Advanced Glycation Endproducts (AGEs) are a group of heterogeneous compounds formed by the non enzymatic reactions between aldehydic group of reducing sugars with proteins, lipids or nucleic acids. Formation and accumulation of AGEs are related with the aging process and are accelerated in diabetes. Type 2 diabetes are the most common form of diabetes, which are characterized by hyperglycemia and insulin resistance associated to a progressive deterioration of beta cell function and mass. The pathogenic role of AGEs in vascular diabetic complications is widely recognised. Recently, other aspects of the detrimental effects of AGEs in type 2 diabetes have emerged: AGEs interfere with the complex molecular pathway of insulin signalling, leading to insulin resistance; AGEs modify the insulin molecule, and consequently, its function; AGEs decrease insulin secretion and insulin content. In this article, we review the role of AGEs in type 2 diabetes, beyond their involvement in vascular complications.
Keywords: Diabetes, advanced glycation end products, pancreatic β-cells, insulin resistance, metabolic syndrome, hyperglycemia, glucose homeostasis, methylglyoxal, glycolaldehyde, AGE pentosidine, phosphorylation, musculoskeletal tissues
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