| Project/Area Number |
26461336
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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 | Osaka University |
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Principal Investigator |
Kawamori Dan 大阪大学, 医学系研究科, 助教 (50622362)
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| Co-Investigator(Kenkyū-buntansha) |
松岡 孝昭 大阪大学, 医学系研究科, 准教授 (10379258)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2016: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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| Keywords | 糖尿病 / グルカゴン / エネルギー代謝 / 代謝異常 / シグナル伝達 / インスリンシグナル / ストレス応答 |
|---|
| Outline of Final Research Achievements |
At this moment, mechanisms for dysregulated glucagon secretion are still unclear. Here, we explored the etiology and underlying molecular mechanisms of glucagon dysregulation. Regular mice were fed by nutritionally modified diets for 16 weeks, and metabolic parameters were examined. The mice fed by highly protein-containing diet promptly exhibited glucose intolerance while smaller increase in body weight than regular diet-fed mice, together with significant elevation of plasma glucagon / insulin ratio suggesting its pathological impact. In vitro glucose load on glucagon-secreting cell-line InR1G induced hypersecretion of glucagon, and increase in oxidative stress and deterioration of insulin signaling were identified as underlying mechanisms. These data elucidate, at least partly, the previously unclear mechanism of abnormal glucagon secretion, providing insights into a potential novel approach to diabetes treatment, targeting glucagon.
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