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Issue 107 Item 11 Advanced Glycation End Products (AGEs) Causes Endothelial Dysf

Apr 23, 2002

Study investigated whether changes in endothelium-dependent vasodilation, a marker of endothelial function, were related to serum AGEs concentrations in patients with type 2 diabetes. Data from experimental studies have suggested that the increased formation of advanced glycation end products (AGEs) is one of the causes of endothelial dysfunction in diabetes.

For this study, 170 patients with type 2 diabetes and 83 healthy nondiabetic control subjects of similar age were recruited. Serum AGEs were assayed by competitive enzyme-linked immunosorbent assay. Endothelium-dependent and -independent vasodilation of the brachial artery was measured by high-resolution vascular ultrasound.

The results of the study showed that Serum AGEs were increased in diabetic patients compared with control subjects, and both endothelium-dependent and endothelium-independent vasodilation were impaired. On univariate analysis of all subjects, serum AGEs correlated with endothelium-dependent vasodilation; a weaker association was found with endothelium-independent vasodilation. On multiple regression analyses including age, sex, smoking status, and plasma lipids, only serum AGEs remained a significant independent determinant of endothelium-dependent vasodilation.

It was concluded that increased serum concentrations of AGEs in patients with type 2 diabetes is associated with endothelial dysfunction, independent of other cardiovascular risk factors. Because endothelial dysfunction contributes to the pathogenesis of both micro- and macroangiopathy in diabetes, it is important to determine whether treatment targeting AGEs will lead to an amelioration of endothelial dysfunction in patients with type 2 diabetes. Therapeutic agents for the treatment of AGE accumulation are currently being developed. Diabetes Care 25:1055-1059, 2002