Mechanism of androgen production in skeletal muscle and muscle atrophy suppression
| Project/Area Number |
24680070
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| Research Category |
Grant-in-Aid for Young Scientists (A)
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| Allocation Type | Partial Multi-year Fund |
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| Research Field |
Sports science
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| Research Institution | Senshu University |
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Principal Investigator |
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥27,430,000 (Direct Cost: ¥21,100,000、Indirect Cost: ¥6,330,000)
Fiscal Year 2014: ¥6,110,000 (Direct Cost: ¥4,700,000、Indirect Cost: ¥1,410,000)
Fiscal Year 2013: ¥6,890,000 (Direct Cost: ¥5,300,000、Indirect Cost: ¥1,590,000)
Fiscal Year 2012: ¥14,430,000 (Direct Cost: ¥11,100,000、Indirect Cost: ¥3,330,000)
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| Keywords | アンドロゲン / サルコペニア / 骨格筋 / 自己分泌 / 身体運動 |
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| Outline of Final Research Achievements |
It is believed that dihydrotestosterone (DHT) is the most powerful androgen converted by testosterone through 5α-reductase (srd5a1). However, it remains to be elucidated whether muscular DHT production through srd5a1 is locally involved in skeletal muscular plasticity. Here we found that local DHT production in skeletal muscle induced muscular hypertrophy with acceleration of the protein synthesis and inhibited muscular atrophy through the suppression of atrophy-related gene expression. Transcriptional regulation of srd5a1 is controlled by early growth response2 (egr2). These observations indicate that bioactive androgen production through srd5a1 locally play an important role in skeletal muscle metabolism.
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Report
(4 results)
Research Products
(21 results)
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[Journal Article] Mucosal immune function comparison between amenorrheic and eumenorrheic distance runners2012
Author(s)
Kazuhiro Shimizu, Natsumi Suzuki, Mariko Nakamura, Katsuji Aizawa, Tomoko Imai, Satomi Suzuki, Nobuhiko Eda, Yukichi Hanaoka, Kikuko Nakao, Naoto Suzuki, Noboru Mesaki, Ichiro Kono, Takao Akama.
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Journal Title
Journal of Strength and Conditioning Research
Volume: 26巻
Pages: 1402-1406
Related Report
Peer Reviewed
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