2017 Fiscal Year Final Research Report
Molecular mechanism underlying pathophysiological insulin secretion during early type 2 diabetes mellitus.
| Project/Area Number |
15K07973
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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 | Showa University |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
MITSUMOTO Asuka (KAIZAKI Asuka) 昭和大学, 薬学部, 講師 (70407443)
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| Research Collaborator |
ISHII Shunichi
TANAKA Maho
HAMAGUCHI Momoe
Ohno Sayuri
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Keywords | 高インスリン血症 / 酸化ストレス / TRPチャネル / 膵島 / 活性酸素 |
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| Outline of Final Research Achievements |
Hyperinsulinemia often observed in the early type 2 diabetes mellitus has been shown to be associated with a higher risk of Alzheimer's disease and colorectal cancer. The present study focuses on characteristics of islet beta cells, which are susceptible to oxidative stress, and aims to clarify its pathophysiological significance.
The present study demonstrated that the redox-sensitive TRP channels activated by reactive oxygen species produced in cells in response to the glucose uptake may have a physiological role in fast-acting insulin secretion. On the other hand, it is suggested that electrophiles produced by sustained high blood glucose levels as well as hyperlipidemia induces persistent activation of the TRP channel, inducing pathological insulin secretion.
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| Free Research Field |
毒性学
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