| Project/Area Number |
26500021
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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 |
Integrated Nutrition Science
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| Research Institution | Kobe Women's University |
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Principal Investigator |
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| Research Collaborator |
NISHIDA Hikaru 神戸女子大学, 大学院・家政学研究科, 院生
YAMAMOTO Yu 神戸女子大学, 大学院・家政学研究科, 院生
WAKE Ikumi 神戸女子大学, 大学院・家政学研究科, 院生
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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: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2014: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 分岐鎖アミノ酸 / 骨格筋 / 成長ホルモン / mTOR / 筋委縮 / IGF-I / 筋萎縮 / グルココルチコイド / LAT1 |
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| Outline of Final Research Achievements |
Branched-chain amino acid (BCAA) prevents muscle atrophy. mTOR complex 1 (mTORC1) plays a pivotal role in the protective actions of BCAA. GH is also known to have a protective effect against muscle atrophy. We examined whether BCAA exerts a protective effect against dexamethasone (Dex)-induced muscle atrophy independently of GH using GH-deficient spontaneous dwarf rats (SDRs). BCAA did not increase cross-sectional area (CSA) of the muscle fibers and did not stimulate the phosphorylation of p70S6K and 4E-BP1, both of which are phosphorylated by mTORC1 and stimulate protein synthesis. In contrast, after GH supplementation, muscle fiber CSA was decreased by Dex and BCAA prevented the Dex-induced decrease in CSA. BCAA increased p70S6K phosphorylation. These findings suggest that GH increases mTORC1 activity to recover the action of BCAA in SDRs and that GH is required for the actions of BCAA in muscles.
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