| Project/Area Number |
16K09799
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Endocrinology
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| Research Institution | Shinshu University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
小島 至 群馬大学, 生体調節研究所, 名誉教授 (60143492)
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| Project Period (FY) |
2016-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2018: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | インスリン / ブドウ糖 / インクレチン / cAMP / インスリン分泌 / パルミチル化 / NADPH / 甘味受容体 |
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| Outline of Final Research Achievements |
During the study period, three achievements on pancreatic β cells were obtained. (1 ) We published as a book about the possibility that sweet taste receptors in pancreatic β cells play an important role in glucose stimulation of insulin secretion (ISBN 978-981-13-0002-8). (2) We found that cytoplasmic thyroid hormone binding protein knockout mice cause glucose intolerance and obesity under high-fat diet load, and examined the details and published them (Biochem Biophys Res Commun. 2019; 508 (3): 914-920 ). (3) There have been many reports that conventional estrogen works to promote insulin transcription activity of pancreatic β cells, but in studies using pancreatic β cell lines, the fact that estrogen suppresses the transcriptional activity of insulin in pancreatic β cells and Its molecular mechanism was elucidated and reported (In Vitro Cell Dev Biol Anim. 2019; 55 (4): 226-236).
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| Academic Significance and Societal Importance of the Research Achievements |
世界的な健康問題である２型糖尿病はインスリン分泌が不足することで発症・進展する。我々は３０年以上にわたりインスリン分泌機構の解明に努めてきた。本研究期間には甘味受容体のインスリン分泌機構への関与に関する最新知見を整理し、さらに環境ホルモンがインスリン分泌を障害し糖尿病の急増に関連しているという魅力的な仮説を支持する基礎データ（エルトロゲンがインスリン転写活性を抑制する）が得られた。また、２型糖尿病の発症促進要因である肥満に関して、その発症に関与する新たな分子基盤を提唱できた。これらのことは２型糖尿病発症機構の解明や治療法の開発に将来的展望を与える。
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