| Project/Area Number |
26350639
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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 |
Rehabilitation science/Welfare engineering
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| Research Institution | Nihon Fukushi University |
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Principal Investigator |
IWATA Masahiro 日本福祉大学, 健康科学部, 准教授 (60448264)
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| Co-Investigator(Kenkyū-buntansha) |
坂野 裕洋 日本福祉大学, 健康科学部, 准教授 (00351205)
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| Co-Investigator(Renkei-kenkyūsha) |
AKIMOTO Takayuki 早稲田大学, スポーツ科学学術院, 教授 (00351205)
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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 |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2016: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2014: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 悪液質 / カヘキシー / 骨格筋 / 萎縮 / 代謝 / メカニカルストレス / 温熱刺激 / ストレッチ |
|---|
| Outline of Final Research Achievements |
In this study, we examined the effects of mechanical stress and heat stress on skeletal muscle dysfunction derived from cachexia. As a result, it was suggested that 1) mechanical stress may induce muscle hypertrophy through promotion of protein synthesis pathway by activation of integrin β1/β3 and mTOR, 2) heat stress may suppress muscle atrophy derived from cachexia through inhibition of protein degradation pathway by inactivation of p38MAPK and FoxO1/3a, and 3) mechanical stress may improve insulin resistance through inactivation of p38MAPK and JNK and activation of AS160/TBC1D1.
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