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http://dx.doi.org/10.5352/JLS.2013.23.9.1163

Fagopyritol, a Derivative of D-chiro-inositol, Induces GLUT4 Translocation via Actin Filament Remodeling in L6-GLUT4myc Skeletal Muscle Cells  

Nam, Hajin (Institute of Natural Medicine, Hallym University)
Hwang, In Koo (Department of Anatomy and Cell Biology, College of Veterinary Medicine, and Research Institute for Veterinary Science, Seoul National University)
Jung, Harry (Department of Medical Genetics, College of Medicine, Hallym University)
Kwon, Seung-Hae (Korea Basic Science Institute Chuncheon Center)
Park, Ok Kyu (Korea Basic Science Institute Chuncheon Center)
Suh, Jun Gyo (Institute of Natural Medicine, Hallym University)
Publication Information
Journal of Life Science / v.23, no.9, 2013 , pp. 1163-1169 More about this Journal
Abstract
Insulin induces glucose transporter 4 (GLUT4) translocation to the muscle cell surface. As fagopyritol has insulin-like effects, the effects of fagopyritol on GLUT4 translocation and filamentous (F) actin remodeling in L6-GLUT4myc skeletal muscle cells were investigated. Fagopyritol significantly increased plasma membrane GLUT4 levels compared with the basal control in L6-GLUT4myc myoblast cells. Phosphatidylinositol (PI) 3-kinase inhibitor (LY294002) treatment prevented GLUT4 translocation to the plasma membrane in the myoblasts. Fagopyritol treatment apparently stimulates F-actin remodeling in myoblasts. In addition, fagopyritol treatment induced GLUT4 translocation and F-actin remodeling in myotubes. Taken together, these results suggest that fagopyritol promotes GLUT4 translocation and F-actin remodeling by activating the PI 3-kinase-dependent signaling pathway.
Keywords
Fagopyritol; Glucose transporter 4 (GLUT4) translocation; Actin filament; D-chiro-inositol; L6-GLUT4myc myoblasts;
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