| Project/Area Number |
24700705
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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 |
Sports science
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| Research Institution | Juntendo University |
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Principal Investigator |
ZHENG DONGMEI 順天堂大学, 医学(系)研究科(研究院), 非常勤助教 (10420829)
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2013: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2012: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | Autophagy / Endurance exercise / LC3 / muscle / mTOR / treadmill / autophagy / endurance exercise / オートファジー / 運動 / 筋肉 / S6 |
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| Research Abstract |
Starvation-induced decrease in insulin and serum amino acids effectively suppresses the mammalian target of rapamycin (mTor) signaling to induce autophagy, a cellular major degradative pathway, in skeletal muscles (soleus, plantaris, and gastrocnemius). I investigated effect of treadmill running exercise on mTor signaling of skeletal muscles of starved mice. I found that mTor signaling pathway once inactivated under starvation conditions was reactivated after treadmill running exercise (12 m/min, 2 h) as revealed by the transition of phosphorylation state of S6-kinase and ribosomal S6. In accordance with this, autophagosomes induced in the skeletal muscles of starved GFP-transgenic mice were markedly suppressed after exercise. Treadmill running exercise caused changes in the expression of glycogenin, galectin-1, etc. However, these changes do not seem to connect to the mechanism of exercise-induced mTor reactivation.
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