| Project/Area Number |
25460113
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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 |
Pharmacology in pharmacy
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| Research Institution | Meiji University of Integrative Medicine |
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Principal Investigator |
KATSURA Masashi 明治国際医療大学, 医学教育研究センター, 教授 (80204452)
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| Co-Investigator(Kenkyū-buntansha) |
佐藤 公道 京都大学, 薬学研究科, 名誉教授 (80025709)
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| Research Collaborator |
SHIGETO Makoto
KAKU Kohei
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| Project Period (FY) |
2013-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2015: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | インスリン分泌 / 膵島細胞 / GLP-1 / Aキナーゼ / Cキナーゼ / 膵β細胞 / ＧＬＰ－１ / Ｃキナーゼ / Ａキナーゼ / インクレチン / インスリン / ＰＬＣ / ＰＫＡ / ＰＫＣ / カルシウム流入 / 糖尿病 / グルカゴン / 膵α細胞 |
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| Outline of Final Research Achievements |
Strategies aimed at mimicking or enhancing the action of the incretin hormone glucagon-like peptide 1 (GLP-1) therapeutically improve glucose-stimulated insulin secretion (GSIS); however, it is not clear whether GLP-1 directly drives insulin secretion in pancreatic islets. In the present study, we examined the mechanisms by which GLP-1 stimulates insulin secretion in mouse and human islets.
Based on results using high concentration of GLP-1, the mechanism of action of GLP-1 has been considered to be PKA-dependent. But it was revealed that at physiologically low concentration of GLP-1, PKC-dependent pathway promotes insulin secretion.
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