期刊文献+

运动与AMPK/mTOR轴介导细胞自噬改善肌肉减少性肥胖的研究进展

Advances in Exercise and AMPK/mTOR Axis-mediated Cellular Autophagy to Improve Sarcopenic Obesity
下载PDF
导出
摘要 肌肉减少性肥胖(SO)是一种与衰老相关的肥胖型疾病,主要病症表现为骨骼肌质量、力量或功能下降,以及脂肪含量的上升.SO中的蛋白质与脂肪的合成分解失衡,体内细胞自噬水平下降或发生障碍是重要因素之一.运动作为重要的代谢调节手段,可通过腺苷酸活化蛋白激酶(AMPK)/哺乳动物雷帕霉素靶蛋白(mTOR)信号通路调控体内自噬水平,促进细胞自噬,起到重塑骨骼肌与调控内环境稳态,维持骨骼肌健康和增加脂肪消耗的作用,是改善和逆转SO的关键. Sarcopenic obesity(SO)is an obesity-related disease associated with aging,characterized by decreased skeletal muscle mass,strength or function,and increased fat content.The imbalance between synthesis and degradation of protein and fat and the decrease or disorder of autophagy in the body are important factors in SO.Exercise is an important metabolic regulator of autophagy in the body through the adenosine monophosphate-activated protein kinase(AMPK)/mammalian target of rapamycin(mTOR)signaling pathway.Promoting autophagy plays a role in remodeling skeletal muscle,regulating homeostasis,maintaining skeletal muscle health and increasing fat consumption and is key to countering and reversing SO.
作者 张军军 ZHANG Junjun(Department of Police Command and Tactics,Fujian Police Academy,Fuzhou,Fujian 350007)
出处 《绵阳师范学院学报》 2023年第8期133-140,共8页 Journal of Mianyang Teachers' College
关键词 肌肉减少性肥胖 AMPK MTOR 自噬 运动 sarcopenia obesity AMPK mTOR autophagy exercise
  • 相关文献

参考文献9

二级参考文献115

  • 1Giovanni Tarantino,Silvia Savastano,Annamaria Colao.Hepatic steatosis,low-grade chronic inflammation and hormone/growth factor/adipokine imbalance[J].World Journal of Gastroenterology,2010,16(38):4773-4783. 被引量:24
  • 2Mackenzie MG, Hamilton DL, Murray JT, et al. mVps34 is activated by an acute bout of resistance exercise. Biochem Soc Trans, 2007, 35 : 1314-1316.
  • 3Fujita S, Dreyer HC, Drummond MJ,et al. Nutrient signalling in the regulation of human muscle protein synthesis. J Physiol, 2007, 582:813 -823.
  • 4Wackerhage H, Ratkevicius A. Signal transduction pathways that regulate muscle growth. Essays Biochem, 2008, 44 : 99 -108.
  • 5Harris TE, Lawrence JC Jr. TOR signaling. Sci STKE, 2003, 212 : re15.
  • 6Bodine SC, Stitt TN, Gonzalez M, et al. Akt/mTOR pathway is a crucial regulator of skeletal muscle hypertrophy and can prevent muscle atrophy in vivo. Nat Cell Biol, 2001, 3 : 1014- 1019.
  • 7Reynolds TH 4th, Bodine SC, Lawrence JC, Jr. Control of Ser2448 phosphorylation in the mammalian target of rapamycin by insulin and skeletal muscle load. J Biol Chem, 2002, 277 : 17657- 17662.
  • 8Baar K, Esser K. Phosphorylation of p70 (S6k) correlates with increased skeletal muscle mass following resistance exercise. Am J Physiol, 1999, 276 :C120- 127.
  • 9Kubica N, Bolster DR, Farrell PA, et al. Resistance exercise increases muscle protein synthesis and translation of eukaryotic initiation factor 2Bepsilon mRNA in a mammalian target of rapamycin-dependent manner. J Biol Chem, 2005, 280 : 7570-7580.
  • 10Kubica N, Kimball SR, Jefferson LS, et al. Alterations in the expression of mRNAs and proteins that code for species relevant to eIF2B activity after an acute bout of resistance exercise. J Appl Physiol, 2004, 96 : 679 -687.

共引文献88

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部