Single bout of running exercise suppressed autophagy in the fasted state

禁食状态下单次跑步运动抑制自噬

• 批准号: 24700705
• 负责人: ZHENG DONGMEI
• 金额: $ 2.83万
• 依托单位: Juntendo University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Young Scientists (B)
• 财政年份: 2012
• 资助国家: 日本
• 起止时间: 2012-04-01 至 2014-03-31
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-24700705/
• 关键词: Autophagy; Endurance exercise; LC3; muscle; mTOR; treadmill; autophagy; endurance exercise; オートファジー; 運動; 筋肉; S6

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.

饥饿引起的胰岛素和血清氨基酸的减少有效抑制了雷帕霉素（mTor）信号的靶细胞诱导自噬，这是骨骼肌（比目鱼肌、跖肌和腓肠肌）的细胞主要降解途径。研究了跑步机运动对饥饿小鼠骨骼肌mTor信号的影响。我发现mTor信号通路在饥饿条件下失活，在跑步机运动（12 m/min, 2 h）后重新激活，这是S6激酶和核糖体S6磷酸化状态的转变所揭示的。由此可见，运动后饥饿gfp转基因小鼠骨骼肌诱导的自噬体明显受到抑制。跑步机运动引起糖原素、半乳糖凝集素-1等表达的变化。然而，这些变化似乎与运动诱导的mTor再激活的机制无关。

项目成果

Ferulic Acid Induces Mammalian Target of Rapamycin Inactivation in Cultured Mammalian Cells

• DOI: 10.1248/bpb.b12-00695
• 发表时间: 2013-01-01
• 期刊: BIOLOGICAL & PHARMACEUTICAL BULLETIN
• 影响因子: 2
• 作者: Bian, Zehua;Furuya, Norihiko;Ueno, Takashi
• 通讯作者: Ueno, Takashi

Autophagy is suppressed in soleus and plantaris muscles by endurance exercise.

耐力运动可抑制比目鱼肌和跖肌中的自噬。

• 发表时间: 2012
• 期刊: Spotology
• 作者: Zheng DM;Bian Z;Furuya N;Takeda-Ezaki M;Oliva Trejo JA;Takahashi K;Hiraoka Y;Fujimura T;Komatsu M;Kominami E;Ueno T;Ezaki J.
• 通讯作者: Ezaki J.

Interleukin-11 Links Oxidative Stress and Compensatory Proliferation

• DOI: 10.1126/scisignal.2002056
• 发表时间: 2012-01-17
• 期刊: SCIENCE SIGNALING
• 影响因子: 7.3
• 作者: Nishina, Takashi;Komazawa-Sakon, Sachiko;Nakano, Hiroyasu
• 通讯作者: Nakano, Hiroyasu