： 0012-1797
Suppression of arthritic bone destruction by adenovirus-mediated dominant-negative Ras gene transfer to synoviocytes and osteoclasts Peer-reviewed

A Yamamoto, A Fukuda, H Seto, T Miyazaki, Y Kadono, Y Sawada, Nakamura, I, H Katagiri, T Asano, Y Tanaka, H Oda, K Nakamura, S Tanaka

ARTHRITIS AND RHEUMATISM　48　(9)　2682-2692　2003/09

DOI： 10.1002/art.11214 　

ISSN： 0004-3591
Coxsackievirus and adenovirus receptor (CAR)-positive immature osteoblasts as targets of adenovirus-mediated gene transfer for fracture healing Peer-reviewed

T Ito, K Tokunaga, H Maruyama, H Kawashima, H Kitahara, T Horikoshi, A Ogose, Y Hotta, R Kuwano, H Katagiri, N Endo

GENE THERAPY　10　(18)　1623-1628　2003/09

DOI： 10.1038/sj.gt.3302060 　

ISSN： 0969-7128
Differing roles of Akt and serum- and glucocorticoid-regulated kinase in glucose metabolism, DNA synthesis, and oncogenic activity Peer-reviewed

H Sakoda, Y Gotoh, H Katagiri, M Kurokawa, H Ono, Y Onishi, M Anai, T Ogihara, M Fujishiro, Y Fukushima, M Abe, N Shojima, M Kikuchi, Y Oka, H Hirai, T Asano

JOURNAL OF BIOLOGICAL CHEMISTRY　278　(28)　25802-25807　2003/07

DOI： 10.1074/jbc.M301127200 　

ISSN： 0021-9258
Structural and functional characterization of gastric mucosa and central nervous system in histamine H-2 receptor-null mice Peer-reviewed

Y Fukushima, T Shindo, M Anai, T Saitoh, YH Wang, M Fujishiro, Y Ohashi, T Ogihara, K Inukai, H Ono, H Sakoda, Y Kurihara, M Honda, N Shojima, H Fukushima, Y Haraikawa-Onishi, H Katagiri, Y Shimizu, M Ichinose, T Ishikawa, M Omata, R Nagai, H Kurihara, T Asano

EUROPEAN JOURNAL OF PHARMACOLOGY　468　(1)　47-58　2003/05

DOI： 10.1016/S0014-2999(03)01668-6 　

ISSN： 0014-2999
Ethanol feeding induces insulin resistance with enhanced PI 3-kinase activation Peer-reviewed

Y Onishi, M Honda, T Ogihara, H Sakoda, M Anai, M Fujishiro, H Ono, N Shojima, Y Fukushima, K Inukai, H Katagiri, M Kikuchi, Y Oka, T Asano

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS　303　(3)　788-794　2003/04

DOI： 10.1016/S0006-291X(03)00407-8 　

ISSN： 0006-291X
Three mitogen-activated protein kinases inhibit insulin signaling by different mechanisms in 3T3-L1 adipocytes Peer-reviewed

M Fujishiro, Y Gotoh, H Katagiri, H Sakoda, T Ogihara, M Anai, Y Onishi, H Ono, W Abe, N Shojima, Y Fukushima, M Kikuchi, Y Oka, T Asano

MOLECULAR ENDOCRINOLOGY　17　(3)　487-497　2003/03

DOI： 10.1210/me.2002.0131 　

ISSN： 0888-8809
Regulation of PPAR gamma transcriptional activity in 3T3-L1 adipocytes Peer-reviewed

M Watanabe, K Inukai, H Katagiri, T Awata, Y Oka, S Katayama

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS　300　(2)　429-436　2003/01

DOI： 10.1016/S0006-291X(02)02860-7 　

ISSN： 0006-291X
Regulation of PPAR gamma transcriptional activity in 3T3-L1 adipocytes Peer-reviewed

M Watanabe, K Inukai, H Katagiri, T Awata, Y Oka, S Katayama

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS　300　(2)　429-436　2003/01

DOI： 10.1016/S0006-291X(02)02860-7 　

ISSN： 0006-291X
Extremely early onset of ranitidine action on human histamine H-2 receptors expressed in HEK293 cells Peer-reviewed

Y Fukushima, T Ishikawa, T Saitoh, K Tateishi, T Ogihara, M Fujishiro, N Shojima, M Honda, A Kushiyama, M Anai, H Sakoda, H Ono, Y Onishi, H Otsuka, H Katagiri, R Nagai, M Omata, T Asano

DIGESTION　68　(2-3)　145-152　2003

DOI： 10.1159/000075349 　

ISSN： 0012-2823
Angiotensin II-induced insulin resistance is associated with enhanced insulin signaling Peer-reviewed

T Ogihara, T Asano, K Ando, Y Chiba, H Sakoda, M Anai, N Shojima, H Ono, Y Onishi, M Fujishiro, H Katagiri, Y Fukushima, M Kikuchi, N Noguchi, H Aburatani, Komuro, I, T Fujita

HYPERTENSION　40　(6)　872-879　2002/12

DOI： 10.1161/01.HYP.0000040262.48405.A8 　

ISSN： 0194-911X
Angiotensin II-induced insulin resistance is associated with enhanced insulin signaling Peer-reviewed

T Ogihara, T Asano, K Ando, Y Chiba, H Sakoda, M Anai, N Shojima, H Ono, Y Onishi, M Fujishiro, H Katagiri, Y Fukushima, M Kikuchi, N Noguchi, H Aburatani, Komuro, I, T Fujita

HYPERTENSION　40　(6)　872-879　2002/12

DOI： 10.1161/01.HYP.0000040262.48405.A8 　

ISSN： 0194-911X
Resistin is regulated by C/EBPs, PPARs, and signal-transducing molecules Peer-reviewed

HY Song, N Shojima, H Sakoda, T Ogihara, M Fujishiro, H Katagiri, M Anai, Y Onishi, H Ono, K Inukai, Y Fukushima, M Kikuchi, H Shimano, N Yamada, Y Oka, T Asano

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS　299　(2)　291-298　2002/11

DOI： 10.1016/s0006-291x(02)02551-2 　

ISSN： 0006-291X
Resistin is regulated by C/EBPs, PPARs, and signal-transducing molecules Peer-reviewed

HY Song, N Shojima, H Sakoda, T Ogihara, M Fujishiro, H Katagiri, M Anai, Y Onishi, H Ono, K Inukai, Y Fukushima, M Kikuchi, H Shimano, N Yamada, Y Oka, T Asano

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS　299　(2)　291-298　2002/11

DOI： 10.1016/S0006-291X(02)02551-2 　

ISSN： 0006-291X
[Glucagon test]. Peer-reviewed

Tsunoda U, Katagiri H

Nihon rinsho. Japanese journal of clinical medicine　60 Suppl 8　308-312　2002/08

ISSN： 0047-1852
Role of PKC isoforms in glucose transport in 3T3-L1 adipocytes: insignificance of atypical PKC Peer-reviewed

M Tsuru, H Katagiri, T Asano, T Yamada, S Ohno, T Ogihara, Y Oka

AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM　283　(2)　E338-E345　2002/08

DOI： 10.1152/ajpendo.00457.2001 　

ISSN： 0193-1849
Humoral regulation of resistin expression in 3T3-L1 and mouse adipose cells Peer-reviewed

N Shojima, H Sakoda, T Ogihara, M Fujishiro, H Katagiri, M Anai, Y Onishi, H Ono, K Inukai, M Abe, Y Fukushima, M Kikuchi, Y Oka, T Asano

DIABETES　51　(6)　1737-1744　2002/06

ISSN： 0012-1797
Role of PDK1 in insulin-signaling pathway for glucose metabolism in 3T3-L1 adipocytes Peer-reviewed

T Yamada, H Katagiri, T Asano, M Tsuru, K Inukai, H Ono, T Kodama, M Kikuchi, Y Oka

AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM　282　(6)　E1385-E1394　2002/06

DOI： 10.1152/ajpendo.00486.2001 　

ISSN： 0193-1849
Activation of AMPK is essential for AICAR-induced glucose uptake by skeletal muscle but not adipocytes Peer-reviewed

H Sakoda, T Ogihara, M Anai, M Fujishiro, H Ono, Y Onishi, H Katagiri, M Abe, Y Fukushima, N Shojima, K Inukai, M Kikuchi, Y Oka, T Asano

AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM　282　(6)　E1239-E1244　2002/06

DOI： 10.1152/ajpendo.00455.2001 　

ISSN： 0193-1849
Acyl-coenzyme a dehydrogenases are localized on GLUT4-containing vesicles via association with insulin-regulated aminopeptidase in a manner dependent on its dileucine motif Peer-reviewed

H Katagiri, T Asano, T Yamada, T Aoyama, Y Fukushima, M Kikuchi, T Kodama, Y Oka

MOLECULAR ENDOCRINOLOGY　16　(5)　1049-1059　2002/05

DOI： 10.1210/mend.16.5.0831 　

ISSN： 0888-8809
Acyl-coenzyme a dehydrogenases are localized on GLUT4-containing vesicles via association with insulin-regulated aminopeptidase in a manner dependent on its dileucine motif Peer-reviewed

H Katagiri, T Asano, T Yamada, T Aoyama, Y Fukushima, M Kikuchi, T Kodama, Y Oka

MOLECULAR ENDOCRINOLOGY　16　(5)　1049-1059　2002/05

DOI： 10.1210/me.16.5.1049 　

ISSN： 0888-8809
Molecular mechanisms of insulin action and the impaired steps in insulin resistant conditions Peer-reviewed

Asano T, Ogihara T, Anai M, Katagiri H

Recent Res Devel Biochem　3　639-651　2002
Akt protein kinase inhibits non-apoptotic programmed cell death induced by ceramide Peer-reviewed

T Mochizuki, A Asai, N Saito, S Tanaka, H Katagiri, T Asano, M Nakane, A Tamura, Y Kuchino, C Kitanaka, T Kirino

JOURNAL OF BIOLOGICAL CHEMISTRY　277　(4)　2790-2797　2002/01

DOI： 10.1074/jbc.M106361200 　

ISSN： 0021-9258
Unique phosphorylation mechanism of Gab1 using PI 3-kinase as an adaptor protein Peer-reviewed

Y Onishi-Haraikawa, M Funaki, N Gotoh, M Shibuya, K Inukai, H Katagiri, Y Fukushima, M Anai, T Ogihara, H Sakoda, H Ono, M Kikuchi, Y Oka, T Asano

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS　288　(2)　476-482　2001/10

DOI： 10.1006/bbrc.2001.5791 　

ISSN： 0006-291X
Regulation of phosphoinositide metabolism, Akt phosphorylation, and glucose transport by PTEN (lhosphatase and tensin homolog deleted on chromosome 10) in 3T3-L1 adipocytes Peer-reviewed

H Ono, H Katagiri, M Funaki, M Anai, K Inukai, Y Fukushima, H Sakoda, T Ogihara, Y Onishi, M Fujishiro, M Kikuchi, Y Oka, T Asano

MOLECULAR ENDOCRINOLOGY　15　(8)　1411-1422　2001/08

DOI： 10.1210/me.15.8.1411 　

ISSN： 0888-8809
MKK6/3 and p38 MAPK pathway activation is not necessary for insulin-induced glucose uptake but regulates glucose transporter expression Peer-reviewed

M Fujishiro, Y Gotoh, H Katagiri, H Sakoda, T Ogihara, M Anai, Y Onishi, H Ono, M Funaki, K Inukai, Y Fukushima, M Kikuchi, Y Oka, T Asano

JOURNAL OF BIOLOGICAL CHEMISTRY　276　(23)　19800-19806　2001/06

DOI： 10.1074/jbc.M101087200 　

ISSN： 0021-9258

eISSN： 1083-351X
Five isoforms of the phosphatidylinositol 3-kinase regulatory subunit exhibit different associations with receptor tyrosine kinases and their tyrosine phosphorylations Peer-reviewed

Inukai, I, M Funaki, M Anai, T Ogihara, H Katagiri, Y Fukushima, H Sakoda, Y Onishi, H Ono, M Fujishiro, M Abe, Y Oka, M Kikuchi, T Asano

FEBS LETTERS　490　(1-2)　32-38　2001/02

DOI： 10.1016/S0014-5793(01)02132-9 　

ISSN： 0014-5793
3-Phosphoinositide-dependent protein kinase 1, an Akt1 kinase, is involved in dephosphorylation of Thr-308 of Akt1 in Chinese hamster ovary cells Peer-reviewed

T Yamada, H Katagiri, T Asano, K Inukai, M Tsuru, T Kodama, M Kikuchi, Y Oka

JOURNAL OF BIOLOGICAL CHEMISTRY　276　(7)　5339-5345　2001/02

DOI： 10.1074/jbc.M005685200 　

ISSN： 0021-9258
Proteins associated with insulin-regulated aminopeptidase in insulin sensitive tissues: a possible role in anchoring GLUT4 Peer-reviewed

Y Oka, T Yamada, H Katagiri, T Asano

CELL-SURFACE AMINOPEPTIDASES: BASIC AND CLINICAL ASPECTS　1218　259-264　2001

ISSN： 0531-5131
Insulin prevents cardiomyocytes from oxidative stress-induced apoptosis through activation of PI3 kinase/Akt Peer-reviewed

R Aikawa, M Nawano, YP Gu, H Katagiri, T Asano, WD Zhu, R Nagai, Komuro, I

CIRCULATION　102　(23)　2873-2879　2000/12

ISSN： 0009-7322
Partial functional recovery of paraplegic rat by adenovirus-mediated gene delivery of constitutively active MEK1 Peer-reviewed

T Miura, S Tanaka, A Seichi, M Arai, T Goto, H Katagiri, T Asano, H Oda, K Nakamura

EXPERIMENTAL NEUROLOGY　166　(1)　115-126　2000/11

DOI： 10.1006/exnr.2000.7493 　

ISSN： 0014-4886
Dexamethasone-induced insulin resistance in 3T3-L1 adipocytes is due to inhibition of glucose transport rather than insulin signal transduction Peer-reviewed

H Sakoda, T Ogihara, M Anai, M Funaki, K Inukai, H Katagiri, Y Fukushima, Y Onishi, H Ono, M Fujishiro, M Kikuchi, Y Oka, T Asano

DIABETES　49　(10)　1700-1708　2000/10

ISSN： 0012-1797
p110 beta is up-regulated during differentiation of 3T3-L1 cells and contributes to the highly insulin-responsive glucose transport activity Peer-reviewed

T Asano, A Kanda, H Katagiri, M Nawano, T Ogihara, K Inukai, M Anai, Y Fukushima, Y Yazaki, M Kikuchi, R Hooshmand-Rad, CH Heldin, Y Oka, M Funaki

JOURNAL OF BIOLOGICAL CHEMISTRY　275　(23)　17671-17676　2000/06

DOI： 10.1074/jbc.M910391199 　

ISSN： 0021-9258
Structure and function of phosphatidylinositol-3,4 kinase Peer-reviewed

M Funaki, H Katagiri, K Inukai, M Kikuchi, T Asano

CELLULAR SIGNALLING　12　(3)　135-142　2000/03

DOI： 10.1016/S0898-6568(99)00086-8 　

ISSN： 0898-6568
The N-terminal 34 residues of the 55 kDa regulatory subunits of phosphoinositide 5-kinase interact with tubulin Peer-reviewed

K Inukai, M Funaki, M Nawano, H Katagiri, T Ogihara, M Anai, Y Onishi, H Sakoda, H Ono, Y Fukushima, M Kikuchi, Y Oka, T Asano

BIOCHEMICAL JOURNAL　346　483-489　2000/03

DOI： 10.1042/0264-6021:3460483 　

ISSN： 0264-6021
Reciprocal role of ERK and NF-kappa B pathways in survival and activation of osteoclasts Peer-reviewed

T Miyazaki, H Katagiri, Y Kanegae, H Takayanagi, Y Sawada, A Yamamoto, MP Pando, T Asano, IM Verma, H Oda, K Nakamura, S Tanaka

JOURNAL OF CELL BIOLOGY　148　(2)　333-342　2000/01

DOI： 10.1083/jcb.148.2.333 　

ISSN： 0021-9525
Clinical relevance of heteroplasmic concentration of mitochondrial A3243 G mutation in leucocytes Peer-reviewed

T Asano, K Tsukuda, H Katagiri, Y Onishi, H Sakoda, H Ono, T Ogihara, M Funaki, M Anai, K Inukai, M Fujishiro, Y Fukushima, T Yamasoba, T Oka, M Kikuchi, Y Oka

DIABETOLOGIA　42　(12)　1439-1440　1999/12

DOI： 10.1007/s001250051316 　

ISSN： 0012-186X
No correlation of plasma cell 1 overexpression with insulin resistance in diabetic rats and 3T3-L1 adipocytes Peer-reviewed

H Sakoda, T Ogihara, M Anai, M Funaki, K Inukai, H Katagiri, Y Fukushima, Y Onishi, H Ono, Y Yazaki, M Kikuchi, Y Oka, T Asano

DIABETES　48　(7)　1365-1371　1999/07

DOI： 10.2337/diabetes.48.7.1365 　

ISSN： 0012-1797
p85/p110-type phosphatidylinositol kinase phosphorylates not only the D-3, but also the D-4 position of the inositol ring Peer-reviewed

M Funaki, H Katagiri, A Kanda, M Anai, R Nawano, T Ogihara, K Inukai, Y Fukushima, H Ono, Y Yazaki, M Kikuchi, Y Oka, T Asano

JOURNAL OF BIOLOGICAL CHEMISTRY　274　(31)　22019-22024　1999/07

DOI： 10.1074/jbc.274.31.22019 　

ISSN： 0021-9258

eISSN： 1083-351X
Enhanced expression of glucose transporter GLUT3 in tumorigenic HeLa cell hybrids associated with tumor suppressor dysfunction Peer-reviewed

T Suzuki, A Iwazaki, H Katagiri, Y Oka, JL Redpath, EJ Stanbridge, T Kitagawa

EUROPEAN JOURNAL OF BIOCHEMISTRY　262　(2)　534-540　1999/06

DOI： 10.1046/j.1432-1327.1999.00421.x 　

ISSN： 0014-2956
Role of JTT-501, a new insulin sensitiser, in restoring impaired GLUT4 translocation in adipocytes of rats fed a high fat diet Peer-reviewed

J Terasaki, M Anai, M Funaki, T Shibata, K Inukai, T Ogihara, H Ishihara, H Katagiri, Y Onishi, H Sakoda, Y Fukushima, Y Yazaki, M Kikuchi, Y Oka, T Asano

