| Project/Area Number |
21790858
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Metabolomics
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| Research Institution | Hirosaki University |
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Principal Investigator |
MIZUKAMI Hiroki Hirosaki University, 大学院・医学研究科, 講師 (00374819)
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| Project Period (FY) |
2009 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2010: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2009: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | スフィンゴ脂質 / β細胞 / 2型糖尿病 / G蛋白共益受容体 / S1P1 / ベータ細胞 / 1型糖尿病 / G蛋白共役受容体 / Gi / β細胞アポトーシス / 膵島移植 / β細胞増殖 / インスリン分泌 |
|---|
| Research Abstract |
To evaluate the function of sphingolipid signaling in pancreatic β cells, β cell specific S1P1 knocked out mouse was generated using Cre-Lox P system. βS1P1KO showed no apparent phenotype in vivo. Forskolin potentiated insulin secretion was promoted in isolated islet of βS1P1KO compared to control. In whole islet patch clump, forskolin stimulated hyper-oscillation of Ca^<2+> was observed inβS1P1KO islet even under 500nM S1P. In islet transplantation experiment, marginal number of βS1P1KO islets (100) successively lowered glucose level in STZ induced type 1 diabetic model mouse, but not of control islets. Collectively, inhibition of S1P1 signaling in β cells can lead to protection against β cell injury and lead to a new type of β cell therapy in diabetes.
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