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We investigated glucose uptake and the trans-location of Akt and caveolin-3 in response to insulin in H9c2 cardiomyoblasts exposed to an experimental insulin resistance condition of 100 nM insulin in a 25 mM glucose containing media for 24 h. The cels under the insulin resistance condition exhibited a decrease in insulin-sti-mulated 2-deoxy[3H]glucose uptake as compared to control cels grown in 5 mM glucose media. translocation to membranes, we observed a sig-nificant decrease in insulin-stimulated membrane asociation of phosphorylated Akt with a con-sequent increase of the cytosolic pol. Actin remodeling in response to insulin was also greatly retarded in the cells. When translocation of Akt and caveolin-3 to caveolae was examined, the insulin resistance condition attenuated locali-zation of Akt and caveolin-3 to caveolae from cytosol. As a result, insulin-stimulated Akt activa-tion in caveolae was significantly decreased. crease of glucose uptake into the cells is related to their reduced levels of caveolin-3, Akt and phosphorylated Akt in caveolae. We conclude that the insulin resistance condition induced the retardation of their translocation to caveolae and in turn caused an attenuation in insulin signaling, namely activation of Akt in caveolae for glucose uptake into H9c2 cardiomyoblasts.