DIABETOLOGIA　41　(4)　400-409　1998/04

DOI： 10.1007/s001250050922 　

ISSN： 0012-186X
Altered expression levels and impaired steps in the pathway to phosphatidylinositol 3-kinase activation via insulin receptor substrates 1 and 2 in Zucker fatty rats Peer-reviewed

M Anai, M Funaki, T Ogihara, J Terasaki, K Inukai, H Katagiri, Y Fukushima, Y Yazaki, M Kikuchi, Y Oka, T Asano

DIABETES　47　(1)　13-23　1998/01

ISSN： 0012-1797
Screening of patients with maternally transmitted diabetes for mitochondrial gene mutations in the tRNA(Leu(UUR)) region Peer-reviewed

K Tsukuda, Y Suzuki, K Kameoka, N Osawa, Y Goto, H Katagiri, T Asano, Y Yazaki, Y Oka

DIABETIC MEDICINE　14　(12)　1032-1037　1997/12

DOI： 10.1002/(SICI)1096-9136(199712)14:12<1032::AID-DIA504>3.0.CO;2-Y 　

ISSN： 0742-3071
Role of the C terminus in histamine H2 receptor signaling, desensitization, and agonist-induced internalization Peer-reviewed

Y Fukushima, T Asano, K Takata, M Funaki, T Ogihara, M Anai, K Tsukuda, T Saitoh, H Katagiri, M Aihara, N Matsuhashi, Y Oka, Y Yazaki, K Sugano

JOURNAL OF BIOLOGICAL CHEMISTRY　272　(31)　19464-19470　1997/08

DOI： 10.1074/jbc.272.31.19464 　

ISSN： 0021-9258
Oligomer formation of histamine H2 receptors expressed in Sf9 and COS7 cells Peer-reviewed

Y Fukushima, T Asano, T Saitoh, M Anai, M Funaki, T Ogihara, H Katagiri, N Matsuhashi, Y Yazaki, K Sugano

FEBS LETTERS　409　(2)　283-286　1997/06

DOI： 10.1016/S0014-5793(97)00531-0 　

ISSN： 0014-5793
Insulin receptor substrate (IRS)-2 is dephosphorylated more rapidly than IRS-1 via its association with phosphatidylinositol 3-kinase in skeletal muscle cells Peer-reviewed

T Ogihara, BC Shin, M Anai, H Katagiri, K Inukai, M Funaki, Y Fukushima, H Ishihara, K Takata, M Kikuchi, Y Yazaki, Y Oka, T Asano

JOURNAL OF BIOLOGICAL CHEMISTRY　272　(19)　12868-12873　1997/05

DOI： 10.1074/jbc.272.19.12868 　

ISSN： 0021-9258
Targeting of GLUT1-GLUT5 chimeric proteins in the polarized cell line Caco-2 Peer-reviewed

K Inukai, K Takata, T Asano, H Katagiri, H Ishihara, M Nakazaki, Y Fukushima, Y Yazaki, M Kikuchi, Y Oka

MOLECULAR ENDOCRINOLOGY　11　(4)　442-449　1997/04

DOI： 10.1210/me.11.4.442 　

ISSN： 0888-8809
Molecular mechanism of insulin-stimulated glucose transport in 3T3-L1 adipocytes. Invited Peer-reviewed

Oka Y, Hosaka T, Katagiri H, Asano T

Jpn J Physiol　47 Suppl 1　S49-S49　1997/04
Co-localization of glucokinase with actin filaments Peer-reviewed

T Murata, H Katagiri, H Ishihara, Y Shibasaki, T Asano, Y Toyoda, B Pekiner, C Pekiner, Miwa, I, Y Oka

FEBS LETTERS　406　(1-2)　109-113　1997/04

DOI： 10.1016/S0014-5793(97)00253-6 　

ISSN： 0014-5793
p85 alpha gene generates three isoforms of regulatory subunit for phosphatidylinositol 3-kinase (PI 3-kinase), p50 alpha, p55 alpha, and p85 alpha, with different PI 3-kinase activity elevating responses to insulin Peer-reviewed

K Inukai, M Funaki, T Ogihara, H Katagiri, A Kanda, M Anai, Y Fukushima, T Hosaka, M Suzuki, BC Shin, K Takata, Y Yazaki, M Kikuchi, Y Oka, T Asano

JOURNAL OF BIOLOGICAL CHEMISTRY　272　(12)　7873-7882　1997/03

DOI： 10.1074/jbc.272.12.7873 　

ISSN： 0021-9258
Roles of PI 3-kinase and Ras on insulin-stimulated glucose transport in 3T3-L1 adipocytes Peer-reviewed

H Katagiri, T Asano, K Inukai, T Ogihara, H Ishihara, Y Shibasaki, T Murata, J Terasaki, M Kikuchi, Y Yazaki, Y Oka

AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM　272　(2)　E326-E331　1997/02

ISSN： 0193-1849
Interaction between the two signal transduction systems of the histamine H2 receptor: Desensitizing and sensitizing effects of histamine stimulation on histamine-dependent cAMP production in Chinese hamster ovary cells Peer-reviewed

Y Fukushima, T Asano, H Katagiri, M Aihara, T Saitoh, M Anai, M Funaki, T Ogihara, K Inukai, N Matsuhashi, Y Oka, Y Yazaki, K Sugano

BIOCHEMICAL JOURNAL　320　27-32　1996/11

ISSN： 0264-6021
Association between HLA and islet cell antibodies in diabetic patients with a mitochondrial DNA mutation at base pair 3243 Peer-reviewed

T Kobayashi, Y Oka, H Katagiri, A Falorni, A Kasuga, Takei, I, K Nakanishi, T Murase, K Kosaka, A Lernmark

DIABETOLOGIA　39　(10)　1196-1200　1996/10

DOI： 10.1007/BF02658506 　

ISSN： 0012-186X
beta-cell loss and glucose induced signalling defects in diabetes mellitus caused by mitochondrial tRNA(Leu)(UUR) gene mutation Peer-reviewed

Y Oka, H Katagiri, H Ishihara, T Asano, T Kobayashi, M Kikuchi

DIABETIC MEDICINE　13　(9)　S98-S102　1996/09

ISSN： 0742-3071
Effect of mitochondrial and/or cytosolic glycerol S-phosphate dehydrogenase overexpression on glucose-stimulated insulin secretion from MIN6 and HIT cells Peer-reviewed

H Ishihara, M Nakazaki, Y Kanegae, K Inukai, T Asano, H Katagiri, Y Yazaki, M Kikuchi, J Miyazaki, Saito, I, Y Oka

DIABETES　45　(9)　1238-1244　1996/09

ISSN： 0012-1797
Cloning of cDNAs encoding two isoforms of 68-kDa type I phosphatidylinositol-4-phosphate 5-kinase Peer-reviewed

H Ishihara, Y Shibasaki, N Kizuki, H Katagiri, Y Yazaki, T Asano, Y Oka

JOURNAL OF BIOLOGICAL CHEMISTRY　271　(39)　23611-23614　1996/09

DOI： 10.1074/jbc.271.39.23611 　

ISSN： 0021-9258
Overexpression of catalytic subunit p110 alpha of phosphatidylinositol 3-kinase increases glucose transport activity with translocation of glucose transporters in 3T3-L1 adipocytes Peer-reviewed

H Katagiri, T Asano, H Ishihara, K Inukai, Y Shibasaki, M Kikuchi, Y Yazaki, Y Oka

JOURNAL OF BIOLOGICAL CHEMISTRY　271　(29)　16987-16990　1996/07

DOI： 10.1074/jbc.271.29.16987 　

ISSN： 0021-9258
A human pancreatic islet inwardly rectifying potassium channel: cDNA cloning, determination of the genomic structure and genetic variations in Japanese NIDDM patients Peer-reviewed

Y Tanizawa, A Matsubara, K Ueda, H Katagiri, A Kuwano, J Ferrer, MA Permutt, Y Oka

DIABETOLOGIA　39　(4)　447-452　1996/04

DOI： 10.1007/s001250050464 　

ISSN： 0012-186X
A novel 55-kDa regulatory subunit for phosphatidylinositol 3-kinase structurally similar to p55PIK is generated by alternative splicing of the p85 alpha gene Peer-reviewed

K Inukai, M Anai, E VanBreda, T Hosaka, H Katagiri, M Funaki, Y Fukushima, T Ogihara, Y Yazaki, M Kikuchi, Y Oka, T Asano

JOURNAL OF BIOLOGICAL CHEMISTRY　271　(10)　5317-5320　1996/03

DOI： 10.1074/jbc.271.10.5317 　

ISSN： 0021-9258
CHARACTERIZATION OF RAT GLUT5 AND FUNCTIONAL-ANALYSIS OF CHIMERIC PROTEINS OF GLUT1 GLUCOSE-TRANSPORTER AND GLUT5 FRUCTOSE TRANSPORTER Peer-reviewed

K INUKAI, H KATAGIRI, K TAKATA, T ASANO, M ANAI, H ISHIHARA, M NAKAZAKI, M KIKUCHI, Y YAZAKI, Y OKA

ENDOCRINOLOGY　136　(11)　4850-4857　1995/11

ISSN： 0013-7227

eISSN： 1945-7170
HUMAN GLUT-2 OVEREXPRESSION DOES NOT AFFECT GLUCOSE-STIMULATED INSULIN-SECRETION IN MIN6 CELLS Peer-reviewed

H ISHIHARA, T ASANO, K TSUKUDA, H KATAGIRI, K INUKAI, M ANAI, Y YAZAKI, J MIYAZAKI, M KIKUCHI, Y OKA

AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM　269　(5)　E897-E902　1995/11

ISSN： 0193-1849
STRUCTURAL AND FUNCTIONAL-ANALYSIS OF THE CANINE HISTAMINE-H2-RECEPTOR BY SITE-DIRECTED MUTAGENESIS - N-GLYCOSYLATION IS NOT VITAL FOR ITS ACTION Peer-reviewed

Y FUKUSHIMA, Y OKA, T SAITOH, H KATAGIRI, T ASANO, N MATSUHASHI, K TAKATA, E VANBREDA, Y YAZAKI, K SUGANO

BIOCHEMICAL JOURNAL　310　553-558　1995/09

ISSN： 0264-6021
INHIBITION OF PANCREATIC BETA-CELL GLUCOKINASE BY ANTISENSE RNA EXPRESSION IN TRANSGENIC MICE - MOUSE STRAIN-DEPENDENT ALTERATION OF GLUCOSE-TOLERANCE Peer-reviewed

H ISHIHARA, F TASHIRO, K IKUTA, T ASANO, H KATAGIRI, K INUKAI, M KIKUCHI, Y YAZAKI, Y OKA, J MIYAZAKI

FEBS LETTERS　371　(3)　329-332　1995/09

DOI： 10.1016/0014-5793(95)00932-Y 　

ISSN： 0014-5793
INSULIN EDEMA IN DIABETES-MELLITUS ASSOCIATED WITH THE 3243-MITOCHONDRIAL TRNA(LEU(UUR)) MUTATION - CASE-REPORTS Peer-reviewed

Y SUZUKI, H KADOWAKI, M TANIYAMA, T KADOWAKI, H KATAGIRI, Y OKA, Y ATSUMI, K HOSOKAWA, Y TANAKA, T ASAHINA, Y MOMIYAMA, K MATSUOKA

DIABETES RESEARCH AND CLINICAL PRACTICE　29　(2)　137-142　1995/08

ISSN： 0168-8227
A PATIENT WITH DIABETES-MELLITUS, CARDIOMYOPATHY, AND A MITOCHONDRIAL GENE MUTATION - CONFIRMATION OF A GENE MUTATION IN CARDIAC-MUSCLE Peer-reviewed

H KITAOKA, K KAMEOKA, Y SUZUKI, E SASAKI, M MAJIMA, K TAKADA, H KATAGIRI, Y OKA, N OHSAWA

DIABETES RESEARCH AND CLINICAL PRACTICE　28　(3)　207-212　1995/06

ISSN： 0168-8227
A CASE OF DIABETIC AMYOTROPHY ASSOCIATED WITH 3243 MITOCHONDRIAL TRNA(LEU UUR) MUTATION AND SUCCESSFUL THERAPY WITH COENZYME-Q10 Peer-reviewed

Y SUZUKI, H KADOWAKI, Y ATSUMI, K HOSOKAWA, H KATAGIRI, T KADOWAKI, Y OKA, K UYAMA, A MOKUBO, T ASAHINA, C MURATA, K MATSUOKA

ENDOCRINE JOURNAL　42　(2)　141-145　1995/04

DOI： 10.1507/endocrj.42.141 　

ISSN： 0918-8959
DESENSITIZATION OF ENDOTHELIN-1 BINDING BY VASOPRESSIN VIA A CAMP-MEDIATED PATHWAY IN RAT CCD Peer-reviewed

F TAKEMOTO, S UCHIDA, H KATAGIRI, Y OKA, A NAKAO, K KUROKAWA

AMERICAN JOURNAL OF PHYSIOLOGY-RENAL FLUID AND ELECTROLYTE PHYSIOLOGY　268　(3)　F385-F390　1995/03

ISSN： 0363-6127
A NOVEL ISOFORM OF SYNTAXIN-BINDING PROTEIN HOMOLOGOUS TO YEAST SEC1 EXPRESSED UBIQUITOUSLY IN MAMMALIAN-CELLS Peer-reviewed

H KATAGIRI, J TERASAKI, T MURATA, H ISHIHARA, T OGIHARA, K INUKAI, Y FUKUSHIMA, M ANAI, M KIKUCHI, J MIYAZAKI, Y YAZAKI, Y OKA

JOURNAL OF BIOLOGICAL CHEMISTRY　270　(10)　4963-4966　1995/03

DOI： 10.1074/jbc.270.10.4963 　

ISSN： 0021-9258
A Case of Mitochondrial Diabetes Mellitus with Various Autonomic Symptoms and Subclinical Cardiac Dysfunction Peer-reviewed

Yoshihiko Suzuki, Yukihiko Momiyama, Yoshihito Atsumi, Kazuhiro Hosokawa, Mitsuru Kimura, Hideki Katagiri, Takashi Kadowaki, Yoshitomo Oka, Kempei Matsuoka

Journal of the Japan Diabetes Society　38　(1)　39-44　1995

DOI： 10.11213/tonyobyo1958.38.39 　

ISSN： 0021-437X
MITOCHONDRIAL DIABETES-MELLITUS - GLUCOSE-INDUCED SIGNALING DEFECTS AND BETA-CELL LOSS Peer-reviewed

Y OKA, H KATAGIRI, H ISHIHARA, T ASANO, M KIKUCHI, T KOBAYASHI

MUSCLE & NERVE　3　S131-S136　1995

ISSN： 0148-639X
REGULATION OF GLUCOSE-TRANSPORTER-1 (GLUT1) GENE-EXPRESSION BY EPIDERMAL GROWTH-FACTOR IN BOVINE CORNEAL ENDOTHELIAL-CELLS Peer-reviewed

K ISHIDA, H YAMASHITA, H KATAGIRI, Y OKA

JAPANESE JOURNAL OF OPHTHALMOLOGY　39　(3)　225-232　1995

ISSN： 0021-5155
REPLACEMENT OF BATH TRYPTOPHAN RESIDUES AT 388 AND 412 COMPLETELY ABOLISHED CYTOCHALASIN-B PHOTOLABELING OF THE GLUT1 GLUCOSE-TRANSPORTER Peer-reviewed

K INUKAI, T ASANO, H KATAGIRI, M ANAI, M FUNAKI, H ISHIHARA, K TSUKUDA, M KIKUCHI, Y YAZAKI, Y OKA

BIOCHEMICAL JOURNAL　302　355-361　1994/09

ISSN： 0264-6021
POSTTREATMENT NEUROPATHY IN DIABETIC SUBJECTS WITH MITOCHONDRIAL TRANSFER-RNA (LEU) MUTATION Peer-reviewed

Y SUZUKI, H KADOWAKI, H KATAGIRI, M SUEMATSU, Y ATSUMI, K HOSOKAWA, T KADOWAKI, Y OKA, Y YAZAKI, K MATSUOKA

DIABETES CARE　17　(7)　777-778　1994/07

ISSN： 0149-5992
MITOCHONDRIAL DIABETES-MELLITUS - PREVALENCE AND CLINICAL CHARACTERIZATION OF DIABETES DUE TO MITOCHONDRIAL TRNA(LEU(UUR)) GENE MUTATION IN JAPANESE PATIENTS Peer-reviewed

H KATAGIRI, T ASANO, H ISHIHARA, K INUKAI, M ANAI, T YAMANOUCHI, K TSUKUDA, M KIKUCHI, H KITAOKA, N OHSAWA, Y YAZAKI, Y OKA

DIABETOLOGIA　37　(5)　504-510　1994/05

ISSN： 0012-186X
Application of reverse transcription-polymerase chain reaction to study the glucose transporter protein gene (GLUT1) expression in preimplantation mouse embryos Peer-reviewed

Morita Y, Tsutsumi O, Oka Y, Katagiri H, Taketani Y

J. Mamm. Ova Res　11　1-7　1994
OVEREXPRESSION OF HEXOKINASE-I BUT NOT GLUT1 GLUCOSE-TRANSPORTER ALTERS CONCENTRATION-DEPENDENCE OF GLUCOSE-STIMULATED INSULIN-SECRETION IN PANCREATIC BETA-CELL LINE MIN6 Peer-reviewed

H ISHIHARA, T ASANO, K TSUKUDA, H KATAGIRI, K INUKAI, M ANAI, M KIKUCHI, Y YAZAKI, J MIYAZAKI, Y OKA

JOURNAL OF BIOLOGICAL CHEMISTRY　269　(4)　3081-3087　1994/01

ISSN： 0021-9258
SUPEROXIDE-DISMUTASE IN DEVELOPING MOUSE RETINA Peer-reviewed

H YAMASHITA, K HORIE, T YAMAMOTO, H KATAGIRI, T ASANO, T HIRANO, T NAGANO, Y OKA

JAPANESE JOURNAL OF OPHTHALMOLOGY　38　(2)　148-161　1994

ISSN： 0021-5155
PANCREATIC BETA-CELL LINE MIN6 EXHIBITS CHARACTERISTICS OF GLUCOSE-METABOLISM AND GLUCOSE-STIMULATED INSULIN-SECRETION SIMILAR TO THOSE OF NORMAL ISLETS Peer-reviewed

