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

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.

Localization of Glucose Transporter 10 to Hair Cells’ Cuticular Plate in the Mouse Inner Ear

“…Additional studies are necessary to elucidate the exact regulation and effects of Glut10 on hair cell movement. Nevertheless, it has been shown that the remodeling of F-actin in myoblasts is influenced by Glut4 and that PI3K signaling is involved [ 26 ]. Aquaporins and Ca 2+ gradient could also be involved in the regulation of Glut5 [ 27 , 28 ].…”