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.
|Number of pages||4|
|Journal||Nippon rinsho. Japanese journal of clinical medicine|
|Publication status||Published - Oct 2002|
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