H ISHIHARA, T ASANO, K TSUKUDA, H KATAGIRI, K INUKAI, M ANAI, M KIKUCHI, Y YAZAKI, JI MIYAZAKI, Y OKA

DIABETOLOGIA　36　(11)　1139-1145　1993/11

ISSN： 0012-186X
CLONING AND INCREASED EXPRESSION WITH FRUCTOSE FEEDING OF RAT JEJUNAL GLUT5 Peer-reviewed

K INUKAI, T ASANO, H KATAGIRI, H ISHIHARA, M ANAI, Y FUKUSHIMA, K TSUKUDA, M KIKUCHI, Y YAZAKI, Y OKA

ENDOCRINOLOGY　133　(5)　2009-2014　1993/11

ISSN： 0013-7227
MITOCHONDRIAL GENE MUTATION IN ISLET-CELL-ANTIBODY-POSITIVE PATIENTS WHO WERE INITIALLY NON-INSULIN-DEPENDENT DIABETICS Peer-reviewed

Y OKA, H KATAGIRI, Y YAZAKI, T MURASE, T KOBAYASHI

LANCET　342　(8870)　527-528　1993/08

DOI： 10.1016/0140-6736(93)91649-7 　

ISSN： 0140-6736
THE ROLE OF N-GLYCOSYLATION IN THE TARGETING AND STABILITY OF GLUT1 GLUCOSE-TRANSPORTER Peer-reviewed

T ASANO, K TAKATA, H KATAGIRI, H ISHIHARA, K INUKAI, M ANAI, H HIRANO, Y YAZAKI, Y OKA

FEBS LETTERS　324　(3)　258-261　1993/06

DOI： 10.1016/0014-5793(93)80129-I 　

ISSN： 0014-5793
ROLE OF TRYPTOPHAN-388 OF GLUT1 GLUCOSE TRANSPORTER IN GLUCOSE-TRANSPORT ACTIVITY AND PHOTOAFFINITY-LABELING WITH FORSKOLIN Peer-reviewed

H KATAGIRI, T ASANO, H ISHIHARA, JL LIN, K INUKAI, MF SHANAHAN, K TSUKUDA, M KIKUCHI, Y YAZAKI, Y OKA

BIOCHEMICAL JOURNAL　291　861-867　1993/05

ISSN： 0264-6021
GLUCOKINASE-DEFECTIVE NIDDM Peer-reviewed

H KATAGIRI, T ASANO, T YAMANOUCHI, Y YAZAKI, Y OKA

LANCET　341　(8850)　961-962　1993/04

ISSN： 0140-6736
EXPRESSION OF GLUT-4 GLUCOSE TRANSPORTER IN UNWEIGHTED SOLEUS MUSCLE OF NORMAL AND STZ-INDUCED DIABETIC RATS Peer-reviewed

H ISHIHARA, T ASANO, H KATAGIRI, JL LIN, K TSUKUDA, K INUKAI, Y YAZAKI, Y OKA

AMERICAN JOURNAL OF PHYSIOLOGY　264　(2)　E301-E307　1993/02

ISSN： 0002-9513
DESENSITIZATION OF CANINE HISTAMINE-H2-RECEPTOR EXPRESSED IN CHINESE-HAMSTER OVARY CELLS Peer-reviewed

Y FUKUSHIMA, Y OKA, H KATAGIRI, T SAITOH, T ASANO, H ISHIHARA, N MATSUHASHI, T KODAMA, Y YAZAKI, K SUGANO

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS　190　(3)　1149-1155　1993/02

DOI： 10.1006/bbrc.1993.1170 　

ISSN： 0006-291X
REPLACEMENT OF INTRACELLULAR C-TERMINAL DOMAIN OF GLUT1 GLUCOSE TRANSPORTER WITH THAT OF GLUT2 INCREASES V(MAX) AND K(M) OF TRANSPORT ACTIVITY Peer-reviewed

H KATAGIRI, T ASANO, H ISHIHARA, K TSUKUDA, JL LIN, K INUKAI, M KIKUCHI, Y YAZAKI, Y OKA

JOURNAL OF BIOLOGICAL CHEMISTRY　267　(31)　22550-22555　1992/11

ISSN： 0021-9258
CHARACTERIZATION OF GLUT3 PROTEIN EXPRESSED IN CHINESE-HAMSTER OVARY CELLS Peer-reviewed

T ASANO, H KATAGIRI, K TAKATA, K TSUKUDA, JL LIN, H ISHIHARA, K INUKAI, H HIRANO, Y YAZAKI, Y OKA

BIOCHEMICAL JOURNAL　288　189-193　1992/11

ISSN： 0264-6021
NONSENSE MUTATION OF GLUCOKINASE GENE IN LATE-ONSET NON-INSULIN-DEPENDENT DIABETES-MELLITUS Peer-reviewed

H KATAGIRI, T ASANO, H ISHIHARA, K INUKAI, M ANAI, J MIYAZAKI, K TSUKUDA, M KIKUCHI, Y YAZAKI, Y OKA

LANCET　340　(8831)　1316-1317　1992/11

DOI： 10.1016/0140-6736(92)92494-Z 　

ISSN： 0140-6736
DOMAINS RESPONSIBLE FOR THE DIFFERENTIAL TARGETING OF GLUCOSE TRANSPORTER ISOFORMS Peer-reviewed

T ASANO, K TAKATA, H KATAGIRI, K TSUKUDA, JL LIN, H ISHIHARA, K INUKAI, H HIRANO, Y YAZAKI, Y OKA

JOURNAL OF BIOLOGICAL CHEMISTRY　267　(27)　19636-19641　1992/09

ISSN： 0021-9258
DELETION OF C-TERMINAL 12 AMINO-ACIDS OF GLUT1 PROTEIN DOES NOT ABOLISH THE TRANSPORT ACTIVITY Peer-reviewed

JL LIN, T ASANO, H KATAGIRI, K TSUKUDA, H ISHIHARA, K INUKAI, Y YAZAKI, Y OKA

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS　184　(2)　865-870　1992/04

DOI： 10.1016/0006-291X(92)90670-G 　

ISSN： 0006-291X
2 GLUCOSE TRANSPORTER ISOFORMS ARE SORTED DIFFERENTIALLY AND ARE EXPRESSED IN DISTINCT CELLULAR COMPARTMENTS Peer-reviewed

Y SHIBASAKI, T ASANO, JL LIN, K TSUKUDA, H KATAGIRI, H ISHIHARA, Y YAZAKI, Y OKA

BIOCHEMICAL JOURNAL　281　829-834　1992/02

ISSN： 0264-6021
GLUCOSE BINDING ENHANCES THE PAPAIN SUSCEPTIBILITY OF THE INTRACELLULAR LOOP OF THE GLUT1 GLUCOSE TRANSPORTER Peer-reviewed

T ASANO, H KATAGIRI, K TSUKUDA, JL LIN, H ISHIHARA, K INUKAI, Y YAZAKI, Y OKA

FEBS LETTERS　298　(2-3)　129-132　1992/02

ISSN： 0014-5793
EXPRESSION OF GLUCOSE TRANSPORTER ISOFORMS WITH AGING Peer-reviewed

Y OKA, T ASANO, JL LIN, K TSUKUDA, H KATAGIRI, H ISHIHARA, K INUKAI, Y YAZAKI

GERONTOLOGY　38　3-9　1992

ISSN： 0304-324X
UP-REGULATION OF GLUT2 MESSENGER-RNA BY GLUCOSE, MANNOSE, AND FRUCTOSE IN ISOLATED RAT HEPATOCYTES Peer-reviewed

T ASANO, H KATAGIRI, K TSUKUDA, JL LIN, H ISHIHARA, Y YAZAKI, Y OKA

DIABETES　41　(1)　22-25　1992/01

ISSN： 0012-1797
THE ROLE OF N-GLYCOSYLATION OF GLUT1 FOR GLUCOSE-TRANSPORT ACTIVITY Peer-reviewed

T ASANO, H KATAGIRI, K TAKATA, JL LIN, H ISHIHARA, K INUKAI, K TSUKUDA, M KIKUCHI, H HIRANO, Y YAZAKI, Y OKA

JOURNAL OF BIOLOGICAL CHEMISTRY　266　(36)　24632-24636　1991/12

ISSN： 0021-9258
EXPRESSION OF THE GLUT1 GLUCOSE TRANSPORTER INCREASES THYMIDINE UPTAKE IN CHINESE-HAMSTER OVARY CELLS AT LOW GLUCOSE-CONCENTRATIONS Peer-reviewed

T ASANO, Y SHIBASAKI, JL LIN, K TSUKUDA, H KATAGIRI, H ISHIHARA, Y YAZAKI, Y OKA

CANCER RESEARCH　51　(16)　4450-4454　1991/08

ISSN： 0008-5472
ALTERED EXPRESSION OF GLUCOSE TRANSPORTER ISOFORMS WITH AGING IN RATS - SELECTIVE DECREASE IN GLUT4 IN THE FAT TISSUE AND SKELETAL-MUSCLE Peer-reviewed

JL LIN, T ASANO, Y SHIBASAKI, K TSUKUDA, H KATAGIRI, H ISHIHARA, F TAKAKU, Y OKA

DIABETOLOGIA　34　(7)　477-482　1991/07

ISSN： 0012-186X
SUBSTITUTION OF LEUCINE FOR TRYPTOPHAN-412 DOES NOT ABOLISH CYTOCHALASIN-B LABELING BUT MARKEDLY DECREASES THE INTRINSIC ACTIVITY OF GLUT1 GLUCOSE TRANSPORTER Peer-reviewed

H KATAGIRI, T ASANO, Y SHIBASAKI, JL LIN, K TSUKUDA, H ISHIHARA, Y AKANUMA, F TAKAKU, Y OKA

JOURNAL OF BIOLOGICAL CHEMISTRY　266　(12)　7769-7773　1991/04

ISSN： 0021-9258
THE GLUCOSE-TRANSPORT ACTIVITY OF GLUT1 IS MARKEDLY DECREASED BY SUBSTITUTION OF A SINGLE AMINO-ACID WITH A DIFFERENT CHARGE AT RESIDUE-415 Peer-reviewed

H ISHIHARA, T ASANO, H KATAGIRI, JL LIN, K TSUKUDA, Y SHIBASAKI, Y YAZAKI, Y OKA

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS　176　(2)　922-930　1991/04

DOI： 10.1016/S0006-291X(05)80274-8 　

ISSN： 0006-291X
PEPTIDE-BASED RADIOIMMUNOASSAY SPECIFIC FOR GLUT1 GLUCOSE TRANSPORTER Peer-reviewed

K TSUKUDA, T ASANO, JL LIN, H KATAGIRI, H ISHIHARA, F TAKAKU, Y OKA

DIABETES　40　(3)　315-318　1991/03

ISSN： 0012-1797
C-TERMINAL TRUNCATED GLUCOSE TRANSPORTER IS LOCKED INTO AN INWARD-FACING FORM WITHOUT TRANSPORT ACTIVITY Peer-reviewed

Y OKA, T ASANO, Y SHIBASAKI, JL LIN, K TSUKUDA, H KATAGIRI, Y AKANUMA, F TAKAKU

NATURE　345　(6275)　550-553　1990/06

DOI： 10.1038/345550a0 　

ISSN： 0028-0836

Show all ︎Show first 5

Misc. 14

神経ネットワークを介した膵α細胞量の調節

椎木幾久子, 田部勝也, 井泉知仁, 吉村充弘, 西村渉, 今井淳太, 奥屋茂, 上田陽一, 片桐秀樹, 谷澤幸生

糖尿病(Web)　66　(Suppl)　2023

ISSN： 1881-588X
2型糖尿病患者におけるLaser speckle flowgraphyによる視神経乳頭領域の眼血流指標と超音波検査による頸動脈血流指標との関係

澤田正二郎, 佐竹千尋, 國方彦志, 安田正幸, 伊藤梓, 黒澤聡子, 児玉慎二郎, 山本淳平, 金子慶三, 今井淳太, 中澤徹, 片桐秀樹

糖尿病　62　(Suppl.1)　S-128　2019/04
Publisher: (一社)日本糖尿病学会
ISSN： 0021-437X
Staphylococcus warneriによる感染性心内膜炎(IE)を発症した1型糖尿病の1例

山本淳平, 遠藤彰, 山本沙織, 秋山正年, 安達理, 金子慶三, 澤田正二郎, 今井淳太, 下川宏明, 齋木佳克, 片桐秀樹

糖尿病　62　(3)　198-198　2019/03
Publisher: (一社)日本糖尿病学会
ISSN： 0021-437X
肝臓・骨格筋いずれでインスリン受容体を後天的に欠損させても全身におけるグルコース酸化はむしろ増加する

高橋圭, 山田哲也, 椙澤貴志, 川田恵子, 児玉慎二郎, 浅井洋一郎, 宗像佑一郎, 高橋広延, 穂坂真一郎, 清家準朗, 井泉知仁, 高俊弘, 宇野健司, 澤田正二郎, 今井淳太, 稲田睦, 片桐秀樹

糖尿病　61　(Suppl.1)　S-363　2018/04
Publisher: (一社)日本糖尿病学会
ISSN： 0021-437X
血管内皮特異的なNF-κB経路の遮断は老齢マウスにおける膵β細胞の老化を抑制する

高橋広延, 山田哲也, 突田壮平, 宗像佑一郎, 高橋圭, 児玉慎二郎, 浅井洋一郎, 穂坂真一郎, 清家準郎, 宇野健司, 澤田正二郎, 今井淳太, 片桐秀樹

糖尿病　61　(Suppl.1)　S-386　2018/04
Publisher: (一社)日本糖尿病学会
ISSN： 0021-437X
頭蓋内胚細胞腫放射線治療後汎下垂体機能低下症患者の難治性視床下部性肥満に対し肥満外科手術を試みた一例

祢津昌広, 工藤正孝, 手塚雄太, 森本玲, 小野美澄, 五十嵐康宏, 澤田正二郎, 田中直樹, 内藤剛, 片桐秀樹, 伊藤貞嘉, 佐藤文俊

日本内分泌学会雑誌　94　(1)　406-406　2018/04
Publisher: (一社)日本内分泌学会
ISSN： 0029-0661
LSG施行後5年目にrevision surgeryとして再LSG/DJBを施行した糖尿病合併重症肥満の1例

伊勢一郎, 田中直樹, 河野えみ子, 土屋堯裕, 井本博文, 渡辺和宏, 長尾宗紀, 武者宏昭, 澤田正二郎, 片桐秀樹, 岡本智子, 武田みゆき, 内藤剛, 海野倫明

日本肥満症治療学会学術集会プログラム・抄録集　34回　75-75　2016/07
Publisher: 日本肥満症治療学会
当科におけるsensor augmented insulin pump(SAP)の使用経験

澤田正二郎, 川名洋平, 児玉慎二郎, 鴇田藍, 宗像佑一郎, 突田壮平, 高橋圭, 宇野健司, 今井淳太, 山田哲也, 片桐秀樹

糖尿病　59　(2)　141-141　2016/02
Publisher: (一社)日本糖尿病学会
ISSN： 0021-437X

eISSN： 1881-588X
Sleeve保険収載1年現状と問題点 Sleeve保険収載1年当院での減量手術の動向と課題

田中直樹, 内藤剛, 井本博文, 宮地智洋, 土屋堯裕, 河野えみ子, 長尾宗紀, 渡辺和宏, 澤田正二郎, 片桐秀樹, 岡本智子, 武田みゆき, 武者宏昭, 元井冬彦, 海野倫明

日本肥満症治療学会学術集会プログラム・抄録集　33回　51-51　2015/06
Publisher: 日本肥満症治療学会
病的肥満症に対する減量手術の安全性と有効性の検討

田中直樹, 内藤剛, 長尾宗紀, 井本博文, 宮地智洋, 土屋堯裕, 河野えみ子, 渡辺和宏, 澤田正二郎, 片桐秀樹, 武者宏昭, 大沼忍, 元井冬彦, 海野倫明

日本肥満症治療学会学術集会プログラム・抄録集　33回　122-122　2015/06
Publisher: 日本肥満症治療学会
急性膵炎の合併を疑った重症糖尿病性ケトアシドーシスの一例

田中満実子, 宇野健司, 角田宇衣子, 高橋圭, 宗像佑一郎, 浅井陽一郎, 今井淳太, 山田哲也, 石垣泰, 岡芳知, 片桐秀樹

糖尿病　55　(4)　296-296　2012/04
Publisher: (一社)日本糖尿病学会
ISSN： 0021-437X

eISSN： 1881-588X
神経を介した臓器間ネットワークによるエネルギー代謝制御機構 Invited

今井淳太, 片桐秀樹

糖尿病診療マスター　9　(1)　21-25　2011/01

DOI： 10.11477/mf.1415101133 　
多発膵腫瘍により膵全摘を余儀なくされインスリン導入となったVHL病の1例

近藤敬一, 檜尾好徳, 丹治泰裕, 工藤宏仁, 突田壮平, 石川素子, 薄井正寛, 冨永竜, 長谷川豊, 山口賢, 石垣泰, 荻原健英, 片桐秀樹, 元井冬彦, 江川新一, 海野倫明, 藤島史喜, 中村保宏, 渡辺みか, 岡芳知

糖尿病　53　(7)　523-523　2010/07
Publisher: (一社)日本糖尿病学会
ISSN： 0021-437X
SU薬二次無効の臨床的研究グリクラジドとグリベンクラミドの比較(第2報) (糖尿病)

佐藤譲, 角田宇衣子, 山田哲也, 田村明, 法西敏宗, 高橋累, 石垣泰, 関川明宏, 石原寿光, 平井完史, 高橋和眞, 片桐秀樹, 檜尾好徳, 鈴木進, 岡芳知

糖尿病　45　(Suppl.2)　S160-S160-623　2002
Publisher: (一社)日本糖尿病学会
ISSN： 0021-437X

eISSN： 1881-588X

Show all ︎Show first 5

Presentations 293

臓器間神経ネットワークによる個体レベルでの代謝恒常性維持機構 Invited

第114回日本病理学会総会　2025/04/19
Neuronal Information Highways for Maintaining Metabolic Homeostasis at the Whole-Body Level Invited

