Effects of Icariin on insulin resistance via the activation of AMPK pathway in C2C12 mouse muscle cells

被引:36
作者
Han, Yunkyung [1 ]
Jung, Hyo Won [1 ,2 ]
Park, Yong-Ki [1 ,2 ]
机构
[1] Dongguk Univ, Korean Med R&D Ctr, Gyeongju 780714, South Korea
[2] Dongguk Univ, Coll Korean Med, Dept Herbol, Gyeongju 780714, South Korea
关键词
Icariin; C2C12; cells; AMPK pathway; Insulin resistance; Skeletal muscle; Type; 2; diabetes; TYPE-2; DIABETES-MELLITUS; SKELETAL-MUSCLE; PROTEIN-KINASE; GLUCOSE-UPTAKE; METFORMIN; ADIPONECTIN; OBESITY; RATS; MICE;
D O I
10.1016/j.ejphar.2015.03.059
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Insulin resistance in skeletal muscle is a major risk factor for the development of type 2 diabetes (T2D). In this study, we investigated the effect of icariin on insulin resistance in C2C12 mouse skeletal muscle cells. C2C12 myoblasts were differentiated into myotubes for five days, then treated with icariin (50 and 100 LIM) or metformin (1 rnM) in the presence of 100 nM insulin for 24 h. Adiponectin production was measured in culture media by ELISA, and AMP-activated protein kinase (AMPK)/insulin signaling pathway activation was assessed by the westem blot analysis. Icariin significantly increased adiponectin production in C2C12 myotubes. Moreover, icariin markedly promoted the phosphorylation of AMPK and acetyl-CoA carboxylase (ACC). Icariin up-regulated the expression of phosphatidylinositol 3-kinase (PI3K) and the phosphorylation of insulin receptor substrate-1 (IRS-1) in C2C12 myotubes. These results suggest that icariin has therapeutic potential for the treatment of T2D via the regulation of insulin resistance in skeletal muscle. (C) 2015 Elsevier B.V. All rights reserved.
引用
收藏
页码:60 / 63
页数:4
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