| Project/Area Number |
15K09398
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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 |
Metabolomics
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| Research Institution | Chiba University (2017)
Saitama Medical University (2015-2016) |
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Principal Investigator |
Ono Hiraku 千葉大学, 大学院医学研究院, 講師 (10570616)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
Fiscal Year 2017: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2016: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2015: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
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| Keywords | Akt / 視床下部 / 摂食 / インスリン感受性 / インスリン / インスリン抵抗性 / 摂食調節 / インスリン情報伝達 / グルコースクランプ法 / 阻害薬 / 糖尿病 / PTEN |
|---|
| Outline of Final Research Achievements |
Insulin is known to function in the arcuate nucleus of the hypothalamus to suppress food intake as well as suppress hepatic glucose production indirectly, via PI 3-kinase pathway. The most important molecule downstream of PI 3-kinase is Akt, while its role in the hypothalamus is unclear. In this study we bidirectionally modified Akt activity specifically in the arcuate nucleus of rats and investigated effects on food intake and glucose metabolism.
Overexpression of constitutively-active Akt or dominant-negative Akt in the arcuate nucleus unexpectedly did not significantly change food intake or body weight. On the other hand, hypothalamic constitutive activation of Akt ameliorated high fat diet-induced hepatic insulin resistance, suggesting a divergence of pathway toward regulation of food intake and that toward glucose metabolism exist downstream of PI 3-kinase, only latter of which is what Akt is responsible.
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