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This Article Accepted manuscript (PDF) All Versions of this Article: JOE-08-0104v1 198/3/561    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Shang, W. Articles by Chen, M. Search for Related Content PubMed PubMed Citation Articles by Shang, W. Articles by Chen, M.

W Shang, Shanghai Institute of Endocrine and Metabolic Diseases, School of Medicine, Shanghai Jiaotong University,, Shanghai, China
Y Yang, Shanghai Institute of Endocrine and Metabolic Diseases, School of Medicine, Shanghai Jiaotong University,, Shanghai, China
L Zhou, Shanghai Institute of Endocrine and Metabolic Diseases, School of Medicine, Shanghai Jiaotong University,, Shanghai, China
B Jiang, Shanghai Institute of Endocrine and Metabolic Diseases, School of Medicine, Shanghai Jiaotong University,, Shanghai, China
H Jin, Shanghai Institute of Endocrine and Metabolic Diseases, School of Medicine, Shanghai Jiaotong University,, Shanghai, China
M Chen, Shanghai Institute of Endocrine and Metabolic Diseases, School of Medicine, Shanghai Jiaotong University, Shanghai, 200025, China

Correspondence: Mingdao Chen, Email: benhinshang{at}yahoo.com

Abstract

A series of clinical trials and animal experiments have demonstrated that ginseng and its major active constituent, ginsenosides, possess glucose lowering action. In our previous study, ginsenoside Rb1 has been shown to regulate PPAR activity to facilitate adipogenesis of 3T3-L1 cells. However, the effect of Rb1 on glucose transport in insulin-sensitive cells and its molecular mechanism need further elucidation. In this study, Rb1 significantly stimulated basal and insulin-mediated glucose uptake in a time- and dose-dependent manner in 3T3-L1 adipocytes and C2C12 myotubes, the maximal effect was achieved at a concentration of 1 µM and a time of 3h. In adipocytes, Rb1 promoted GLUT1 and GLUT4 translocation to the cell surface which was examined by analyzing their distribution in subcellular membrane fractions, and enhanced translocation of GLUT4 was confirmed using the transfection of GLUT4-eGFP in CHO cells. Meanwhile, Rb1 increased the phosphorylation of IRS-1 and AKT, and stimulated PI3K activity in the absence of the activation of the insulin receptor. Rb1-induced glucose uptake as well as GLUT1 and GLUT4 translocation was inhibited by the PI3K inhibitor. These results suggest that ginsenoside Rb1 stimulates glucose transport in insulin-sensitive cells by promoting translocations of GLUT1 and GLUT4 by partially activating insulin signaling pathway. These findings are useful in understanding the hypoglycemic and anti-diabetic properties of ginseng and ginsenosides.