A prepared anti-MSTN polyclonal antibody reverses insulin resistance of diet-induced obese rats via regulation of PI3K/Akt/mTOR&FoxO1 signal pathways

被引:36
作者
Tang, Liang [1 ]
Liu, Chen-tao [2 ]
Wang, Xu-dan [1 ]
Luo, Kai [1 ]
Zhang, Di-di [1 ]
Chi, Ai-ping [1 ]
Zhang, Jing [1 ]
Sun, Li-jun [1 ,3 ]
机构
[1] Shaanxi Normal Univ, Inst Sports Biol, Xian 710062, Peoples R China
[2] Northwest Univ, Dept Phys Educ, Xian 710069, Peoples R China
[3] Shaanxi Normal Univ, Postdoctoral Res Stn Biol, Xian 710062, Peoples R China
关键词
Anti-myostatin polyclonal antibody; GLUT4; Insulin resistance; Myostatin; Obesity; Polyclonal antibody; PI3K/Akt/mTOR&FoxO1; Signal pathways; SKELETAL-MUSCLE MASS; MYOSTATIN; HYPERTROPHY;
D O I
10.1007/s10529-014-1617-z
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 [微生物学]; 090105 [作物生产系统与生态工程];
摘要
Suppression of myostatin (MSTN) is associated with skeletal muscle atrophy and insulin resistance. However, the mechanisms by which MSTN regulates insulin resistance are not well known. We have explored the signaling pathways through which MSTN regulates insulin resistance in diet-induced obese rats using a polyclonal antibody for MSTN. The anti-MSTN polyclonal antibody significantly improved insulin resistance and whole-body insulin sensitivity, decreased MSTN protein expression in muscle samples by 39 % in diet-induced obese rats. Furthermore, the anti-MSTN polyclonal antibody significantly enhanced PI3K activity (140 %), Akt phosphorylation (86 %), GLUT4 protein expression (23 %), the phosphorylation of mTOR (21 %), and inhibited the phosphorylation of FoxO1 (57 %), but did not affect the phosphorylation of GSK-3 beta. Thus, suppression of MSTN by the anti-MSTN polyclonal antibody reverses insulin resistance of diet-induced obesity via MSTN/PI3K/Akt/mTOR and MSTN/PI3K/Akt/FoxO1 signaling pathways.
引用
收藏
页码:2417 / 2423
页数:7
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