| Project/Area Number |
20590854
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Circulatory organs internal medicine
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| Research Institution | Hokkaido University |
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Principal Investigator |
KINUGAWA Shintaro Hokkaido University, 大学院・医学研究科, 助教 (60399871)
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| Co-Investigator(Kenkyū-buntansha) |
TSUTSUI Hiroyuki 北海道大学, 大学院・医学研究科, 教授 (70264017)
FURUMOTO Tomoo 北海道大学, 大学院・医学研究科, 特任助教 (10399925)
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| Co-Investigator(Renkei-kenkyūsha) |
OKITA Koichi 北翔大学, 大学院・生涯学習研究科, 教授 (80382539)
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| Project Period (FY) |
2008 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2010: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2009: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2008: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | メタボリックシンドローム / 運動能力 / 酸化ストレス / ミトコンドリア機能 / 骨格筋 / 小動物用トレッドミル |
|---|
| Research Abstract |
The exercise capacity was impaired in metabolic syndrome mice, which was associated with mitochondrial dysfunction in the skeletal muscle. Furthermore, NAD (P) H oxidase-dependent oxidative stress in skeletal muscle played an important role in the impaired exercise capacity and mitochondrial dysfunction. The present study demonstrated that therapies designed to regulate oxidative stress and maintain mitochondrial function could be beneficial to improve the exercise capacity in metabolic syndrome.
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