Objective: Angiotensin II (ATII) can increase insulin resistance by interfering insulin signaling pathway at the various steps in insulin target tissues in individuals with hypertension, obesity, or type 2 DM. Interfering insulin signaling pathway at the various steps in insulin target tissues is thought to be the underlying mechanism of insulin resistance by ATII. Insulin should bind to insulin receptor to have biological actions. We have already observed ATII inhibited insulin binding to insulin receptor in bovine aortic endothelial cells. However, the effect of ATII on insulin binding in muscle is still unclear. In this study, we investigated the effect of ATII on the binding capacity between insulin and insulin receptors in L6 cells. Methods: To observe whether insulin binding was affected by ATII, we treated 10-7 M ATII for 10 minutes to L6 cells, with or without ATII receptor blocker (eprosartan, 0.02, 0.2, 2, 20 and 200 μM) for 30 minutes. We also investigated Akt phosphorylation (ser473) after ATII treatment. Results: ATII increased insulin binding capacity up to 15% in L6 cells. Pretreating with eprosartan dose dependently recovered decreased insulin binding capacity by ATII. AT II decreased Akt phosphorylation. Conclusion: The increase of insulin binding capacity by ATII might be due to compensate mechanism for inhibited insulin signaling by ATII. ATII increased insulin binding capacity but decreased Akt phosphorylation in L6 cells. Decreased insulin binding capacity by ATII was recovered after ATII receptor blocker treatment. ATII might effect insulin resistance by diversiform mechanisms depending on tissue types.