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Vol. 17, Issue 5, 2322-2330, May 2006

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Protein Kinase C Mediates Insulin-induced Glucose Transport through Actin Remodeling in L6 Muscle Cells

Li-Zhong Liu ^* , Hai-Lu Zhao , Jin Zuo ^*, Stanley K.S. Ho , Juliana C.N. Chan , Yan Meng ^*, Fu-De Fang ^*, and Peter C.Y. Tong 

^* Department of Biochemistry, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences and Peking Union Medical College, 100005 Beijing, China; Department of Medicine and Therapeutics, Prince of Wales Hospital, Chinese University of Hong Kong, Shatin, N.T., Hong Kong, China

Submitted October 24, 2005; Revised January 23, 2006; Accepted March 1, 2006
Monitoring Editor: Carl-Henrik Heldin

Protein kinase C (PKC) has been implicated in insulin-induced glucose uptake in skeletal muscle cell, although the underlying mechanism remains unknown. In this study, we investigated the effect of PKC on actin remodeling and glucose transport in differentiated rat L6 muscle cells expressing myc-tagged glucose transporter 4 (GLUT4). On insulin stimulation, PKC translocated from low-density microsomes to plasma membrane accompanied by increase in GLUT4 translocation and glucose uptake. Z-scan confocal microscopy revealed a spatial colocalization of relocated PKC with the small GTPase Rac-1, actin, and GLUT4 after insulin stimulation. The insulin-mediated colocalization, PKC distribution, GLUT4 translocation, and glucose uptake were inhibited by wortmannin and cell-permeable PKC pseudosubstrate peptide. In stable transfected cells, overexpression of PKC caused an insulin-like effect on actin remodeling accompanied by a 2.1-fold increase in GLUT4 translocation and 1.7-fold increase in glucose uptake in the absence of insulin. The effects of PKC overexpression were abolished by cell-permeable PKC pseudosubstrate peptide, but not wortmannin. Transient transfection of constitutively active Rac-1 recruited PKC to new structures resembling actin remodeling, whereas dominant negative Rac-1 prevented the insulin-mediated PKC translocation. Together, these results suggest that PKC mediates insulin effect on glucose transport through actin remodeling in muscle cells.

Address correspondence to: Peter C.Y. Tong (ptong{at}cuhk.edu.hk), Fu-De Fang (fangfd{at}public3.bta.net.cn), or Yan Meng (ymengsmile{at}yahoo.com).

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