| Project/Area Number |
21790286
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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 |
General medical chemistry
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| Research Institution | Kumamoto University |
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Principal Investigator |
YANO Masato Kumamoto University, 大学院・生命科学研究部, 助教 (60315299)
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| Project Period (FY) |
2009 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
|
| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2010: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2009: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | スフィンゴ脂質 / セラミド / インスリン / 酸化ストレス / ミトコンドリア / 活性酸素種 / スフィンゴミエリン / 膵β細胞 / 電子伝達系 / スフィゴミエリン |
|---|
| Research Abstract |
Sphingomyelin synthase 1 (SMS1) catalyzes the conversion of ceramide to sphingomyelin, and has a central role in controlling sphingolipid homeostasis in the cell. In this study, we analyzed the pathogenesis of SMS1 null mice, which exhibit insulin secretion deficiency. As results, we found that disturbance of sphingolipid homeostasis and increased oxidative stress accompanied with mitochondrial dysfunction underlies insulin secretion deficiency observed in pancreatic beta-cells of SMS1 null mice. Furthermore, anti-oxidant treatment recovered insulin secretion deficiency in SMS1 null mice.
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