| Project/Area Number |
25860750
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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 |
Metabolomics
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| Research Institution | Kobe University |
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Principal Investigator |
TATEYA Sanshiro 神戸大学, 医学(系)研究科(研究院), 研究員 (70639260)
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| Co-Investigator(Renkei-kenkyūsha) |
TAMORI Yoshikazu 神戸大学, 大学院医学研究科, 客員教授 (90379397)
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
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| Keywords | インスリン抵抗性 / 慢性炎症 / 一酸化窒素 / VASP |
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| Outline of Final Research Achievements |
Entire mechanisms during the development of diabetes and obesity have not revealed yet. Endothelial function has been impaired at the beginning of diabetes, however, whether or not, this impairment causes or worsens diabetes is still unknown. We found that endothelial-derived nitric oxide (NO) is indispensable for the intact insulin signaling in the neighboring cells such as hepatocytes or adipocytes. NO/cGMP/PKG/VASP signaling contributes to the suppression of obesity-induced inflammation and insulin resistance. This findings, we believe, could be a promising target for the treatment of diabetes.
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