Exercise induces autophagy in peripheral tissues and in the brain.
Exercise induces autophagy in peripheral tissues and in the brain.
复制标题
DOI：
10.4161/auto.21327
复制
发表时间：
2012-10
期刊：
影响因子：
13.3
通讯作者：
Levine B
中科院分区：
文献类型：
--
作者：
He C;Sumpter R Jr;Levine B
我们最近发现体育锻炼是体内自噬的一种新的诱因。运动引起多个参与代谢调节的器官的自噬，如肌肉、肝脏、胰腺和脂肪组织。为了研究运动诱导的自噬的生理作用，我们产生了bcl2(Thr69Ala，Ser70Ala和Ser84Ala)(BCL2 AAA)的敲入非磷酸化突变的小鼠，这些小鼠在运动和饥饿诱导的自噬中存在缺陷，但在基础自噬中没有缺陷。我们发现，BCL2 AAA小鼠不能像野生型小鼠那样在跑步机上跑步，也不会经历运动介导的骨骼肌葡萄糖摄取增加。与野生型小鼠不同，BCL2 AAA小鼠在8周的运动训练后未能逆转高脂饮食诱导的葡萄糖耐受，这可能是由于调节运动期间肌肉葡萄糖吸收和代谢的信号通路存在缺陷。综上所述，这些发现表明，自噬在调节运动诱导的代谢益处方面发挥了迄今未知的重要作用。在本附录中，我们展示了跑步机运动也能诱导成年小鼠大脑皮层的自噬。这一观察提出了一个有趣的问题，即自噬是否在一定程度上中介了运动在神经退化、成人神经发生和认知功能改善方面的有益效果。
We recently identified physical exercise as a newly defined inducer of autophagy in vivo. Exercise induced autophagy in multiple organs involved in metabolic regulation, such as muscle, liver, pancreas and adipose tissue. To study the physiological role of exercise-induced autophagy, we generated mice with a knock-in nonphosphorylatable mutation in BCL2 (Thr69Ala, Ser70Ala and Ser84Ala) (BCL2 AAA) that are defective in exercise- and starvation-induced autophagy but not in basal autophagy. We found that BCL2 AAA mice could not run on a treadmill as long as wild-type mice, and did not undergo exercise-mediated increases in skeletal glucose muscle uptake. Unlike wild-type mice, the BCL2 AAA mice failed to reverse high-fat diet-induced glucose intolerance after 8 weeks of exercise training, possibly due to defects in signaling pathways that regulate muscle glucose uptake and metabolism during exercise. Together, these findings suggested a hitherto unknown important role of autophagy in mediating exercise-induced metabolic benefits. In the present addendum, we show that treadmill exercise also induces autophagy in the cerebral cortex of adult mice. This observation raises the intriguing question of whether autophagy may in part mediate the beneficial effects of exercise in neurodegeneration, adult neurogenesis and improved cognitive function.
登录
查看更多内容
影响因子：
158.5
作者：
Knowler, WC;Barrett-Connor, E;Nathan, DM
通讯作者：
Nathan, DM
运动和PGC1alpha在炎症和慢性疾病中的作用。
影响因子：
64.8
作者：
Handschin, Christoph;Spiegelman, Bruce M.
通讯作者：
Spiegelman, Bruce M.
影响因子：
16
作者：
Kroemer G;Mariño G;Levine B
通讯作者：
Levine B
影响因子：
3.3
作者：
Mizushima, N;Yamamoto, A;Ohsumi, Y
通讯作者：
Ohsumi, Y
影响因子：
64.8
作者：
He, Congcong;Bassik, Michael C.;Moresi, Viviana;Sun, Kai;Wei, Yongjie;Zou, Zhongju;An, Zhenyi;Loh, Joy;Fisher, Jill;Sun, Qihua;Korsmeyer, Stanley;Packer, Milton;May, Herman I.;Hill, Joseph A.;Virgin, Herbert W.;Gilpin, Christopher;Xiao, Guanghua;Bassel-Duby, Rhonda;Scherer, Philipp E.;Levine, Beth
通讯作者：
Levine, Beth