Abstract
Insulin resistance is characterized by an impaired responsiveness to the action of insulin at its multiple target organs. The accumulation of advanced glycation endproducts (AGEs) has been demonstrated in clinical settings of insulin resistance such as in diabetes, hypertension, and obesity. In this review we have focused on advanced glycation as a modulator of insulin resistance. Structural and functional abnormalities of the insulin molecule by glycation and methylglyoxal may contribute to the pathogenesis of insulin resistance. In addition, it is likely that AGEs interfere in the complex molecular pathways of insulin signaling and as such in insulin resistance.
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