An update on the potential role of advanced glycation end products in glycolipid metabolism.

Advanced glycation end products (AGEs) play a crucial role in many major diseases, such as diabetes and atherosclerosis. AGE accumulation in the body is generally considered a consequence of hyperglycaemia. However, recent studies have shown that AGEs may also be an important cause of the initial pathogenesis of diabetes and atherosclerosis. The objective of the present review is to provide an update on the AGE-induced mechanisms involved in the pathophysiology of glucose and lipid metabolism, even though the unique mechanisms involved in these diseases are not well understood. AGE precursors (methylglyoxal) and AGE receptors have been demonstrated in animal models to mediate insulin resistance and lipid metabolism disorders. Although we have not yet achieved a complete understanding of the role of AGEs, emerging therapeutic interventions targeting AGE reduction and AGE-RAGE signalling have yielded some beneficial clinical outcomes. Additional studies are needed to evaluate the utility and mechanism of circulating and tissue AGEs to support the identification of efficient and specific interventions.