Katagiri Hideki

APPW2025　2025/03/18
被災後の糖尿病薬剤選択～東日本大震災の経験を踏まえて～ Invited

片桐秀樹

第59回糖尿病学の進歩　2025/01/25
（若手研究奨励賞）Calcineurin/NFATc3-FoxM1経路を介した肥満代償性膵β細胞増殖機構の解明

木幡将人, 今井淳太, 井泉知仁, 川名洋平, 遠藤彰, 菅原裕人, 高橋圭, 金子慶三, 片桐秀樹

第35回分子糖尿病学シンポジウム　2024/12/07
臓器間ネットワークによる個体レベルでの代謝制御機構～発見から応用へ～ Invited

片桐秀樹

第77回日本自律神経学会総会　2024/10/26
（日本肥満学会学会賞）臓器間ネットワークによる個体レベルでの代謝制御から見た肥満・肥満症研究 Invited

片桐秀樹

第45回日本肥満学会　2024/10/20
（実地医家アワード最優秀賞）アルドステロン新測定系におけるアルドステロン産生腺腫スクリーニングカットオフの検討

小野美澄, 手塚雄太, 山崎有人, 小黒草太, 高瀬圭, 伊藤明宏, 鈴木貴, 田中哲洋, 片桐秀樹, 佐藤文俊

第46回日本高血圧学会総会　2024/10/12
臓器間ネットワークによる個体レベルでの代謝制御～発見から応用へ～ Invited

片桐秀樹

第78回全国臨床糖尿病医会学術集会　2024/09/07
（若手研究奨励賞）出産後膵島ではマクロファージが増加し、貪食により膵β細胞量減少を促進する

遠藤彰, 今井淳太, 川名洋平, 菅原裕人, 木幡将人, 高橋圭, 金子慶三, 片桐秀樹

第97回日本内分泌学会学術総会　2024/06/06
（若手研究奨励賞）肝糖新生は基質選択的に低強度および高強度走行の運動能に影響を及ぼす

堀内嵩弘, 金子慶三, 穂坂真一郎, 冨山晴太郎, 高橋圭, 大和真弥, 今井淳太, 片桐秀樹

第67回日本糖尿病学会年次学術集会　2024/05/17
Regulation of pancreatic β cells by liver-β cell-inter-organ neuronal network Invited

Junta Imai, Hideki Katagiri

第67回日本糖尿病学会年次学術集会　2024/05/17
『災害時糖尿病診療マニュアル 2024』3章個々の糖尿病病態への対応 ①～⑥ Invited

片桐秀樹

第67回日本糖尿病学会年次学術集会　2024/05/17
（若手研究奨励賞）Calcineurin/NFATc3-FoxM1経路を介した肥満代償性膵β細胞増殖機構の解明

木幡将人, 今井淳太, 井泉知仁, 川名洋平, 遠藤彰, 菅原裕人, 高橋圭, 金子慶三, 片桐秀樹

第37回日本糖尿病・肥満動物学会年次学術集会　2024/03/15
臓器間ネットワークによる個体レベルでの代謝制御機構～発見から応用へ～ Invited

片桐秀樹

第37回日本糖尿病・肥満動物学会年次学術集会　2024/03/16
臓器間ネットワークによる個体レベルでの代謝制御機構 Invited

片桐秀樹

第58回糖尿病学の進歩　2024/02/17
臓器間ネットワークによる個体レベルでの代謝制御 Invited

片桐秀樹

第57回日本成人病（生活習慣病）学会学術集会　2024/01/13
脳神経系による組織の適応修復の分子細胞機構 Invited

片桐秀樹

第97回日本薬理学会年会　2023/12/15
高度肥満症に伴うGH-IGF-1軸の機能的障害と臨床的因子に関する検討

久保晴丸, 澤田正二郎, 遠藤彰, 穂坂真一郎, 菅原裕人, 川名洋平, 浅井洋一郎, 児玉慎二郎, 高橋圭, 金子慶三, 今井淳太, 片桐秀樹

第44回日本肥満学会・第41回日本肥満症治療学会学術集会　2023/11/25
（若手研究奨励賞）光遺伝学的迷走神経刺激はグルコース応答性インスリン分泌を増強し膵β細胞増殖を誘導する

川名洋平, 今井淳太, 片桐秀樹

第44回日本肥満学会・第41回日本肥満症治療学会学術集会　2023/11/25
臓器間神経ネットワークによる膵β細胞増殖機構の解明とその制御 Invited

川名洋平, 今井淳太, 片桐秀樹

第44回日本肥満学会・第41回日本肥満症治療学会学術集会　2023/11/25
彰往察来～肥満研究と臓器間ネットワーク～ Invited

片桐秀樹

第44回日本肥満学会・第41回日本肥満症治療学会学術集会　2023/11/25
（若手研究奨励賞）細胞増殖レポーターマウスを用いたin vivoでの膵β細胞増殖の経時的観察

菅原裕人, 今井淳太, 川名洋平, 遠藤彰, 木幡将人, 清家準朗, 児玉慎二郎, 高橋圭, 金子慶三, 片桐秀樹

第96回日本内分泌学会学術総会
未病段階から寿命に関わる糖尿病 Invited

片桐秀樹

第31回日本医学会総会　2023/04/22
臓器間ネットワークによる代謝調節機構 Invited

片桐秀樹

第57回糖尿病学の進歩
臓器間ネットワークによる個体レベルでの代謝恒常性維持機構 Invited

片桐秀樹

第43回日本炎症・再生医学会　2022/07/07
Glucose metabolism and lifespan Invited

2022/05/14
臓器間相互作用（臓器代謝ネットワーク）から見た動脈硬化の進展予防 Invited

片桐秀樹

第53回日本動脈硬化学会総会・学術集会　2021/10/24
臓器間神経ネットワークによる個体レベルでの代謝制御機構 Invited

片桐秀樹

第74回日本自律神経学会総会　2021/10/24
Neuronal Information Highways for Systemic Regulation of Glucose Metabolism Invited

Hideki Katagiri

THE UEHARA INTERNATIONAL SYMPOSIUM 2021　2021/06/08
（若手研究奨励賞）出産後膵島ではマクロファージが増加し、エフェロサイトーシスにより膵β細胞量減少を促進する Invited

遠藤彰, 今井淳太, 井泉知仁, 川名洋平, 菅原裕人, 木幡将人, 児玉慎二郎, 高橋圭, 金子慶三, 片桐秀樹

第64回日本糖尿病学学会年次学術集会　2021/05/20
肝臓のインスリン作用の減弱に起因し個体レベルのエネルギー代謝を制御する新規の肝臓－脳－褐色脂肪組織連関の発見 Invited

高橋圭, 山田哲也, 片桐秀樹

第64回日本糖尿病学学会年次学術集会　2021/05/22
迷走神経シグナルによる膵β細胞量調節機構 Invited

今井淳太, 片桐秀樹

第64回日本糖尿病学学会年次学術集会　2021/05/20
肝と臓器連関～個体レベルでの代謝調節における肝臓の新たな役割～ Invited

片桐秀樹

第43回日本肝臓学会東部会
（若手研究奨励賞）生体内における膵β細胞の増殖を同一個体で経時的に観察できる高感度手法の樹立 Invited

菅原裕人, 今井淳太, 山本淳平, 井泉知仁, 川名洋平, 遠藤彰, 木幡将人, 金子慶三, 澤田正二郎, 片桐秀樹

第63回日本糖尿病学会年次学術集会
糖尿病・糖尿病合併症発症機序における臓器連関肝臓からの臓器連関によるエネルギー代謝 Invited

高橋圭, 山田哲也, 片桐秀樹

第63回日本糖尿病学会年次学術集会
（ハーゲドーン賞受賞講演）臓器間神経ネットワークによる個体レベルの代謝調節と糖尿病 Invited

Hideki Katagiri

2020/10/10
Vagal nerve signal-mediated regulation of pancreatic β cells Invited

Junta Imai, Hideki Katagiri

2020/10/05
Neuronal and endothelial signals involved in senescence of parenchymal cells International-presentation Invited

Hideki Katagiri

Cold Spring Harbor Laboratory Meeting- Mechanism of Aging（Virtual Meeting）　2020/09/23
臓器連関による代謝調節 Invited

片桐秀樹

第117回日本内科学会講演会　2020/08/07
臓器間ネットワークによる個体レベルの代謝調節と糖尿病 Invited

2020/05/15
臓器間神経ネットワークによる膵β細胞増殖システム Invited

2020/04/11
"Vagal nerve signal-regulated cell proliferation for maintaining whole body homeostasis" Invited

Junta Imai, Hideki Katagiri

2020/03/17
Neuronal Information Highways for Maintaining Metabolic Homeostasis at the Whole-Body Level Invited

Hideki Katagiri

AMED-CREST/PRIME Joint International Symposium “Homeostasis & Adaptation/Repair”　2020/02/01
光遺伝学的迷走神経刺激は膵β細胞増殖を誘導しstreptozotocin誘発糖尿病の血糖上昇を抑制する Invited

2019/12/07
Role of Vagal Nerve in Pancreatic β Cell Function International-presentation Invited

Hideki Katagiri

EuroDIA Meeting (EDM)　2019/11/21
Neuronal Information Highways for Maintaining Metabolic Homeostasis at the Whole-Body Level Invited

Hideki Katagiri

University of Lyon　2019/11/19
Regulation of beta cell function by the liver: nerve implication International-presentation Invited

Hideki Katagiri

55th Annual Meeting of the European Association for the Study of Diabetes（EASD）　2019/09/19
Blockade of the NF-κB pathway in the endothelium prolongs longevity and suppresses senescence of pancreatic β-cells Invited

Hideki Katagiri
臓器連関と内分泌代謝学 Invited

Hideki Katagiri

2019/07/06
A型インスリン抵抗症とインスリンシグナル伝達病 Invited

小川渉, 廣田勇士, 門脇弘子, 依藤亨, 石垣泰, 片桐, 秀樹

第62回日本糖尿病学会学術総会
本邦におけるB型インスリン抵抗症の実態 Invited

片桐秀樹, 石垣泰, 門脇弘子, 依藤亨, 廣田勇士, 小川渉

第62回日本糖尿病学会学術総会
（若手研究奨励賞）光遺伝学的迷走神経刺激はグルコース応答性インスリン分泌を増強し膵β細胞増殖を誘導する Invited
Vagal signal-mediated tissue regeneration and its therapeutic potential in aged animals Invited

Tomohito Izumi, Junta Imai, Junpei Yamamoto, Hideki Katagiri
Regulation of β cell proliferation by vagal nerve signals Invited

Junta Imai, Hideki Katagiri
Post-Disaster Diabetes Care -Lessons from experiences with the Great East Japan Earthquake- Invited

Hideki Katagiri

JDS/AASD/IDF-WPR Joint Sympsium on Diabetes Management and Natural Disaster　2019/05/24
恒常性維持のための迷走神経シグナルを介した細胞増殖制御機構 Invited

Junta Imai, Hideki Katagiri

2019/05/10
"Systemic glucose oxidation is enhanced in acquired liver and muscle insulin receptor knockout mice " International-presentation Invited

Kei Takahashi, Tetsuya Yamada, Takashi Sugisawa, Keiko Kawata, Yoichiro Asai, Yuichiro Munakata, Shinjiro Kodama, Shojiro Sawada, Junta Imai, Makoto Inada, Hideki Katagiri

The 9th Federation of the Asian and Oceanian Physiological Societies Congress in conjunction with the 96th Annual Meeting of the Physiological Society of Japan
迷走神経シグナルによる代償性膵β細胞増殖制御機構 Invited

Junta Imai, Hideki Katagiri

2019/03/16
迷走神経による膵β細胞制御 Invited

Junta Imai, Hideki Katagiri

2019/03/01
臓器間ネットワークと代謝疾患 Invited

Hideki Katagiri

2018/12/02
臓器間神経ネットワークによる個体レベルでの代謝調節システム Invited

Hideki Katagiri

2018/10/26
Metabolic Information Highways～臓器間ネットワークによる個体レベルの代謝調節機構 Invited

Hideki Katagiri

2018/10/20
肝臓からの臓器連関によるエネルギー代謝調節とメタボリックシンドロームの病態解明 Invited

Tetsuya Yamada, Hideki Katagiri
肥満症と臓器間ネットワーク Invited

Hideki Katagiri
Neuronal Information Highways for Systemic Regulation of Glucose and Energy Metabolism Invited

Hideki Katagiri, Junta Imai

2018/07/26
臓器間ネットワークと代謝恒常性

Hideki Katagiri

2018/07/20
臓器連関による肥満の際の代謝調節―肥満2型糖尿病を考える― Invited

Hideki Katagiri
神経シグナルによる膵β細胞量の調節 Invited
迷走神経シグナルによる膵β細胞増殖機構 Invited
臓器/細胞連関から肥満・糖尿病の病態および治療を考える Invited

Tetsuya Yamada, Hideki Katagiri
臓器間神経ネットワークと糖尿病 Invited

Hideki Katagiri
肥満症の病態形成における肝臓からの臓器連関の役割 Invited

Tetsuya Yamada, Hideki Katagiri

2017/11/24
脂肪肝における低酸素応答は胆石形成を促進する Invited

2017/10/28
Aging and Neuronal Information Highways for Systemic Regulation of Glucose and Energy Metabolism International-presentation Invited

Hideki Katagiri

2017/10/11
膵β細胞老化における血管内皮の役割 Invited

2017/10/08
臓器間ネットワークによる個体レベルでの代謝制御機構とメタボリックシンドローム Invited

Hideki Katagiri
臓器間ネットワークによる個体レベルの代謝制御機構 Invited

Hideki Katagiri

2017/09/20
糖尿病創薬をめざした臓器間ネットワーク研究 Invited

Hideki Katagiri
臓器連関から肥満症の病態・治療を考える Invited

Tetsuya Yamada, Hideki Katagir

2017/08/19
臓器間ネットワークによる個体レベルの代謝調節機構 Invited

Hideki Katagiri

2017/07/14
臓器間ネットワークによる個体レベルでの代謝調節システムとメタボリックシンドローム Invited

Hideki Katagiri
臓器間ネットワークと個体レベルの代謝調節 Invited

Hideki Katagiri
（若手研究奨励賞）脂肪肝における低酸素応答はアクアポリン８の発現抑制により胆石形成を促進する Invited
Molecular mechanisms of cell proliferation and organ regeneration mediated by vagal nerve signals Invited

Tomohito Izumi, Junta Imai, Junpei Yamamoto, Hideki Katagiri
インスリン抵抗性やインスリン分泌に関与する臓器間ネットワークと個体レベルの糖代謝調節 Invited

Hideki Katagiri
臓器間ネットワークによる個体レベルでの糖・エネルギー・脂質代謝制御機構 Invited

Hideki Katagiri
肥満症の病態形成における肝臓からの臓器連関の役割 Invited

Tetsuya Yamada, Hideki Katagiri
臓器間神経ネットワークが担う新たな栄養素間ネットワーク機構 Invited

Kenji Uno, Hideki Katagiri
肝臓からの臓器間神経ネットワークによるエネルギー代謝調節機構の解明 Invited

Tetsuya Yamada, Hideki Katagiri
臓器間神経ネットワークが有するメタボリックシンドローム発症機序 Invited

Kenji Uno, Hideki Katagiri

2016/10/02
臓器間神経ネットワークによる個体レベルでの代謝制御機構とメタボリックシンドローム Invited

Hideki Katagiri

2016/09/26
臓器間神経ネットワークによる個体レベルでの糖・エネルギー・脂質代謝制御機構 Invited

Hideki Katagiri

2016/09/09
臓器間ネットワークによる個体レベルでの代謝制御とメタボリックシンドローム Invited

Hideki Katagiri

2016/08/20
Emotional behavior and the common hepatic branch of the vagus nerve Invited

Masayuki Sekiguchi, Daisuke Yamada, Peter Koppensteiner, Saori Odagiri, Tetsuya Yamada, Hideki Katagiri, Keiji Wada

"The 39th Annual Meeting of the Japan Neuroscience Society Yokohama"　2016/07/20
Role of the inter-organ neural network from the liver in systemic energy metabolism. (Joint Symposium by the Presidents of Japan Neuroscience Society and Japanese Society for Neurochemistry: Dynamic neural processes for whole body multiorgan network as a complexity system) Invited

Tetsuya Yamada, Hideki Katagiri

"The 39th Annual Meeting of the Japan Neuroscience Society Yokohama"　2016/07/20
自律神経を介して脳が統御する糖・エネルギー代謝調節機構の解明 Invited

Tetsuya Yamada, Hideki Katagiri

2016/07/08
老化と臓器間ネットワーク Invited

Hideki Katagiri

2016/06/09
臓器間神経ネットワークによる個体レベルでの代謝制御機構 Invited

Hideki Katagiri

2016/05/31
Role of the inter-organ network from the liver in systemic energy metabolism Invited

Tetsuya Yamada, Hideki Katagiri
Regulation of pancreatic beta-cells by vagal nerve signals Invited

Junta Imai, Hideki Katagiri
（若手研究奨励賞）嗅覚受容体は膵β細胞に発現しグルコース応答性インスリン分泌を促進する Invited

宗像佑一郎, 山田哲也, 今井淳太, 突田壮平, 高橋圭, 白井勇太, 児玉慎二郎, 浅井洋一郎, 椙澤貴志, 千葉弓子, 高橋広延, 穂坂真一郎, 井泉知仁, 高俊弘, 宇野健司, 澤田正二郎, 畠山裕康, 神崎展, 宮崎純一, 片桐秀樹
代謝調節系の新たな視点～臓器連関による糖代謝調節系の理解～ Invited

Hideki Katagiri
Neuronal network from the liver regulates systemic lipid metabolism Invited

Kenji Uno, Hideki Katagiri

The 93th Annual Meeting of the Physiological Society of Japan
個体レベルのエネルギー代謝調節における肝臓の役割－臓器間神経ネットワークの観点から－ Invited

Tetsuya Yamada, Hideki Katagiri

2016/03/10
臓器間ネットワークと老化 Invited

Hideki Katagiri

2015/12/19
臓器間神経ネットワークによる個体レベルの糖・エネルギー・脂質代謝制御機構 Invited

Hideki Katagiri
個体レベルのエネルギー代謝調節における肝臓の役割－臓器間神経ネットワークの観点から－

Tetsuya Yamada, Hideki Katagiri
Inter-organ neural network mediate the regulation of systemic energy metabolism International-presentation Invited

Tetsuya Yamada, Hideki Katagiri

The 36th Annual Meeting of Japan Society for the Study of Obesity, The 46th NIPS International Symposium (Homeostatic mechanisms among interacting organ systems – Key to understanding obesity)
糖尿病における臓器間代謝情報ネットワークメカニズム Invited

Hideki Katagiri

2015/09/13
臓器間ネットワークによる個体レベルでの糖・エネルギー・脂質代謝制御機構 Invited

Hideki Katagiri
Metabolic Information Highways ～個体レベルでの糖・エネルギー・脂質代謝制御機構～ Invited

Hideki Katagiri
臓器間神経ネットワークによる個体レベルでのエネルギー・糖・脂質代謝制御機構 Invited

Hideki Katagiri
Neuronal signals from the hepatic amino acid/mTOR/S6K pathway regulates systemic lipid metabolism International-presentation Invited

