2012 Fiscal Year Final Research Report
Involvement of TRPM2 in insulin secretion and diabetes pathogenesis
| Project/Area Number |
23790267
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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 | 大学共同利用機関法人自然科学研究機構(岡崎共通研究施設) (2012)
National Institutes of Natural Sciences Okazaki Research Facilities (2011) |
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Principal Investigator |
UCHIDA Kunitoshi 大学共同利用機関法人自然科学研究機構(岡崎共通研究施設), 岡崎統合バイオサイエンスセンター, 助教 (20581135)
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| Project Period (FY) |
2011 – 2012
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| Keywords | 分子 / 細胞生理学 |
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| Research Abstract |
Insulin secretion from pancreatic b-cells is the only efficient means to decrease blood glucose concentrations. Many electrophysiological studies have shown that not only ATP-sensitive K+ and voltage-gated Ca2+ channels, but also many other ion channels are involved in insulin secretion. We previously revealed that TRPM2 is expressed in pancreatic β-cells and could be involved in insulin secretion. To clarify whether TRPM2 could be a target for the diabetes therapy, we analyzed the wild-type (WT) and TRPM2-KO mice fed a high fat diet. WT mice fed a high fat diet exhibited high blood glucose levels, despite high plasma insulin levels. That is because insulin resistance developed in WT mice. On the other hand, TRPM2-KO mice fed a high fat diet did not exhibit drastic changes in blood glucose levels and plasma insulin levels compared with TRPM2-KO mice fed a normal diet. In addition, insulin resistance did not develop in TRPM2-KO mice. In WT mice fed a high fat diet, TRPM2 mRNA expression levels in islets, liver and white adipose tissue were higher than those in WT mice fed a normal diet. These results suggest that TRPM2 could be involved in diabetes pathogenesis.
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Research Products
(4 results)
