TOHOKU UNIVERSITY Researchers

Research History 3

2022/04 - Present

東北大学大学院医学系研究科糖尿病代謝内科学分野　助教
2019/04 - 2022/03

東北大学大学院医学系研究科糖尿病代謝内科学分野　医員
2015/04 - 2019/03

東北大学大学院医学系研究科糖尿病代謝内科学分野　博士課程

Education 1

山梨大学

2007/04 - 2013/03

Research Interests 1

代謝学、糖尿病、膵β細胞

Research Areas 1

Life sciences / Metabolism and endocrinology /

Awards 1

日本糖尿病学会第11回若手研究奨励賞

2021/05

Papers 9

Phagocytosis by macrophages promotes pancreatic β cell mass reduction after parturition in mice

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　2023/09
Publisher: Elsevier BV
DOI： 10.1016/j.devcel.2023.08.002 　

ISSN： 1534-5807
A highly sensitive strategy for monitoring real-time proliferation of targeted cell types in vivo

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.
Roles of <scp>FoxM1</scp>‐driven basal β‐cell proliferation in maintenance of β‐cell mass and glucose tolerance during adulthood

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　2022/07/15
Publisher: Wiley
DOI： 10.1111/jdi.13846 　

ISSN： 2040-1116

eISSN： 2040-1124

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ABSTRACT 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.
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

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
Publisher: Elsevier BV
DOI： 10.1016/j.amjmed.2020.03.021 　

ISSN： 0002-9343
Native Valve Endocarditis due to<i> Staphylococcus warneri</i> Developing in a Patient with Type 1 Diabetes

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　59　(18)　2269-2274　2020/09/15
Publisher: Japanese Society of Internal Medicine
DOI： 10.2169/internalmedicine.4661-20 　

ISSN： 0918-2918

eISSN： 1349-7235
Vascular resistance of carotid and vertebral arteries is associated with retinal microcirculation measured by laser speckle flowgraphy in patients with type 2 diabetes mellitus

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
Publisher: Elsevier BV
DOI： 10.1016/j.diabres.2020.108240 　

ISSN： 0168-8227
Inhibition of Plasminogen Activator Inhibitor-1 Activation Suppresses High Fat Diet-Induced Weight Gain via Alleviation of Hypothalamic Leptin Resistance

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　2020/06/24
Publisher: Frontiers Media SA
DOI： 10.3389/fphar.2020.00943 　

eISSN： 1663-9812
Vagus-macrophage-hepatocyte link promotes post-injury liver regeneration and whole-body survival through hepatic FoxM1 activation

Tomohito Izumi, Junta Imai, Junpei Yamamoto, Yohei Kawana, Akira Endo, Hiroto Sugawara, Masato Kohata, Yoichiro Asai, Kei Takahashi, Shinjiro Kodama, Keizo Kaneko, Junhong Gao, Kenji Uno, Shojiro Sawada, Vladimir V. Kalinichenko, Yasushi Ishigaki, Tetsuya Yamada, Hideki Katagiri

Nature Communications　9　(1)　2018/12/13
Publisher: Springer Science and Business Media LLC
DOI： 10.1038/s41467-018-07747-0 　

eISSN： 2041-1723

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Abstract 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.

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