Kenji Uno, Hideki Katagiri

75th Scientific Sessions,American Diabetes Association
迷走神経シグナルによる膵β細胞増殖機構 Invited

Junta Imai, Hideki Katagiri
臓器間ネットワークによる個体レベルでの糖・エネルギー・脂質代謝調節機構 Invited

Hideki Katagiri

2015/04/22
臓器間神経ネットワークによる個体レベルでの糖・エネルギー・脂質代謝制御機構 Invited

Hideki Katagiri
エネルギー代謝調節における臓器間神経ネットワーク機構の役割 Invited

Tetsuya Yamada, Hideki Katagiri

2015/03/20
臓器間神経ネットワークによる糖・エネルギー代謝調節機構の解明 Invited

Tetsuya Yamada, Hideki Katagiri

2015/02/07
Hepatic glucokinase triggers obesity development by negatively regulating BAT thermogenesis via neural signals Invited

Hideki Katagiri

2014/11/25
Neuronal Information Highways for Metabolic Regulation at the Whole Body Level Invited

Hideki Katagiri

2014/11/25
迷走神経シグナルによる膵β細胞制御機構 Invited

Junta Imai, Hideki Katagiri
Metabolic Surgery 後の代謝改善効果〜神経系による代謝調節の面から Invited

Hideki Katagiri
CHOP Modulates Adipose Tissue Macrophage Polarization International-presentation Invited

Toru Suzuki, Junhong Gao, Keiichi Kondo, Yasushi Ishigaki, Junta Imai, Tetsuya Yamada, Hideki Katagiri

74th Scientific Sessions Amarican Diabetes Association
CHOP Involvement in Hepatic Glucose Production and Insulin Resistance International-presentation Invited

Keiichi Kondo, Junhong Gao, Toru Suzuki, Yasushi Ishigaki, Junta Imai, Tetsuya Yamada, Hideki Katagiri

74th Scientific Sessions Amarican Diabetes Association
CSIIとCGMからみた糖尿病治療の展望 Invited
神経シグナルと膵β細胞量の調節 Invited

Junta Imai, Hideki Katagiri
エネルギー代謝における臓器間相互作用 Invited

Tetsuya Yamada, Hideki Katagiri
Inter-organ neural network mediate body weight regulation. Invited

Tetsuya Yamada, Sohei Tsukita, Hideki Katagiri

The 91st Annual Meeting of the Physiological Society of Japan
A cerebral cortical region that responds to amino acid injection into the hepatic portal vein. Invited

Sekiguchi Masayuki, Koppensteiner Peter, Odagiri Saori, Hatanaka Yusuke, Yamada Daisuke, Yamada Tetsuya, Katagiri Hideki, Wada Keiji

The 91st Annual Meeting of the Physiological Society of Japan
臓器間ネットワークからみた肥満・２型糖尿病 Invited

Tetsuya Yamada, Hideki Katagiri
臓器間ネットワークから血管病を紐解 Invited

Hideki Katagiri

2014/02/02
Metabolic Information Highways ～個体レベルの糖エネルギー代謝調節機構～ Invited

Hideki Katagiri

2013/12/17
メタボリックインフォメーションハイウェイ Invited

Hideki Katagiri
Neuronal information highways for systemic regulation of glucose and energy metabolism.Neuronal information highways for systemic regulation of glucose and energy metabolism. Invited

Hideki Katagiri

The 36th Naito Conference
肝からの臓器間ネットワークによるエネルギー代謝制御 Invited
臓器間神経ネットワークによる個体ﾚﾍﾞﾙでのｴﾈﾙｷﾞｰ代謝制御機構 Invited

Hideki Katagiri
Hepatic glucokinase triggers obesity development by negatively regulating BAT thermogenesis via neural signals Invited

2013/02/01
個体レベルでの代謝制御と老化・寿命 Invited

Hideki Katagiri

2012/12/08
Regulation of pancreatic beta-cells by Inter-organ Networks International-presentation Invited

Junta Imai, Hideki Katagiri

2012/11/27
神経系を介した臓器間相互作用による体重調整 Invited

2012/11/24
Metabolic Information Highway～個体レベルでの代謝制御機構～ Invited

Hideki Katagiri

2012/10/27
Metabolic Information Highway〜個体レベルでの代謝制御機構〜

片桐秀樹

神経組織の成長・再生・移植研究会第27回学術集会　2012/10/27
Systemic regulation of glucose and energy metabolism via inter-organ neuronal network International-presentation Invited

Hideki Katagiri

The 9th Nikko International Symposium 2012　2012/10/12
Bach1 deficiency protects pancreatic beta cells from oxidative stress injury International-presentation Invited

Keiichi Kondo, Y. Ishigaki, J. Gao, T. Yamada, J. Imai, S. Sawada, A. Muto, Y. Oka, K. Igarashi, H. Katagiri

48th EASD Annual Meeting
血管内皮細胞におけるNF-kＢ経路が代謝や老化・寿命に及ぼす役割 Invited

2012/09/27
個体レベルでの代謝調節と循環〜血圧から寿命の制御まで〜

片桐秀樹

第1回日本肺循環学会学術集会　2012/09/22
糖尿病と肥満〜その仕組みと予防〜

片桐秀樹

第7回東北大学病院市民公開講座　2012/07/22
動脈硬化を操る代謝シグナルネットワークの解明から治療へ The atherosclerosis puzzle:Bringing up new Matabolic pieces

片桐秀樹

第44回日本動脈硬化学会総会・学術集会　2012/07/19
Hepatic DEPTOR expression improves systemic Insulin Resistance International-presentation Invited

Yumiko Chiba, Kenji Uno, Hideki Katagiri

American Diabetes Association 72nd Scientific Sessions　2012/06/09
Chronic mild stress alters circadian expressions of molecular clock genes in the liver International-presentation Invited

Kei Takahashi, Tetsuya Yamada, Yoshitomo Oka, Hideki Katagiri

American Diabetes Association 72nd Scientific Sessions　2012/06/09
Hepatic Glucokinase Negatively Regulates BAT Thermogenesis via a Neural Pathway International-presentation Invited

Sohei Tsukita, Tetsuya Yamada, Kenji Uno, Yoshitomo Oka, Hideki Katagiri

American Diabetes Association 72nd Scientific Sessions
糖代謝と自律神経：神経ネットワークの解明

片桐秀樹

第55回日本糖尿病学会年次学術集会　2012/05/17
神経系を介した臓器間相互作用による体重調節機構 Invited

2012/04/21
臓器間ネットワークによる膵β細胞制御機構 Invited

Junta Imai, Hideki Katagiri

2012/04/21
臓器間ネットワークとメタボリックシンドローム

片桐秀樹

第49回日本臨床分子医学会学術集会　2012/04/13
糖尿病と栄養 –東日本大震災を乗り越えて-

片桐秀樹

第19回日本健康体力栄養学会　2012/03/10
全身における代謝調節と臓器間神経ネットワーク Invited

Hideki Katagiri

第46回糖尿病学の進歩　2012/03/01
糖尿病と肥満その仕組みと対策

片桐秀樹

市民公開セミナードクターサーチみやぎ健康セミナー「糖尿病」　2011/11/13
東日本大震災における避難所巡回診療

児玉慎二郎, 石垣泰, 片桐秀樹

日本糖尿病学会第49回東北地方会　2011/11/05
高度肥満に腹腔鏡下袖状胃切除術を施行した２例

本藏理恵子, 長谷川豊, 近藤敬一, 今井淳太, 山田哲也, 石垣泰, 内藤剛, 柴田近, 岡芳知, 片桐秀樹

日本糖尿病学会第49回東北地方会　2011/11/05
非侵襲的陽圧換気療法の使用により著明な体重減少を呈した肥満低換気症候群の一例

浅井洋一郎, 田中満実子, 宗像佑一郎, 高橋圭, 角田宇衣子, 宇野健司, 今井淳太, 山田哲也, 石垣泰, 岡芳知, 片桐秀樹

日本糖尿病学会第49回東北地方会　2011/11/05
糖尿病ケトーシスを契機に診断された先端巨大症の一例

宗像佑一郎, 宇野健司, 高橋圭, 浅井洋一郎, 田中満実子, 山田哲也, 森本玲, 佐藤文俊, 伊藤貞嘉, 岡芳知, 片桐秀樹

日本糖尿病学会第49回東北地方会　2011/11/05
糖尿病性ケトアシドーシスの加療中に低リン血症とそれに伴う筋障害を呈した1例

山本淳平, 今井淳太, 山口賢, 角田宇衣子, 佐竹千尋, 渡辺崇, 河野ひろ子, 山田哲也, 石垣泰, 岡芳知, 片桐秀樹

日本糖尿病学会第49回東北地方会　2011/11/05
震災後ケトアシドーシスを発症し、肺血栓塞栓症、敗血症を合併した2型糖尿病の一例

白井勇太, 宇野健司, 角田宇衣子, 丹治泰裕, 渡辺崇, 高橋圭, 今井淳太, 山田哲也, 石垣泰, 岡芳知, 片桐秀樹

日本糖尿病学会第49回東北地方会　2011/11/05
膵動静脈奇形に対する膵全摘後に自家膵島移植を施行した1例

井泉知仁, 長谷川豊, 山口賢, 角田宇衣子, 澤田正二郎, 後藤昌史, 海野倫明, 里見進, 岡芳知, 片桐秀樹

日本糖尿病学会第49回東北地方会　2011/11/05
糖尿病性心筋症を合併した1型糖尿病の一例

澤田正二郎, 白井勇太, 宇野健司, 金子慶三, 鴇田藍, 児玉慎二郎, 後岡広太郎, 下川宏明, 今井淳太, 山田哲也, 石垣泰, 岡芳知, 片桐秀樹

日本糖尿病学会第49回東北地方会　2011/11/05
急性膵炎の合併を疑った重症糖尿病性ケトアシドーシスの一例

田中満実子, 宇野健司, 角田宇衣子, 高橋圭, 宗像佑一郎, 浅井洋一郎, 今井淳太, 山田哲也, 石垣泰, 岡芳知, 片桐秀樹

日本糖尿病学会第49回東北地方会　2011/11/05
膵腎同時移植によりインスリン量の減量・慢性維持透析治療から離脱できた１型糖尿病の１例

本間緑, 長谷川豊, 井泉知仁, 澤田正二郎, 石垣泰, 川岸直樹, 関口悟, 里見進, 岡芳知, 片桐秀樹

日本糖尿病学会第49回東北地方会　2011/11/05
経管栄養中に高血糖高浸透圧昏睡にて救急搬入された初回治療２型糖尿病の1例

鈴木亨, 山口賢, 角田宇衣子, 長谷川豊, 丹治泰裕, 山本淳平, 今井淳太, 山田哲也, 石垣泰, 岡芳知, 片桐秀樹

日本糖尿病学会第49回東北地方会　2011/11/05
Regulation of insulin secretion by inter-organ networks International-presentation

Junta Imai, Yoshitomo Oka, Hideki Katagiri

Programming Beta Cell Development, Impairment and regeneration　2011/10/23
災害時の糖尿病医療〜東日本大震災の経験をふまえて〜

片桐秀樹

2011年宮城県糖尿病看護セミナー　2011/10/22
WFS1遺伝子欠損マウスにおけるDPP-4阻害薬（vildagliptin）の膵β細胞保護効果の検討

丹治泰裕, 山口賢, 薄井正寛, 冨永竜, 近藤敬一, 石垣泰, 岡芳知, 片桐秀樹, 石原寿光

第54回日本糖尿病学会年次学術集会　2011/10/21
多臓器円環のダイナミクス研究に関する学術的意義と推進上の課題

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学術シンポジウム「多臓器円環のダイナミクス」　2011/10/08
肥満と糖尿病〜なぜ太る・血糖値が上がる〜

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東北大学健康フェア　2011/10/01
臓器間神経ネットワークによる全身での代謝調節

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第32回日本肥満学会　2011/09/23
臓器間神経ネットワークによる糖・エネルギー代謝の恒常性維持機構

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第34回日本神経科学大会　2011/09/14
Neuronal Information Highways for Maintaining Glucose and Energy Homeostasis

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Neuroscience 2011（第34回日本神経科学大会）　2011/09/14
第一線の研究者からの発信

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ＲＵ11シンポジウム　2011/09/11
Metabolic Information Highways〜神経ネットワークによる個体レベルでの代謝調節機構〜

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第29回内分泌代謝学サマーセミナー　2011/07/07
脳神経科学と内科疾患との融合研究事例

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科学技術振興機構研究開発戦略センター戦略イニシアティブ「ホメオダイナミクス」フォローアップワークショップ　2011/06/18
全ゲノムCNV解析による若年発症2型糖尿病患者における高頻度ゲノム欠失成人期疾患のCNV研究

工藤宏仁, 山田哲也, 岡芳知, 片桐秀樹

遺伝医学合同学術集会 2011　2011/06/16
Japan Statement for Metabolic surgery 代謝内科からみたmetabolic surgeryの有用性

石垣泰, 片桐秀樹

第29回日本肥満症治療学会学術集会　2011/06/10
糖尿病の診療・研究の最前線

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ノバルティスファーマ株式会社主催講演会　2011/06/03
災害時の対策

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市民公開講座　2011/05/21
褐色脂肪組織における熱産生抑制につながる組織間ネットワーク

突田壮平, 山田哲也, 宇野健司, 高橋圭, 白井勇太, 宗像佑一郎, 金子慶三, 澤田正二郎, 長谷川豊, 今井淳太, 石垣泰, 岡芳知, 片桐秀樹

第54回日本糖尿病学会年次学術集会　2011/05/19
飢餓における自律神経を介した肝・脂肪代謝制御の解明―Hepato-vagal nerve pathway modulates carbohydrate-lipid balancing―

泉田欣彦, 矢作直也, 武内謙憲, 山田哲也, 西真貴子, 升田紫, 久保田みどり, 熊谷真義, 太田啓介, 高梨幹生, 高瀬暁, 五十嵐正樹, 関谷元博, 飯塚陽子, 大橋健, 大須賀

第54回日本糖尿病学会年次学術集会　2011/05/19
動脈硬化発症・進展におけるWSF1の役割の検討

高俊弘, 石垣泰, 澤田正二郎, 近藤敬一, 井泉知仁, 宇野健司, 長谷川豊, 山口賢, 金子慶三, 突田壮平, 高橋圭, 今井淳太, 山田哲也, 石原寿

第54回日本糖尿病学会年次学術集会　2011/05/19
ATF6α欠損マウスを用いた、ATF6α欠損が耐糖能に与える影響についての検討

薄井正寛, 石原寿光, 鈴木千登世, 山口賢, 石垣泰, 福本学, 森和俊, 岡芳知, 片桐秀樹

第54回日本糖尿病学会年次学術集会　2011/05/19
（緊急シンポジウム）大学病院／地域の中核病院の役割は

石垣泰, 片桐秀樹

第54回日本糖尿病学会年次学術集会　2011/05/19
Cutting-edge Research in Insulin Secretion Regulation of Insulin Secretion by Inter-Organ Communications

Junta Imai, Hideki Katagiri

第54回日本糖尿病学会年次学術集会　2011/05/19
変わる！「糖尿病」新しい時代の、新しい糖尿病医療

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第54回日本糖尿病学会年次学術集会　2011/05/19
全身における代謝調節と臓器間神経ネットワーク

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第46回糖尿病学の進歩　2011/03/01
脳神経科学と内科疾患との融合研究事例

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科学技術振興機構研究開発戦略センター科学技術未来戦略ワークショップ「恒常性維持機構の解明研究」　2011/01/29
脳死下膵腎同時移植によりインスリン治療から離脱した1 型糖尿病の一例

高橋圭, 長谷川豊, 近藤敬一, 金子慶三, 宇野健司, 今井淳太, 山田哲也, 石垣泰, 片桐秀樹, 里見進, 岡芳知

第48回日本糖尿病学会東北地方会　2010/11/06
自己免疫性1 型糖尿病の良好な加療経過中に、劇症型に類似した急激な病態増悪を呈した一例

山本淳平, 金子慶三, 河野ひろ子, 高橋圭, 佐竹千尋, 角田宇衣子, 今井淳太, 山田哲也, 石垣泰, 片桐秀樹, 岡芳知

第48回日本糖尿病学会東北地方会　2010/11/06
10年にわたりインスリン非依存性に経過している緩徐進行1 型糖尿病の一例

宗像佑一郎, 宇野健司, 佐竹千尋, 角田宇衣子, 井泉知仁, 白井勇太, 今井淳太, 山田哲也, 石垣泰, 片桐秀樹, 岡芳知

第48回日本糖尿病学会東北地方会　2010/11/06
インスリン抵抗性が示唆された拡張型心筋症の2例

澤田正二郎, 鈴木俊伸, 金子慶三, 今井淳太, 山田哲也, 石垣泰, 片桐秀樹, 岡芳知

第48回日本糖尿病学会東北地方会　2010/11/06
インスリン自己免疫症候群様の低血糖に、インスリンアレルギーを合併した一例

白井勇太, 宇野健司, 佐竹千尋, 角田宇衣子, 井泉知仁, 宗像佑一郎, 今井淳太, 山田哲也, 石垣泰, 片桐秀樹, 岡芳和

第48回日本糖尿病学会東北地方会　2010/11/06
敗血症・DIC を経て無事出産に至った1 型糖尿病の1例

角田宇衣子, 石垣泰, 工藤宏仁, 丹治泰裕, 山口賢, 今井淳太, 山田哲也, 檜尾好徳, 片桐秀樹, 岡芳知

第48回日本糖尿病学会東北地方会　2010/11/06
低血糖脳症からの遷延した脳機能改善を認めた一例― SPECT画像による検討

工藤宏仁, 石垣泰, 丹治泰裕, 角田宇衣子, 山口賢, 今井淳太, 山田哲也, 檜尾好徳, 片桐秀樹, 岡芳知

第48回日本糖尿病学会東北地方会　2010/11/06
画像所見上異なる特徴を示したインスリノーマの2例

井泉知仁, 宇野健司, 白井勇太, 宗像佑一郎, 金子慶三, 今井淳太, 山田哲也, 石垣泰, 片桐秀樹, 岡芳知

第48回日本糖尿病学会東北地方会　2010/11/06
Metabolic Information Highways 〜糖尿病研究の新展開〜

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第７回香川糖尿病フォーラム　2010/10/27
糖負荷後の血糖上昇が血管性状に及ぼす影響の検討

石垣泰, 鴇田藍, 長谷川英之, 金井浩, 片桐秀樹, 佐々木毅, 岡芳知

第25回日本糖尿病合併症学会　2010/10/22
中枢と末梢のコーディネートエネルギー代謝に関わる末梢組織のバイオロジー

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第31回日本肥満学会　2010/10/01
Metabolilc Harmony〜肥満・糖尿病研究の新展開〜

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日本糖尿病医会　2010/09/11
Meet the Professor Metabolic Harmony 〜肥満・糖尿病研究の新展開〜

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第52回全国臨床糖尿病医会学術集会　2010/09/11
糖負荷後血糖上昇と血管性状変化の検討

石垣泰, 鴇田藍, 長谷川英之, 金井浩, 片桐秀樹, 佐々木毅, 岡芳知

第3回日本肥満症治療学会学術集会　2010/09/10
Metabolilc Harmony〜神経系による糖・エネルギー代謝の臓器間調節〜

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第6回Summer Vascular Conference　2010/09/04
生命科学は人類に何をもたらすか」糖尿病・代謝学からの報告

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日本学術会議第二部　2010/08/27
ER stress responses, both in macrophages and vascular cells, play important roles in the development of arteriosclerosis.

