| Project/Area Number |
16K19540
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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 | Kyushu University |
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Principal Investigator |
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| Research Collaborator |
Nomura Masatoshi
Tatsushima Keita
Hasuzawa Nao
Ogata Masatoshi
Terada Eriko
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| Project Period (FY) |
2016-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2018: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2017: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | プリン作動性化学伝達 / 小胞型ヌクレオチドトランスポーター / 糖代謝 / ATP / VNUT / インスリン分泌 / インスリン抵抗性 / 糖 / 脂質 / 薬理学 |
|---|
| Outline of Final Research Achievements |
Vesicular Nucleotide Transporter(VNUT) is essential for vesicular storage of ATP and subsequent purinergic chemical transmission. The purpose of this research was to clarify the role and the molecular mechanism of purinergic chemical transmission in glucose metabolism. We revealed that VNUT regulates insulin sensitivity in the liver through the direct action on hepatocytes and indirect action on inflammatory cells. Furthermore, we found that the inhibitor of VNUT affects the pancreas and the liver and these effects lead to the improvement of insulin secretion and insulin sensitivity respectively. These results suggest that the inhibitor of VNUT could be a new therapeutic drug for diabetes mellitus.
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| Academic Significance and Societal Importance of the Research Achievements |
本研究においてVNUTを介したプリン作動性化学伝達が糖代謝において果たす役割とその分子メカニズムを解明することが出来た。プリン作動性化学伝達による糖代謝制御メカニズムの解明は待ち望まれている新たな糖尿病治療の開発へとつながることが期待され、VNUT阻害作用をもつクロドロン酸が細胞および個体レベルで糖代謝を改善することを本研究で明らかに出来たことは、今後の糖尿病治療の発展に貢献できると考えられた。
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