Musclin inhibits insulin activation of Akt/protein kinase B in rat skeletal muscle

被引:54
作者
Liu, Y. [1 ]
Huo, X. [2 ]
Pang, X. F. [3 ]
Zong, Z. H. [4 ]
Meng, X. [1 ]
Liu, G. L. [1 ]
机构
[1] China Med Univ, Dept Endocrinol, Hosp 1, Shenyang 110001, Liaoning, Peoples R China
[2] China Med Univ, Dept Gen Surg 3, Hosp 1, Shenyang 110001, Liaoning, Peoples R China
[3] China Med Univ, Dept Cardiol, Hosp 1, Shenyang 110001, Liaoning, Peoples R China
[4] China Med Univ, Dept Biochem & Mol Biol, Shenyang 110001, Liaoning, Peoples R China
关键词
rosiglitazone; thiazolidinedione; diabetes mellitus; rats; musclin; insulin resistance; PPAR gamma; LXR alpha; PI3K; AkT/PKB;
D O I
10.1177/147323000803600314
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 [基础医学];
摘要
Musclin is a muscle-derived secretory peptide that induces insulin resistance in vitro. We studied the effect of musclin (0.5 mu g/ml) on insulin-stimulated glucose uptake in rat skeletal muscles and also the effect of rosiglitazone (0.4 mu g/ml). Preincubation of muscles with musclin resulted in decreased insulin-stimulated glucose uptake. Musclin also reduced expression of peroxisome proliferator-activated receptor gamma (PPAR gamma) and liver X receptor a (LXR alpha) mRNAs, although expression of glucose transporter 4 mRNA was unaltered. Rosiglitazone attenuated the effects of musclin on glucose uptake and PPAR gamma and LXR alpha mRNA expression. Western blotting demonstrated that activation of protein kinase B (Akt/PKB) in the insulin-signalling cascade was decreased by musclin but corrected by rosiglitazone. These findings suggest that musclin-induced impairment of insulin-stimulated glucose uptake in skeletal muscle is related to Akt/PKB inhibition and might be modulated by PPAR gamma/ LXR alpha.
引用
收藏
页码:496 / 504
页数:9
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