Exp Clin Endocrinol Diabetes 2010; 118(9): 657-661
DOI: 10.1055/s-0030-1252069
Short Communication

© Georg Thieme Verlag KG Stuttgart · New York

Palmitate Induced Insulin Resistance by PKCtheta-Dependent Activation of mTOR/S6K Pathway in C2C12 Myotubes

X. Wang1 [*] , W. Yu2 [*] , A. Nawaz3 , F. Guan3 , S. Sun4 , C. Wang3
  • 1Department of Pathophysiology, Yunyang Medical College, Shiyan, China
  • 2Department of Physiology, Yangtze University School of Medicine, Jingzhou, China
  • 3Department of Pathophysiology, Wuhan University School of Medicine, Wuhan, China
  • 4Department of Breast and Thyroid Surgery, Wuhan University Renmin Hospital, Wuhan, China
Further Information

Publication History

received 11.11.2009 first decision 26.01.2010

accepted 24.03.2010

Publication Date:
28 April 2010 (online)


The underlying mechanism of palmitate-induced insulin resistance in skeletal muscle cells is obscure. In this study, we showed that palmitate inhibited the insulin signaling in C2C12 myotubes, accompanied with the enhanced phosphorylation of protein kinase C-theta (PKCΘ). The inhibitory effects of palmitate on the insulin signaling were diminished in PKCΘ- and mTOR (mammalian target of rapamycin)-deficient C2C12 myotubes, and C2C12 myotubes pre-treated with rapamycin. In addition, the phosphorylation of mTOR and p70 ribosomal S6 kinase (S6K) enhanced by palmitate was attenuated in PKCΘ-deficient C2C12 myotubes and in C2C12 myotubes treated with PKCΘ pseudosubstrate. Taken together, our results suggested that palmitate-induced insulin resistance in C2C12 myotubes is mediated by PKCΘ/mTOR/S6K pathway.


1 Equal contribution to paper


C. WangMD & PhD 

Department of Pathophysiology

Wuhan University School of Medicine

185 Donghu Road


430071 Hubei


Email: chwang0525@whu.edu.cn