| Project/Area Number |
26750037
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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 |
Eating habits
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| Research Institution | Ochanomizu University |
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Principal Investigator |
Naka Ayano お茶の水女子大学, 生活科学部, 学部教育研究協力員 (00709181)
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| Project Period (FY) |
2014-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2014: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | イソフラボン / 骨格筋 / ミトコンドリア / 脂質代謝 / 転写因子 / 大豆イソフラボン / 遺伝子 / C2C12細胞 / ERRα / 脂質酸化 |
|---|
| Outline of Final Research Achievements |
This study aimed to examine whether soy isoflavone regulate mitochondrial biogenesis and fat oxidation in skeletal muscles. For this purpose, we used the C2C12 murine muscle cell line. When C2C12 myotubes were treated with 25-50 μM daidzein, there were significant increases in the expression of mitochondrial transcription factor A (Tfam) and its targets such as ATP5b, Cytochrome b and COX1. Daidzein also increased the expression of Mcad and Pdk4 that are involved in fatty acid oxidation. Using several mutant Tfam promoter fragments, we found that the transcription factor, nuclear respiratory factor (NRF) were necessary for the effect of daidzein on Tfam expression. In addition, study using a reporter assay based on the Pdk4 promoter suggested that transcription factor ERRα was involved in daidzein-induced enhancement of Pdk4. These results suggest that daidzein would be beneficial to protect against a wide range of diseases caused by muscle metabolic dysfunction.
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