| Project/Area Number |
25860172
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
General physiology
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| Research Institution | Kyoto Prefectural University of Medicine (2014)
Okazaki Research Facilities, National Institutes of Natural Sciences (2013) |
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Principal Investigator |
KASHIO Makiko 京都府立医科大学, 医学(系)研究科(研究院), 助教 (20631394)
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2014: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2013: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | TRPM2 / レドックスシグナル / 温度 / インスリン |
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| Outline of Final Research Achievements |
Pancreatic b-cells secrete hypoglycemic insulin upon blood glucose elevation to keep its concentration in the range of physiological levels. Insulin secretion from pancreatic b-cell is well known to be mediated by KATP channel-dependent canonical pathway in which KATP channel closure by intracellular ATP elevation causes membrane depolarization and activation of voltage-dependent Ca channel. However, beside the canonical pathway, KATP channel-independet pathways are recently elucidated to be involved in insulin secretion. As one of them, we have clarified the involvement of TRPM2 function in insulin secretion focusing on redox signal-mediated TRPM2-sensitization leading its activation at body temperature.
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