| Project/Area Number |
25461383
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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) |
SUZUKI Satoru 福島県立医科大学, 医学部, 教授 (30222061)
NISHIO Shin-ichi 信州大学, 学術研究院医学系(医学部附属病院), 講師 (30467146)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | インスリン分泌 / 膵β細胞 / インクレチン / ブドウ糖 / カルシウム |
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| Outline of Final Research Achievements |
In search of mechanisms of glucose-stimulates insulin secretion, we established two different aspects of findings as follows.
1)We demonstrated that glucose could trigger rapid insulin release independent from its action on both KATP channel and voltage-dependent Ca2+ channel. Namely, with diazoxide, an opener of KATP channel, and nifedipine, a blocker of L-type voltage-dependent Ca2+ channel, glucose triggered insulin secretion from rat pancreatic islets in the presence of forskolin, an activator of adenylyl cyclase. 2)Lactisole, an inhibitor of sweet taste receptor, inhibited insulin secretion induced by sweeteners. It attenuated the elevation of cytoplasmic Ca2+ concentrations induced by these sweeteners. It also inhibited action of glucose. These results indicate that lactisole may be useful in assessing the role of the glucose-sensing receptor in pancreatic β-cells.
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