| Project/Area Number |
23791050
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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 |
Endocrinology
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| Research Institution | The University of Tokyo |
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Principal Investigator |
SHIMIZU Noriaki 東京大学, 医科学研究所, 特任研究員 (30396890)
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| Research Collaborator |
MARUYAMA Takako 東京大学, 医科学研究所・学術支援専門, 職員
KURIBARA Akiko 東京大学, 医科学研究所, 臨床検査技師
ITO Naoki 東京工業大学, 大学院・生命理工学研究科, 大学院生
MATSUHASHI Tomohiro 慶應義塾大学, 大学院・医学研究科, 大学院生
MA Yanxia 東京大学, 大学院・医学系研究科, 大学院生
MATSUMIYA Ryo 東京大学, 医科学研究所, 後期研修医
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| Project Period (FY) |
2011 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2012: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2011: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | ミオパチー / 筋萎縮 / ロコモティブシンドローム / ステロイド副作用 / 栄養 |
|---|
| Research Abstract |
We showed that glucocorticoid receptor (GR) regulates expression of diverse genes in skeletal muscle through inducing the expression of multiple transcription factors. The target genes bring about both enhancement of catabolism and suppression of anabolism, causing skeletal muscle atrophy. Using animal models, we also showed that oral administration of branched-chain amino acids at a dose above physiological level suppressed transcriptional activation of the target genes via reducing the recruitment of GR onto promoters of the target genes and prevented development of skeletal muscle atrophy caused by a pharmacological dose of glucocorticoids.
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