Yasushi Ishigaki, Junhong Gao, Hideki Katagiri, Yoshitomo Oka

第42回日本動脈硬化学会総会　2010/07/15
Carotidarterial elasticity potentially evaluate minute vascular changes with postprandial hyperglycemia in non-diabetic subjects

Ai Tokita, Yasushi Ishigaki, Hisashi Okimoto, Hideyuki Hasegawa, Yosio Koiwa, Makoto Katou, Tetsuya yamada, Yoshinori Hinokio, Hideki Katagiri, Hiroshi Kanai, Takeshi Sasaki, Yoshitomo Oka

第42回日本動脈硬化学会総会　2010/07/15
Metabolic harmony via neuronal information highways

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第16回日本遺伝子治療学会年次学術集会　2010/07/01
The Role of CHOP Expressed in Vascular and Hematopoietic Cells in Vascular Remodeling International-presentation

Keiichi Kondo, Junhong Gao, Yasushi Ishigaki, Yoshitomo Oka, Hideki Katagiri

American Diabetes Association 70th Scientific Sessions　2010/06/25
Interleukin-6 Enhances Glucose-Stimulated Insulin Secretion from Pancreatic β-Cells International-presentation

Junta Imai, Toshinobu Suzuki, Yoshitomo Oka, Hideki Katagiri

American Diabetes Association 70th Scientific Sessions　2010/06/25
Importance of the Endothelium in Vascular Remodeling and Aortic Aneurysm Formation through NF-kB Pathway International-presentation

Saito T, Hasegawa Y, Oka Y, Katagiri H

American Diabetes Association, 70th Scientific Sessions　2010/06/25
医療につながる分子生物学」「糖尿病と肥満〜分子機構から治療法研究まで〜」

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日本分子生物学会第10回春季シンポジウム　2010/06/06
糖尿病倫隔月誌「Diabetes Frontier」掲載座談会『膵臓機能研究の最前線に迫る〜日本人のIslet Biologyを考慮した新しい糖尿病治療策略を考える〜』

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糖尿病倫隔月誌「Diabetes Frontier」掲載座談会　2010/05/29
肝臓病学におけるパラダイム創生「Metabolic Harmony：自律神経による糖・エネルギー代謝の協調的調節」

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第46回日本肝臓学会総会　2010/05/27
Meet the Expert Metabolilc Harmony〜自律神経による糖・エネルギー代謝の協調的調節〜

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第53回日本糖尿病学会年次学術集会　2010/05/27
動脈硬化発症・進展におけるWFS1の役割の検討

高俊弘, 片桐秀樹, 石垣泰, 石原寿光, 山田哲也, 今井淳太, 澤田正二郎, 宇野健司, 長谷川豊, 山口賢, 金子慶三, 鈴木俊伸, 齋藤徳郎, 突田壮

第53回日本糖尿病学会年次学術集会　2010/05/27
血管内皮細胞NF-ｋBの血管病変形性に果たす役割

齋藤徳郎, 片桐秀樹, 長谷川豊, 荻原健英, 下澤達雄, 石垣泰, 山田哲也, 今井淳太, 宇野健司, 高俊弘, 金子慶三, 檜尾好徳, 浅野知一郎, 藤田敏郎

第53回日本糖尿病学会年次学術集会　2010/05/27
肥満に伴う高血圧発症における肝臓の意義

宇野健司, 片桐秀樹, 山田哲也, 石垣泰, 今井淳太, 長谷川豊, 高俊弘, 金子慶三, 澤田正二郎, 松末公彦, 岡芳知

第53回日本糖尿病学会年次学術集会　2010/05/27
Apaf1-interacting protein (APIP) 遺伝子多型と2型糖尿病との相関研究

角田宇衣子, 檜尾好徳, 石垣泰, 安田和基, 谷澤幸生, 今井潤, 片桐秀樹, 岡芳知

第53回日本糖尿病学会年次学術集会　2010/05/27
膵β細胞における小胞体ストレス応答と酸化ストレス応答のクロストーク

冨永竜, 石原寿光, 山口賢, 佐竹千尋, 薄井正寛, 丹治泰裕, 鈴木千登世, 石垣泰, 山田哲也, 檜尾好徳, 片桐秀樹, 岡芳知

第53回日本糖尿病学会年次学術集　2010/05/27
新規小胞体ストレス蛋白・CRELD2の蛋白特性についての検討

山口賢, 石原寿光, 宗像佑一郎, 佐竹千尋, 薄井正寛, 冨永竜, 丹治泰裕, 鈴木千登世, 石垣泰, 山田哲也, 檜尾好徳, 片桐秀樹, 岡芳知

第53回日本糖尿病学会年次学術集会　2010/05/27
飢餓での自律神経を介した肝・脂肪組織代謝制御の解明？Hepato-vagel pathway modulates carbohydrate-lipid balancing？

泉田欣彦, 矢作直也, 武内謙憲, 西真貴子, 山田哲也, 久保田みどり, 熊谷真義, 太田啓介, 高梨幹生, 高瀬暁, 五十嵐正樹, 関谷元博, 飯塚陽子, 影山晴秋, 塩田清二

第53回日本糖尿病学会年次学術集会　2010/05/27
糖負荷試験における血糖値上昇と頸動脈血管弾性特性の検討

鴇田藍, 石垣泰, 沖本久志, 長谷川英之, 小岩喜郎, 加藤真, 長谷川豊, 澤田正二郎, 今井淳太, 山田哲也, 檜尾好徳, 片桐秀樹, 金井浩, 佐々木毅

第53回日本糖尿病学会年次学術集会　2010/05/27
肝臓病学におけるパラダイム創生「Metabolic Harmony：自律神経による糖・エネルギー代謝の協調的調節」

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第46回日本肝臓学会総会　2010/05/27
臓器間神経ネットワークによる糖代謝・エネルギー代謝の協調的調節

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第64回日本栄養・食糧学会大会　2010/05/21
Metabolic Harmony〜臓器間神経ネットワークによる糖代謝・エネルギー代謝の協調的調節〜

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第３回北東北インスリン糖尿病学研究会　2010/05/08
Metabolilc Harmony〜自律神経による糖・エネルギー代謝の協調的調節〜

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第47回日本臨床分子医学会　2010/04/10
Metabolic Harmony〜臓器間神経ネットワークによる糖代謝・エネルギー代謝の協調的調節〜

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第6回兵庫県糖尿病フォーラム　2010/04/03
神経ネットワークによる臓器間代謝調節

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第44回糖尿病学の進歩　2010/03/05
メタボリックシンドロームの最前線 -基礎から臨床- Neuronal Involvement in Inter-organ Metabolic Communication

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日本循環器病学会　2010/03/05
Metabolilc Harmony〜糖尿病研究の新展開〜

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第2回How to 糖尿病治療　2010/02/16
Metabolilc Harmony〜自律神経による臓器間の協調的代謝調節機構〜

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第35回関東Lipid Artery研究会　2009/11/25
Metabolilc Harmony〜臓器間神経ネットワークによる糖代謝・エネルギー代謝の協調的調節システム〜

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名古屋大学GCOEニューロサイエンスコース　2009/11/20
Metabolic Harmony〜自律神経による糖・エネルギー代謝の協調的調節機構〜

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第31回内分泌セミナー特別講演会　2009/11/19
Metabolic Information Highways 〜糖尿病研究の新展開〜

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第１５回北野糖尿病・内分泌倶楽部　2009/11/15
Metabolic Harmony〜自律神経による糖・エネルギー代謝の協調的調節機構〜

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東京大学大学院薬学研究科G-COEセミナー　2009/11/06
ストレス応答の新機軸神経系による糖・エネルギー代謝の協調的調節

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第82回日本生化学会　2009/10/21
Metabolic Harmony〜自律神経による糖・エネルギー代謝の協調的調節機構〜 International-presentation

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第13回Molecular Cardiovascular Conference　2009/09/04
Metabolic Information Highways 〜糖尿病研究の新展開〜

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Ten Topics in Endocrinology and Metabolism　2009/08/01
Metabolilc Harmony 〜自律神経による臓器間の協調的代謝調節機構〜

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宇都宮地区糖尿病治療研究会　2009/07/03
Metabolic Information Highways〜糖尿病研究の新展開〜

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第7回香川糖尿病フォーラム　2009/06/26
Metabolic Information Highways 〜肝からの求心性神経シグナルによる糖・エネルギー代謝調節〜

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第２回Metabolic Hepatology研究会　2009/06/25
肥満・糖尿病の成因とその対策

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日本内科学会東北地方会生涯教育講演会　2009/06/20
Metabolic Information Highways 〜自律神経による糖・エネルギー代謝の協調的調節機構〜

片桐秀樹

第61回仙南五市郡医師会総会講演会・宮城県医師会医師研修講習会　2009/06/20
Metabolic Information Highways 〜自律神経による糖・エネルギー代謝の協調的調節機構〜

片桐秀樹

東北大学大学院歯学研究科第43回学術フォーラム　2009/05/26
肝からの神経を介した、肥満に伴う高血圧の発症機序

宇野健司, 片桐秀樹, 山田哲也, 石垣泰, 今井淳太, 長谷川豊, 高俊弘, 金子慶三, 齋藤徳郎, 鈴木俊伸, 荻原健英, 岡芳知

第52回日本糖尿病学会年次学術集会　2009/05/21
動脈硬化症・進展におけるCHOPの役割の検討

高俊弘, 片桐秀樹, 石垣泰, 石原寿光, 山田哲也, 澤田正二郎, 荻原健英, 今井淳太, 宇野健司, 長谷川豊, 金子慶三, 鈴木俊伸, 齋藤徳郎

第52回日本糖尿病学会年次学術集会　2009/05/21
腹部内臓脂肪面積の頸動脈血管弾性特性に及ぼす影響の検討

鴇田藍, 石垣泰, 沖本久志, 長谷川英之, 小岩喜郎, 加藤真, 長谷川豊, 山口賢, 澤田正二郎, 今井淳太, 山田哲也, 石原寿光, 檜尾好徳, 片桐秀樹

第52回日本糖尿病学会年次学術集会　2009/05/21
膵β細胞の分化増殖と臨床展開臓器間連関による膵β細胞再生機構

片桐秀樹

第82回日本内分泌学会学術総会　2009/04/23
Metabolic Information Highways 〜自律神経による糖・エネルギー代謝の協調的調節機構〜

片桐秀樹

宮城県インスリン情報交換会　2009/04/14
肝臓からの神経シグナルによる糖・エネルギー代謝調節機構

片桐秀樹

第43回糖尿病学の進歩　2009/02/20
肝からの神経を介した臓器間ネットワークとメタボリックシンドローム

宇野健司, 山田哲也, 岡芳知, 片桐秀樹

第29回日本肥満学会　2008/10/17
Metabolic Information Highway 〜自律神経による糖・エネルギー代謝の協調的調節機構〜

片桐秀樹

千里ライフサイエンスセミナー　2008/10/03
脂肪組織からの求心性神経シグナルによる食欲調節機構

片桐秀樹

第50回歯科基礎医学会学術大会・総会　2008/09/23
肝からの神経による臓器間ネットワークとメタボリックシンドローム

宇野健司, 片桐秀樹

第51回日本糖尿病学会　2008/05/22
自律神経による臓器間代謝情報ネットワークとメタボリックシンドローム

片桐秀樹

日本内分泌学会学術総会　2008/05/16
Metabolic Information Highway〜肥満・糖尿病研究の新展開〜

片桐秀樹

第７回日本内分泌学会東海支部学術集会　2008/02/23
肝からの神経シグナルによる臓器間代謝情報ネットワーク

片桐秀樹

第２２回日本糖尿病・肥満動物学会　2008/02/08
自律神経系による臓器間代謝情報ネットワーク機構

片桐秀樹

BMB2007 （第30回日本分子生物学会年会第80回日本生化学会合同大会）　2007/12/12
肝におけるインスリン産生細胞の創生と骨髄細胞動員による膵β細胞の再生

片桐秀樹, 荻原健英, 今井淳太, 長谷川豊, 岡芳知

日本糖尿病学会年次学術総会　2007/10/30
自律神経を介した臓器（組織）間代謝情報ネットワーク

片桐秀樹

第28回日本肥満学会　2007/10/19
Neuronal pathway from the liver modulates energy expenditure and systemic insulin sensitivity International-presentation

Yamada T, Katagiri H, Uno K, Oka Y

Congress of the International Society for Autonomic Neuroscience　2007/10/05
Metabolic Information Highway〜メタボリックシンドローム研究の新展開〜

片桐秀樹

第62回日本体力医学会大会　2007/09/15
Activation of Hepatic ERK Pathway Promotes Pancreatic Beta Cell Proliferation International-presentation

Imai J, Katagiri H, Oka Y

Office of Life Sciences/National University of Singapore – Tohoku University/Centre of Excellence Joint Symposium　2007/09/05
Inter-organ communication via autonomic nerve circuits modulates systemic energy and glucose metabolism International-presentation

Katagiri H

The 25th JES Summer Seminar on Endocrinology & Metabolism　2007/07/17
Functional Role of Sortilin in Myogenesis and the Development of Insulin-Responsive Glucose Transport System in C2C12 Myocytes International-presentation

Ariga M, Nedachi T, Katagiri H, Kanzaki M

American Diabetes Association, 67th Scientific Sessions　2007/06/22
Activation of Hepatic ERK Pathway Promotes Pancreatic Beta Cell Proliferation. International-presentation

Imai J, Katagiri H, Suzuki T, Oka Y

American Diabetes Association, 67th Scientific Sessions　2007/06/22
臓器間連関によるインスリン抵抗性改善機構

片桐秀樹

第80回日本内分泌学会学術総会　2007/06/14
Metabolic Information Highway〜糖尿病・メタボリックシンドローム研究の新展開〜

片桐秀樹

東北バイオサイエンスシンポジウム　2007/06/04
自律神経系を介した臓器間ネットワークによる糖・エネルギー代謝の協調的調節機構

片桐秀樹

第50回日本糖尿病学会　2007/05/24
生体内での膵β細胞再生を目指した治療法開発

片桐秀樹

第46回日本生体医工学会　2007/04/25
Autonomic nerve circuits modulate energy and glucose metabolism International-presentation

Yamada T, Katagiri H

Okazaki Symposium 2007 on Obesity and Diabetes　2007/04/14
臓器間情報ネットワークによる糖・エネルギー代謝の協調的調節

片桐秀樹

宮崎サイエンスキャンプ　2007/02/16
臓器間情報ネットワークによる糖・エネルギー代謝の協調的調節

片桐秀樹

日本糖尿病動物研究会年次学術集会　2007/02/09
臓器間代謝情報ネットワークによる糖・エネルギー代謝の協調的調節

片桐秀樹

体温調節、温度受容研究会　2007/01/11
Neuronal Pathway from the Liver Modulates Energy Expenditureand Systemic Insulin Sensitivity International-presentation

Uno K, Katagiri H, Yamada T, Oka Y

Tohoku University 21st century COE program The 3rd International Symposium　2006/11/09
Bone Marrow Transplantation Promotes β Cell Regeneration after Acute Injury through Bone Marrow Cell Mobilization International-presentation

Hasegawa Y, Katagiri H, Ogihara T, Saito T, Oka Y

Tohoku University 21st century COE program The 3rd International Symposium　2006/11/09
自律神経系を介した協調的エネルギー代謝調節機構

片桐秀樹

日本肥満学会　2006/10/27
個体におけるエネルギー代謝調節〜臓器間代謝情報ネットワークとその治療応用の可能性〜

片桐秀樹

東京肥満研究会　2006/09/20
Novel Inter-Organ Communication Involved in Glucose and Energy Homeostasis International-presentation

Katagiri H

The 11th Adiposcience Symposium　2006/08/19
Bone Marrow-derived Cell Recruitment Is Involved in Regeneration after Pancreatic Beta Cell Injury International-presentation

Ogihara T, Katagiri H, Hasegawa Y. Oka Y

20th IUBMB International Congress of Biochemistry and Molecular Biology　2006/06/18
Neuronal Pathway from the Liver Modulates Energy Expenditure and Systemic Insulin Sensitivity International-presentation

Katagiri H, Uno K, Yamada T, Oka Y

American Diabetes Association, 66th Scientific Sessions　2006/06/09
Signals from Intra-Abdominal Fat Modulate Insulin and Leptin Sensitivity through Different Mechanisms: Neuronal Involvement in Food Intake International-presentation

Yamada T, Katagiri H, Ishigaki Y, Oka Y

American Diabetes Association, 66th Scientific Sessions　2006/06/09
Apolipoprotein E Involvement in Excess Fat Accumulation and Insulin Resistance International-presentation

Gao J, Katagiri H, Ishigaki Y, Oka Y

American Diabetes Association, 66th Scientific Sessions　2006/06/09
肝におけるインスリン産生細胞の創生と骨髄細胞動員による膵β細胞の再生

片桐秀樹, 荻原健英, 今井淳太, 長谷川豊, 岡芳知

日本糖尿病学会年次学術総会　2006/05/25
骨髄移植を利用した再生医療骨髄移植を利用した膵β細胞の再生治療

荻原健英, 片桐秀樹, 長谷川豊, 岡芳知

日本内分泌学会学術総会　2006/05/19
臓器間ネットワークによる個体レベルの代謝制御システム Invited

Hideki Katagiri
（若手研究奨励賞）脂肪肝における低酸素応答はアクアポリン８の発現抑制により胆石形成を促進する Invited
神経シグナルを介した膵β細胞量制御機構 Invited

Junta Imai, Hideki Katagiri

2013/05/16

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Research Projects 25

Elucidation of mechanisms underlying glucose homeostasis mediated by inter-organ communication and development of diabetes therapies.

