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TC10 Is Required for Insulin-Stimulated Glucose Uptake in Adipocytes

Department of Internal Medicine and Physiology (A.R.S.) and Life Sciences Institute (L.C., S.-H.C., A.R.S.), University of Michigan Medical Center, Ann Arbor, Michigan 48109

Address all correspondence and requests for reprints to: Alan R. Saltiel, Life Sciences Institute, University of Michigan, 210 Washtenaw Avenue, Ann Arbor, Michigan 48109-2216. E-mail: saltiel{at}umich.edu.

Previous studies have suggested that activation of the Rho family member GTPase TC10 is necessary but not sufficient for the stimulation of glucose transport by insulin. We show here that endogenous TC10 is rapidly activated in response to insulin in 3T3L1 adipocytes in a phosphatidylinositol 3-kinase-independent manner, whereas platelet-derived growth factor was without effect. Knockdown of TC10 but not TC10ß by RNA interference inhibited insulin-stimulated glucose uptake as well as the translocation of the insulin-sensitive glucose transporter GLUT4 from intracellular sites to the plasma membrane. In contrast, loss of TC10 had no effect on the stimulation of Akt by insulin. Additionally, knockdown of TC10 inhibited insulin-stimulated translocation of its effector CIP4. These data indicate that TC10 is specifically required for insulin-stimulated glucose uptake in adipocytes.

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