| Project/Area Number |
23790819
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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 |
Gastroenterology
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| Research Institution | Kyoto Pharmaceutical University |
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Principal Investigator |
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| Project Period (FY) |
2011 – 2012
|
| Project Status |
Completed (Fiscal Year 2012)
|
| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2012: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
Fiscal Year 2011: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | レチノイン酸 / タミバロテン / インスリン抵抗性 / レプチン / STAT3 / 肝臓 / NAFLD / NASH / アンチセンスRNA |
|---|
| Research Abstract |
Based on our original finding, the leptin-dependent hepatic insulinsensitization by retinoid, I investigated its precise mechanisms. It was demonstrated thatretinoid activates hepatic leptin signaling by directly inducing leptin receptor expressionvia retinoid receptor. A synthetic rtinoid, tamibarotene, also showed the same effect,suggesting its potential as a novel insulin-resistance treatment. Moreover, AntiX wasidentified as a target gene of hepatic leptin signaling, and the expression level of AntiX inthe liver was significantly correlated with the pathological status of insulin resistance.
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