Offer Organization: Japan Society for the Promotion of Science

System: Grants-in-Aid for Scientific Research

Category: Grant-in-Aid for Scientific Research (S)

Institution: Tohoku University

2020/08/31 - 2025/03/31
恒常性の理解と制御による糖尿病および併発疾患の克服

片桐秀樹

Offer Organization: 科学技術振興機構

System: 戦略的な研究開発の推進ムーンショット型研究開発事業

Institution: 東北大学

2020 - 2025

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AI・数理モデル解析などを活用して、代謝・循環の調節に重要である自律神経を介した臓器間ネットワークの機序を包括的に解明し、その制御手法を開発し、未病期段階の状態をより精密に検出します。それにより、2050年には、糖尿病および併発疾患の発症を未然に防ぐ社会の実現を目指します。
Elucidation of vagal mechanism underlying glucose homeostasis

Katagiri Hideki

Offer Organization: Japan Society for the Promotion of Science

System: Grants-in-Aid for Scientific Research

Category: Grant-in-Aid for Scientific Research (A)

Institution: Tohoku University

2017/04/01 - 2021/03/31

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Neuronal relay systems play critical roles in communicating metabolic information among organs/tissues and maintaining glucose homeostasis at the whole-body level. We have further advanced our previous achievements. This study showed the molecular mechanisms of neuron-derived pancreatic β cell proliferation. First, combination of acetylcholine and PACAP induced β cell proliferation. In addition, we showed the FoxM1 pathway in β cells to enhance cell cycle, leading to beta cell proliferation. Furthermore, stimulation of abdominal vagal nerve per se was shown to promote both insulin secretion acutely and β cell proliferation chronically.
Anatomical and biochemical analyses of paprasympathetic ganglia in the pancreas

KATAGIRI Hideki, TAKAHASHI Hironori, KAWANA Yohei, SUGAWARA Hiroto

Offer Organization: Japan Society for the Promotion of Science

System: Grants-in-Aid for Scientific Research

Category: Grant-in-Aid for Challenging Exploratory Research

Institution: Tohoku University

2016/04/01 - 2018/03/31

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We previously reported a liver-brain-pancreas neuronal relay to play an important role in promoting pancreatic β cell proliferation. Here, we elucidated anatomical and biochemical mechanisms of the neuronal signals within the pancreas. First, the tissue clearing method, CUBIC, revealed a major part of parasympathetic ganglia to be located in the vicinity of pancreatic islets. In addition, ex vivo analyses showed that combined stimulation with several neurotransmitters released by vagal nerves enabled β cells to be efficiently proliferated. This neuronal signal-mediated mechanism, elucidated by this research program, holds potential for developing novel approaches to regenerating pancreatic β cells.
Inter-organ communication via the neuronal system in response to external environment

Katagiri Hideki, IZUMI Tomohito, ASAI Yoichiro, MUNAKATA Yuichiro, YAMAMOTO Junpei, SHIRAI Yuta

Offer Organization: Japan Society for the Promotion of Science

System: Grants-in-Aid for Scientific Research

Category: Grant-in-Aid for Scientific Research (A)

Institution: Tohoku University

2013/04/01 - 2017/03/31

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In multi-organ creatures, including human beings, inter-organ metabolic communication is essential to regulate systemic metabolism. We examined how the inter-organ communication functions in response to alterations in external environment. Thereafter, we elucidated that 1) increased amino acid intake induces hypertriglyceridemia via a neuronal relay system, 2) hypoxic responses in steatotic liver are involved in gallstone formation, and 3) fatty acids promote glucose-stimulated insulin secretion via a newly-identified receptor family. Thus, a variety of inter-organ systems for metabolic homeostasis are ironically involved in obesity-related disorders.
Mechanism of determining genomic copy number according to analyses of early-onset diabetic patients

KATAGIRI Hideki, Kondo Keiichi, Kodama Shinjiro

Offer Organization: Japan Society for the Promotion of Science

System: Grants-in-Aid for Scientific Research

Category: Grant-in-Aid for Challenging Exploratory Research

Institution: Tohoku University

2014/04/01 - 2016/03/31

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Genetic factors play very important roles in the onset and progression of type 2 diabetes mellitus (T2DM). We reported that copy number losses in the subtelomeric region on chromosome 4p16.3 were detected in early-onset Japanese T2DM patients at a high frequency. In this study, we found two novel copy number losses within the subtelomeric regions, which have significant associations with early-onset Japanese T2DM. In addition, using the MassArray system, we detected a “one-copy” region in four diabetic patients within the chromosome 4p16.3 region, indicating some genomic alterations in these affected subjects. Furthermore, the 4p16.3 region and whole exomes of 11 diabetic patients was sequenced by the next generation sequencer. Although the big sequencing data are now analyzing, we obtained novel findings which suggest genomic alterations in one allele of several affected subjects.
Molecular Mechanism of Regulating Glucose and Energy Metabolism via Inter-organ Neuronal Network System

KATAGIRI Hideki

Offer Organization: Japan Society for the Promotion of Science

System: Grants-in-Aid for Scientific Research

Category: Grant-in-Aid for Scientific Research on Innovative Areas (Research in a proposed research area)

Institution: Tohoku University

2010/04/01 - 2015/03/31

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We have recently discovered that neuronal networks among organs/tissues play important roles in maintaining metabolic homeostasis in the whole body. In this study, we first focused on the inter-organ neuronal network system, originated in hepatic PPARγ expression, which promotes energy expenditure and lipolysis, and found that FSP27 mediates this signal downstream from PPARγ in the liver. Next, we newly discovered another inter-ogran communication system which regulates energy metabolism originating in the liver. Hepatic glucokinase expression, which induces glucose uptake, suppressed brown adipose tissue activity and adaptive thermogenesis via a novel neuronal network, consisting of the vagal afferents and sympathetic efferents. Furthermore, this neuronal network determines obesity predisposition among murine strains. Collectively, these discoveries further highlight the importance of inter-organ neuronal network for regulation of systemic homeostasis.
Molecular basis and disorders of control of appetite and fat accumulation

KANGAWA Kenji, HOSODA Kiminori, KOJIMA Masayasu, SHIODA Seiji, MINOKOSHI Yasuhiko, KATAGIRI Hideki, YAMAUCHI Toshimasa, FUNAHASHI Tohru, NAKAZATO Masamitsu, SHIMIZU Hiroyuki, OGAWA Wataru, HOSODA Kiminori

Offer Organization: Japan Society for the Promotion of Science

System: Grants-in-Aid for Scientific Research

Category: Grant-in-Aid for Scientific Research on Innovative Areas (Research in a proposed research area)

Institution: National Cardiovascular Center Research Institute

2010/04/01 - 2015/03/31

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We developed the general research policy and plan of this innovative area, and adjusted and supported research plans of each group. We held a regular meeting every year for the purpose of the exchange of information, organic communication and promoting collaborative investigation among research groups, Furthermore, we held a public international symposium in 2012 and 2014, and established the homepage of this project to make the information public.
New Conceptual Framework for Copy Number Variation-associated Diabetes

KATAGIRI Hideki, MATSUZAKA Takashi

Offer Organization: Japan Society for the Promotion of Science

System: Grants-in-Aid for Scientific Research

Category: Grant-in-Aid for Challenging Exploratory Research

Institution: Tohoku University

2012/04/01 - 2014/03/31

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Genetic factors play very important roles in the onset and progression of type 2 diabetes mellitus (T2DM). We previously found that copy number losses in the subtelomeric region on chromosome 4p16.3 were detected in early-onset Japanese T2DM patients at a high frequency. Herein, we additionally found two novel copy number losses within the subtelomeric regions on chromosomes 16q24 and 22q13, which have significant associations with early-onset Japanese T2DM. Furthermore, copy number variation (CNV) analysis of the whole genome verified simultaneous copy number losses in all three subtelomeric regions in 11 of our 100 T2DM subjects, while none of 100 non-diabetic controls showed the copy number losses in all three regions. Thus, CNV within multiple subtelomeric regions are strongly associated with early-onset T2DM and examination of simultaneous CNVs in these three regions may lead to the development of an accurate and selective procedure for detecting genetic susceptibility to T2DM.
Discovery of a novel inter-organ metabolic communication system

KATAGIRI Hideki

Offer Organization: Japan Society for the Promotion of Science

System: Grants-in-Aid for Scientific Research

Category: Grant-in-Aid for Scientific Research (B)

Institution: Tohoku University

2011 - 2012

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We have found that adaptive thermogenesis induced by brown adipose tissue (BAT) was markedly suppressed, when hepatic glucose metabolism was enhanced by glucokinase overexpression. This liver-to-BAT communication is mediated by a neuronal relay consisting of afferent vagal and efferent sympathetic nerves. This inter-tissue system seems to function as a feed-forward mechanism favoring energy storage. This mechanism might have worked advantageously under conditions of repetitive excesses and shortagesof food. Unfortunately, however, in the current age of constant plenty, this system seems to trigger obesity development. In fact, we further found that this system contributes to determining obesity predisposition among murine strains.
酸化LDL選択的除去による動脈硬化改善治療への挑戦

片桐秀樹, 澤田正二郎

Offer Organization: 日本学術振興会

System: 科学研究費助成事業

Category: 挑戦的萌芽研究

Institution: 東北大学

2009 - 2010

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動脈硬化の発症の機序として、low density lipoprotein(LDL)の果たす役割が重要であることは周知のことである。我々は、以前、高LDLにより動脈硬化をきたすモデルマウス(apoE欠損マウス)を用い、肝に酸化LDL受容体として知られるLOX-1タンパクを過剰発現させることにより、高LDL血症の状況で酸化LDLを選択的に除去することを試みたところ、アデノウィルスによる短期(1週間程度)のLOX-1発現により、4週間の動脈硬化の進展をほぼ完全に抑制するという結果を得た。そこで、LOX-1発現を長期に行い、数ヶ月にわたり酸化LDLを減少させると、動脈硬化病変を縮小させることができるのではないかという挑戦的な仮説を立て、長期発現を試みた。長期発現を得るため、さまざまな発現モデルを試した結果、長期発現改変アデノウィルスを用いることにより、数ヶ月にわたる発現を得ることに成功した。そこで、遺伝子発現系を用い、動脈硬化が進展した週齢でのapoE欠損マウスの動脈硬化病変に与える影響を検討している。 LOX-1遺伝子アデノウィルスの静脈注射により、apoE欠損マウスの肝にLOX-1は発現し、酸化LDLの肝への取り込みが認められた。動脈硬化の進展は肝LOX-1発現により、著明に抑制されたが、高コレステロールapoE欠損マウス食モデルでは、縮小効果までは見出せなかった。現在、普通食のapoE欠損マウスによる、長期間での動脈硬化の進展に対する影響を検討している。本成果は、酸化LDLの動脈硬化の進展や退縮における役割の検討につながるものと期待する。
Role of Neuronal Network System in Development of the Metabolic Syndrome

KATAGIRI Hideki, ISHIGAKI Yasushi

Offer Organization: Japan Society for the Promotion of Science

System: Grants-in-Aid for Scientific Research

Category: Grant-in-Aid for Scientific Research (B)

Institution: Tohoku University

2008 - 2010

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We have recently discovered that neuronal networks among organs/tissues play important roles in maintaining metabolic homeostasis in the whole body. In this study, we examined how the inter-organ neuronal networks contribute to the development of the metabolic syndrome. First, we found that hepatic ERK activation induced insulin hypersecretion and pancreatic beta cell proliferation. This liver-to-pancreas coordination is mediated by a novel neuronal network, consisting the splanchnic afferents and vagal efferents. Furthermore, this neuronal network is involved in obesity-induced hyperinsulinemia. In addition, we have found that another neuronal network originating in hepatic PPARgamma expression causes hypertension associated with obesity. Thus, this study has revealed the mechanisms underlying obesity-induced hyperinsulinemia and hypertension, which are major features of the metabolic syndrome. The mechanisms involve two types of inter-organ metabolic networks, which are potential therapeutic targets for the metabolic syndrome.
Mechanism of pancreatic beta-cell regulation by signals from the liver

IMAI Junta, OKA Yoshitomo, KATAGIRI Hideki

Offer Organization: Japan Society for the Promotion of Science

System: Grants-in-Aid for Scientific Research

Category: Grant-in-Aid for Young Scientists (B)

Institution: Tohoku University

2008 - 2009

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The mechanism underlying compensatory beta-cell responses against insulin resistance is not well understood. We have identified that a neuronal relay, originating in the liver, is involved in compensatory beta-cell responses during obesity development. In addition, we have shown that modulation of this neuronal relay may serve as a potential strategy for beta-cell regenerative medicine. These results were published in Science, one of the most famous scientific journals in the world, and were transmitted all over the world via various media.
メタボリックシンドロームにおける動脈硬化発症機序の解明

片桐秀樹, 高俊弘, GAO J.

Offer Organization: 日本学術振興会

System: 科学研究費助成事業

Category: 特別研究員奨励費

Institution: 東北大学

2008 - 2009

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動脈硬化の発症・進展における分子機序の解明を目指した研究を行っている。昨年度は、酸化LDLの酸化LDLが動脈硬化の発症・進展に関与することを示し、酸化LDLやそれによりもたらされる酸化ストレスの重要性を証明した。本年度は、もう一つのストレス応答系である小胞体ストレスについて検討を進めた。小胞体ストレスによる細胞死を惹起すると考えられているCHOPを欠損したマウスを用い、apoE欠損マウスとの交配による粥状動脈硬化への影響、および、カフモデルによる内膜肥厚に及ぼす影響を検討した。どちらの系においても、動脈硬化の発症はCHOP欠損マウスで著明に抑制され、さらに、血管内における炎症反応が軽減していることがその機序であることが示された。この結果は、動脈硬化における小胞体ストレス応用の意義を示したものとして意義深いとともに、CHOPの炎症反応惹起に関わる役割を解明したことにおいても、重要なものと考えられる。
Elucidation of beta-cell regeneration after Bone marrow transplantation.

HASEGAWA Yutaka, OKA Yoshitomo, KATAGIRI Hideki

Offer Organization: Japan Society for the Promotion of Science

System: Grants-in-Aid for Scientific Research

Category: Grant-in-Aid for Young Scientists (Start-up)

Institution: Tohoku University

2007 - 2008
Unraveling liver-derived signals against obesity and diabetes

KATAGIRI Hideki, OGIHARA Takehide, ISHIGAKI Yasushi, YAMADA Tetsuya

Offer Organization: Japan Society for the Promotion of Science

System: Grants-in-Aid for Scientific Research

Category: Grant-in-Aid for Scientific Research (B)

Institution: Tohoku University

2006 - 2007

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Metabolism is coordinated and regulated among different organs/tissues throughout the body. This coordinated metabolic regulation is apparently essential for maintaining systemic homeostasis, particularly glucose and energy metabolism. Therefore, communication among organs/tissues is extremely important and perturbation of this control system may lead to the development of metabolic disorders. During this decade, the versatility of adipose tissue as an endocrine organ and as a contributor to disease development has been established. However, a number of recent studies have shown that tissue-specific knockout mice exhibit unexpected phenotypes, suggesting the presence of many as yet unknown forms of cross-talk among organs/tissues. We have identified several systems consisting of autonomic nerve circuits, i.e. metabolic information highways, which play important roles in conveying inter-organ communication regarding metabolism. This is exemplified by the discovery of involvement of the afferent hepatic vagus in energy expenditure and fat accumulation. We expressed PPAR_γ in the liver, resulting in enhanced lipolysis in fat tissue and increased systemic energy expenditure. Thus, in response to lipid accumulation in the liver, hepatic vagal afferents transmit information regarding excess energy accumulation to the brain, thereby increasing sympathetic outflow to enhance energy expenditure. Our findings indicate that the brain obtains a variety of metabolic information from peripheral organs/tissues, resulting in cooperative metabolic regulation among tissues/organs throughout the body. Furthermore, these systems appear to contribute to pathological features of the metabolic syndrome under the condition of long-term excess calorie intake. Thus, elucidation of these regulatory systems may facilitate unraveling the mechanisms underlying metabolic homeostasis and those underlying development of the metabolic syndrome.
The role of genes of forkhead transcription factors in type2 diabetes and obesity.

