The mechanisms of Notch2 for insulin resistance in skeletal muscle and its association with exercise and diet
| Project/Area Number |
25882024
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Single-year Grants |
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| Research Field |
Applied health science
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| Research Institution | Nagasaki University |
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Principal Investigator |
MASUDA Shinya 長崎大学, 原爆後障害医療研究所, 産学官連携研究員 (80638403)
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| Project Period (FY) |
2013-08-30 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
Fiscal Year 2014: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | Notch / 筋萎縮 / Notch2 / 骨格筋 / インスリン抵抗性 / Notchシグナル |
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| Outline of Final Research Achievements |
To elucidate functional roles of Notch2 signaling in fully-differentiated myofibers, we generated transgenic mice overexpressing intracellular domain of Notch2 specifically in myofibers (N2ICD-Tg mice). Glucose tolerance test revealed that N2ICD-Tg mice tended to show higher blood glucose level compared to control mice. N2ICD-Tg mice exhibited muscle atrophy in fast-type muscle. We examined the expression of Notch1-4 genes in myofibers isolated from whole muscle tissues, and found that only Notch2 gene was expressed in myofibers. Notch2 gene was also expressed in the isolated myofibers in which satellite cells were depleted, indicating that the detected Notch2 genes derived from differentiated myofibers instead of satellite cells. Constitutively activated Notch2 signaling induced skeletal muscle atrophy, which could be concerned with less glucose tolerance.
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Report
(3 results)
Research Products
(6 results)
