TC10α is required for insulin-stimulated glucose uptake in adipocytes

被引:62
作者
Chang, Louise
Chiang, Shian-Huey
Saltiel, Alan R.
机构
[1] Univ Michigan, Med Ctr, Dept Internal Med & Physiol, Ann Arbor, MI 48109 USA
[2] Univ Michigan, Med Ctr, Inst Life Sci, Ann Arbor, MI 48109 USA
关键词
D O I
10.1210/en.2006-1167
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
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 alpha 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 alpha but not TC10 beta 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 alpha had no effect on the stimulation of Akt by insulin. Additionally, knockdown of TC10 alpha inhibited insulin-stimulated translocation of its effector CIP4. These data indicate that TC10 alpha is specifically required for insulin-stimulated glucose uptake in adipocytes.
引用
收藏
页码:27 / 33
页数:7
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