HINOKIO Yoshinori, SUZUKI Susumu, KATAGIRI Hideki, ISHIHARA Hisamitsu

Offer Organization: Japan Society for the Promotion of Science

System: Grants-in-Aid for Scientific Research

Category: Grant-in-Aid for Scientific Research (C)

Institution: Tohoku University

2004 - 2005

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With DNA extracted from blood samples of unrelated Japanese type 1 and type 2 diabetic patients and non-diabetic controls, we screened mutations and polymorphisms with direct sequencing in the Foxa-2 gene. The screening revealed four polymorphisms of Foxa-2 gene. We have found that two alleles among the polymorphisms in Foxa-2 gene. The frequencies of A alleles of two polymorphisms, nt 537 and codon279, in the gene were significantly higher than those of the opposite allele (p<0.05). From these facts, it is suggested that the polymorphisms in Foxa-2 gene are involved with clinical characteristics of early-onset diabetes. With DNA extracted from blood samples of 96 Japanese type2 diabetic patients and 102 non-diabetic controls, we screened mutations and polymorphisms with direct sequencing in heme oxygenase (HO-1) gene. With the screening of HO-1 gene, we identified three polymorphisms, SNPHO1(A/T), SNPHO2(A/G) and (GT)n repeat in the gene. The allele frequencies SNPHO1 and ANPHO2 were not significantly different between diabetic group and control group. We determined the number of GT repeats in the HO-1 promoter in diabetics and controls and compared the frequencies of short repeat (class S) and long repeat (class L) alleles. In non-diabetic group, the number of patients with hyperlipidemia was significantly larger in class L than in class S (Chi-square test p<0.05). Both the systolic and diastolic pressures in diabetic group were significantly higher in class L than in class S (p<0.05). In non-diabetic group, the number of patients with hyperlipidemia was significantly larger in the case with A/A allele in the SNPHO1 than in the case with A/T allele or T/T allele (Chi-square test p<0.05). Both the systolic and diastolic pressures in diabetic group were significantly higher in the case with A/A allele in SNPHO1 than in with A/T allele or T/T allele. Taken together, these data may suggest a role of polymorphisms of Foxa-2 gene and HO-1 gene in diabetes, hyperlipidemia and hypertension. That requires further investigation to test these hypotheses.
Elucidation of abnormality of plasma membrane microdomain in type 2 diabetes mellitus

SUZUKI Susumu, MIYAGI Taeko, HINOKIO Yoshinori, KATAGIRI Hideki, ISHIHARA Hisamitsu

Offer Organization: Japan Society for the Promotion of Science

System: Grants-in-Aid for Scientific Research

Category: Grant-in-Aid for Scientific Research (B)

Institution: Tohoku University

2004 - 2005

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Membrane microdomains rich in gangliosides are recognized as being critical for proper compartmentalization of insulin signaling. Plasma membrane-associated sialidase, NEU3, is a key enzyme for ganglioside hydrolysis. We previously reported that the mice overexpressing NEU3 developed severe insulin-resistant diabetes. To examine possible the contributions of NEU3 to in vivo insulin sensitivity and glucose tolerance, NEU3 was expressed using adenoviral vectors in the livers of C57BL/6 mice on standard and high-fat diets, and insulin-resistant KKAy mice on standard diets. Hepatic NEU3 overexpression significantly improved glucose tolerance and insulin sensitivity in the C57BL/6 mice fed standard diets, and glucose tolerance in the C57BL/6 mice fed high-fat diets and in KKAy mice. Hepatic NEU3 overexpression increased hepatic glycogen deposition and triglyceride accumulation, and enhanced the hepatic PPARg and fetuin expression in the C57BL/6 mice on standard and high-fat diets, and in KKAy mice. TLC analysis demonstrated increased levels of GM1 and markedly reduced GM3 in the livers of mice with hepatic NEU3 overexpression (NEU3 mice). Basal and insulin-stimulated tyrosine phosphorylations of insulin receptor substrate 1 (IRS1) were significantly increased, but tyrosine phosphorylations of the insulin receptor and IRS2 in the NEU3 liver were unchanged. Insulin-stimulated tyrosine phosphorylations of the insulin receptor were increased in adipose tissues of NEU3 mice. These results suggest that hepatic NEU3 overexpression improves insulin sensitivity and glucose tolerance through modification of ganglioside composition and PPARγ signaling. Our findings also provide further evidence that NEU3 is an important regulator of insulin sensitivity and glucose tolerance.
Elucidation of diabetes-related genes

OKA Yoshitomo, KATAGIRI Hideki, HINOKIO Yoshinori, ISHIHARA Hisamitsu

Offer Organization: Japan Society for the Promotion of Science

System: Grants-in-Aid for Scientific Research

Category: Grant-in-Aid for Scientific Research on Priority Areas

Institution: Tohoku University

2001 - 2005

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Wolfram syndrome, an autosomal recessive disorder associated with diabetes mellitus and optic atrophy is caused by mutations in the WFS1 gene encoding an endoplasmic reticulum (ER) membrane protein. We herein report that pancreatic islets of wfs1-deficient mice exhibit increases in PKR-like ER kinase phosphorylation, chaperone gene expressions and active XBP1 protein levels, indicating an enhanced ER stress response. We established wfsl-deficient MIN6 clonal β-cells by crossing wfsl-deficient mice with mice expressing simian virus 40 large T antigen in β-cells. These cells show essentially the same alterations in ER stress responses as wfsl-deficient islets, which were reversed by re-expression of WFS1 protein or overexpression of GRP78, a master regulator of ER stress. In contrast, these changes are observed neither in heart, skeletal muscle, nor brown adipose tissues with WFS1-deficiency. The enhanced ER stress results in increased caspase 3 cleavage and reduced BrdU incorporation, indicating accelerated apoptotic processes and impaired cell cycle progression in the mutant islets. These changes are associated with increased expression of p21^<CIP1> in wfsl-deficient islets and clonal β-cells. Treatment of islets with thapsigargin, an ER stress inducer increased p21^<CIP1> expression, and forced expression of p21^<CIP1> reduced MIN6 β-cell numbers, suggesting that the ER stress-induced increase in p21^<CIP1> expression to be involved in β-cell loss in the mutant islets. These data indicate that WFS1-deficiency activates the ER stress response specifically in β-cells, causing β-cell loss through increased apoptosis and impaired cell cycle progression.
肝インスリンシグナルの個体糖脂質代謝における役割-ノックダウン法を用いての解析-

片桐秀樹, 高橋和眞, 石垣泰

Offer Organization: 日本学術振興会

System: 科学研究費助成事業

Category: 萌芽研究

Institution: 東北大学

2003 - 2004

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最近、植物や線虫等で見出されていたRNA interferenceと呼ばれる現象が哺乳類細胞でも確認され、特異的に蛋白の発現を抑制する手法として、注目されつつある。目的の蛋白のmRNA配列の一部(20塩基前後)に匹敵する2本鎖RNA (siRNA)を細胞内に導入することで、その蛋白の発現をほぼ完全に抑制することができるというものである。そこで、この技術を用いて、肝細胞におけるインスリンシグナルの抑制が、個体全身における糖代謝の恒常性維持にどのような役割を果たしているか、解明することを目的として、以下の実験を行った。 adenovirusにこのsiRNAを発現するカセットを組み込み、マウスに静注することで肝臓におけるインスリン受容体の発現を抑制することにより、急性に肝臓のインスリンシグナルが減弱した場合、全身の糖代謝にどのような影響を及ぼすか検討した。が、そこで、効果的に遺伝子発現抑制を起こすsiRNAベクターの開発を試みた。昨年、10種類のベクターを作製し、その中で最も強力に抑制するベクターを選択した。本年は、これを実際にマウス個体に投与したところ、肝におけるインスリン受容体の発現は有意に抑制され、約1週間で肝臓の重量は著明に縮小を示した。血中インスリン濃度は約2倍に上昇し、肝におけるインスリンシグナルの低下に代償的に増加したものと考えられた。一方、空腹時血糖値は有意差を認めず、経静脈的糖負荷後の血糖曲線も、変化を認めなかった。これらより、肝におけるインスリン受容体シグナルの突然の遮断が生じ、肝重量の低下を招いても、糖代謝は、インスリン分泌の亢進により代償しうることが示された。
Development of gene therapy for diabetes associated with obesity

KATAGIRI Hideki, TAKAHASHI Kazuma, ISHIHARA Hisamitsu, ISHIGAKI Yasushi

Offer Organization: Japan Society for the Promotion of Science

System: Grants-in-Aid for Scientific Research

Category: Grant-in-Aid for Scientific Research (B)

Institution: Tohoku University

2003 - 2004

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An explosive increase in the number of diabetic patients, which has become a major public health concern in most industrialized countries in recent decades, is mainly the result of excess energy intake and physical inactivity. Excess energy intake results in obesity, a common condition associated with diabetes, hyperlipidemia and premature heart disease. However, the major treatment modalities for diabetes, including insulin injection and oral sulfonylureas, aim at lowering blood glucose levels by driving glucose into cells in peripheral tissues such as muscle and fat. This further exacerbates insulin resistance when energy intake is in excess, resulting in a vicious cycle. Therefore, novel therapies which promote increased energy expenditure are needed. Inefficient metabolism, such as the generation of heat instead of ATP, is a potential treatment strategy for type 2 diabetes associated with obesity. Therefore, to examine whether dissipating excess energy in the liver is a possible therapeutic approach to high fat diet-induced metabolic disorders, we attempted to express uncoupling protein-1 (UCP1) ectopically in murine liver using adenoviral vectors. Once diabetes with obesity developed, hepatic UCP1 expression increased energy expenditure, decreased body weight, and reduced fat in the liver and adipose tissues, resulting in markedly improved insulin resistance, and thus, diabetes and dyslipidemia. Hepatic UCP1 expression also reversed high fat diet-induced hyperphagia and hypothalamic leptin resistance, as well as insulin resistance in muscle. In contrast, intriguingly, in standard chow-fed lean mice, hepatic UCP1 expression did not significantly affect energy expenditure or hepatic ATP contents. Furthermore, no alterations in blood glucose levels, body weight, or adiposity were observed. These findings suggest that ectopic UCP1 in the liver dissipates surplus energy without affecting required energy and exerts minimal metabolic effects in lean mice. Thus, this gene therapy is a new potential therapeutic strategy for the metabolic syndrome.
The role of phospholipase D in the development of diabetes mellitus

HIRAI Masashi, KATAGIRI Hideki, HINOKIO Yoshinori, SUZUKI Susumu, ISHIHARA Hisamitu

Offer Organization: Japan Society for the Promotion of Science

System: Grants-in-Aid for Scientific Research

Category: Grant-in-Aid for Scientific Research (C)

Institution: TOHOKU UNIVERSITY

2002 - 2003

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Glycosylphosphatidylinositol(GPI)-specific phospholipase D(GPI-PLD) cleaves GPI anchor and produces inositol glycan, which is thought to be a second messenger of insulin action. GPI-PLD also has been reported to be involved in insulin secretion. Thus, genetic variations of GPI-PLD could cause diabetes mellitus. Gene analysis was performed in type 2 diabetic patients (DM), the subjects with impaired glucose tolerance (IGT), and the subjects with normal glucose tolerance (NGT). There were totally six mutations resulting in amino acid replacement in exon 1,11,21,22. There are three haplotype alleles according to the combination of Leu/Val polymorphism in the 17th amino acid and Val/Leu in 30th amino acid in exon 1. The frequency of haplotype allele was significantly different among the three groups. The frequency of the mutant type allele was significantly higher in DM and IGT compared to NGT. The analysis of HOMAC (β) using NGT suggested that the subjects with the mutant allele had lower insulin secretary capacity compared to those with the wild type allele. The state of diabetic complications and therapies tended to be different according to the haplotype alleles. To examine the role of GPI-PLD in insulin secretion, we have suppressed the expression of GPI-PLD in insulin secreting cells (INS-1 cells) by introducing synthesized RNAi oligonucleotide and adenovirus RNAi. Furthermore, we have constructed cell lines expressing high levels of GPI-PLD by adenovirus expression vector. It is suggested that genetic variation of GPI-PLD was associated with diabetes us in Japanese due to the decreased insulin secretary capacity.
The role of plasma membrane type sialidase gene Neu3 on the pathogenesis of type 2 diabetes mellitusin Japanese.

SUZUKI Susumu, HIRAI Masashi, YOSHINORI Hinokio, MIYAGI Taeko, ISHIHARA Hisamitsu, KATAGIRI Hideki

Offer Organization: Japan Society for the Promotion of Science

System: Grants-in-Aid for Scientific Research

Category: Grant-in-Aid for Scientific Research (B)

Institution: Tohoku University

2002 - 2003

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Gangliosides are a family of sialic acid-containing glycosphingolipids present in the cell surface membranes. Several lines of evidence suggest their important functional roles in regulating a wide range of biological processes including cell growth, cell differentiation, and transmembrane signaling. Plasma membrane-associated sialidase (Neu3) is a key enzyme for ganglioside hydrolysis, thereby playing crucial roles in regulation of cell surface functions. We have investigated effects of overexpression in transgenic mice by using the human NEU3 cDNA. We demonstrated that mice overexpressing the human NEU3 develop diabetic phenotype associated with hyperinsulinemia, islet hyperplasia, and increased beta-cell mass. As compared with the wild type, insulin-stimulated phosphorylation of the insulin receptor (IR) and insulin receptor substrate I was significantly reduced, and activities of phosphatidylinositol 3-kinase and glycogen synthase were low in transgenic muscle. IR phosphorylation was already attenuated in the younger mice before manifestation of cemia. Transient transfection of NEU3 into 3T3-L1 adipocytes and L6 myocytes caused a significant decrease in IR signaling. In response to insulin, NEU3 was found to undergo tyrosine phosphorylation and subsequent association with the Grb2 protein, thus being activated and causing negative regulation of insulin signaling. In fact, accumulation of GM1 and GM2, the possible sialidase products in transgenic tissues, caused inhibition of IR phosphorylation in vitro, and blocking of association with Grb2 resulted in reversion of impaired insulin signaling in L6 cells. The data indicate that NEU3 indeed participates in the control of insulin signaling, probably via modulation of gangliosides and interaction with Grb2, and that the mice can serve as a valuable model for human insulin-resistant diabetes. We also investigate the possible contribution of single nucleotide polymorphisms (SNPs) in NEU3 to the development of type 2 diabetes. We surveyed SNPs in the NEU3 gene in 298 Japanese subjects with type 2 diabetes mellitus and two control Japanese populations : one consisting of 148 elderly subjects who met stringent criteria for being non-diabetic including age above 60 years and no evidence of diabetes (HbA1c<5.6%), and another 308 subjects with normal glucose tolerance (NGT). We identified eight SNPs with and five SNPs without amino acid substitutions in their coding regions. The allele frequency of one of SNPs was significantly higher in type 2 diabetic patients than in both elderly normal and NGT subjects, whereas the allele frequency of other SNPs was essentially identical in these three groups. Furthermore, in the NGT subjects, the SNP was associated with a significantly lower insulin sensitivity index on oral glucose tolerance test. These results strongly suggest that, in Japanese, the SNP in the NEU32 gene is associated with the development of type 2 diabetes, via reduced insulin signaling.
Studies on mechanisms of insulin-stimulated glucose transport : analysis of downstream signaling and real-time monitoring of GLUT4 translocation

OKA Yoshitomo, HINOKIO Yoshinori, HIRAI Masashi, KATAGIRI Hideki

Offer Organization: Japan Society for the Promotion of Science

System: Grants-in-Aid for Scientific Research

Category: Grant-in-Aid for Scientific Research (B)

Institution: Tohoku University

2001 - 2002

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To elucidate the involvement of protein kinase C (PKC) isoforms in insulin-induced glucose transport, we expressed several PKC isoforms, conventional PKC-α, novel PKC-δ, and atypical PKC isoforms of PKC-λ and PKC-ζ, and their mutants in 3T3-L1 adipocytes using an adenovirus-mediated gene transduction system. Endogenous expression and the activities of PKC-αand PKC-λ/ζ, but not of PKC-δ, were detected in 3T3-L1 adipocytes. Overexpression of each wild-type PKC isoform induced a large amount of PKC activity in 3T3-L1 adipocytes. Atypical PKC-λ/ζ was not significantly activated by insulin, and expression of the wild-type, constitutively active, and domimant-negative mutants of atypical PKC did not affect either basal or insulin-stimulated glucose transport. Thus atypical PKC enzymes do not play a major role in insulin-stimulated glucose transport in 3T3-L1 adipocytes. Insulin-regulated aminopeptidase (IRAP) is known to be localized on the GLUT4-containing vesicles. The region of IRAP fused with glutathione-S-transferase [GST-IRAP(55-82)] was incubated with lysates from 3T3-L1 adipocytes, leading to identification of long-chain, medium-chain, and short-chain acyl-coenzyme A dehydrogenases (ACDs) as the proteins associated with IRAP. Immunoblotting of fractions prepared from sucrose gradient ultracentrifugation and vesicles immunopurified with anti-GLUT4 antibody revealed these ACDs to be localized on GLUT4-containing vesicles. Furthermore, 3-mercaptopropionic acid and hexanoyl-CoA, inhibitors of long-chain and medium-chain ACDs, respectively, induced dissociation of long-chain acyl-coenzyme A dehydrogenase and/or medium-chain acyl-coenzyme A dehydrogenase from IRAP in vitro as well as recruitment of GLUT4 to the plasma membrane and stimulation of glucose transport activity in permeabilized 3T3-L1 adipocytes. These findings suggest that ACDs are localized on GLUT4-containing vesicles via association with IRAP in a manner dependent on its dileucine motif and play a role in retention of GLUT4-containing vesicles to an intracellular compartment.
Generation of Wolfram syndrome mice, aiming at development of new therapeutics for diabetes through preserving pancreatic beta cells

OKA Yoshitomo, TAKAHASHI Kazuma, HINOKIO Yoshinori, KATAGIRI Hedeki, ISHIHARA Hisamitsu, HIRAI Masashi

Offer Organization: Japan Society for the Promotion of Science

System: Grants-in-Aid for Scientific Research

Category: Grant-in-Aid for Scientific Research (A)

2000 - 2002

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Wolfram syndrome is an autosomal recessive disorder associated with juvenile onset diabetes mellitus, optic atrophy, sensorineural deafness and diabetes insipidus. We identified, employing positional cloning, a gene responsible for this disorder and designated it WFS1. We also showed WFS1 protein to be localized in the ER membrane. In addition, WFS1 shares some sequence similarity with yeast Hrd3p, which is involved in ER-associated degradation of malfolded proteins. Thus, though WFS1 protein appears to play a role in the ER-stress response, its precise function remains to be clarified. To elucidate the functions of this novel protein and the pathophysiology of Wolfram syndrome, we have generated mice lacking the WFS1 gene (WFS1-KO). WFS1-KO mice are normal in appearance, growth and fertility Blood glucose levels in male WFS1-KO mice start to rise at around 12 weeks and are significantly higher than those of wild-type mice at 24 weeks (267±33 vs 146±34 mg/dl). This is associated with loss of islet β cells; whole pancreatic insulin content in WFS1-KO mice was 30-times lower than that in wild-type mice (11±4 vs 287±34 ng/mg pancreas). Immunohistochemical analysis of the pancreas using an anti-WFS1 protein antibody revealed that WFS1 protein is absent from exocrine tissue, but is strongly expressed in endocrine β cells. WFS1 protein is not expressed in glucagon-positive cells and the majority of somatostatin-, and pancreatic polypeptide-positive cells are devoid of WFS1 immunoreactivity. In WFS1-KO mice, β cell number fell with age, while a cells were somewhat increased and were scattered throughout the islet. These results strongly suggest WFS1 protein to play a critical role in survival and/or regeneration of β cells and progressive loss of islet β cells to be the major cause of diabetes in this disorder.

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研究業績が報道された
[日本国内] 「未来のノーベル賞候補者顕彰」日本学術振興会賞に25氏

2007/01/12 -

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臓器間相互作用の意義を初提唱片桐秀樹・東北大学大学院医学系研究科教授として、日本学術振興会賞受賞が報道された。
[日本国内] 肝臓肥満防止に一役脳に指令代謝促進―東北大発見

2006/06/16 -

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研究業績が全国紙1面に報道された
[日本国内] 脂肪肝から肥満改善指令東北大院・片桐教授らが明らかに

2006/06/16 -

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研究業績が報道された
[日本国内] 肝臓から脂肪燃焼信号東北大大学院教授らが発見「やせ薬」に応用も

2006/06/16 -

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研究業績が報道された

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Media Coverage 1

[日本国内] 肝臓から脂肪燃焼信号

NHK

2006/06/16

Type: TV or radio program

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全国ニュースで研究業績が報道された