Effect of angiotensin II receptor blocker on insulin signaling in skeletal muscle cells

Impairment of insulin-dependent glucose uptake in skeletal muscles plays a major role in the pathogenesis of diabetes mellitus. Angiotensin converting-enzyme inhibitor (ACEI) has been demonstrated to improve insulin-sensitivity in diabetic patients, partly through the increase in peripheral blood flow mediated by either suppressed angiotensin II or elevated bradykinin. Recently, angiotensin II type-1 receptor blocker (ARB) has been shown to produce similar effects, postulating the importance of intracellular signaling cross-talk between angiotensin II and insulin. In this brief review, we focused on insulin receptor substrate-1(IRS-1) in skeletal muscle cells, and the significance of its serine(612)-phosphorylation was discussed.