Abstract
Increased formation of advanced glycation endproducts (AGEs) constitutes a potential mechanism by which hyperglycaemia and its immediate biochemical sequelae induce micro- and macrovascular complications in diabetes. In type 1 diabetes, circulating levels of AGEs, including the major AGE Ne-(carboxymethyl)lysine (CML), have been shown to be increased and associated with the development of cardiovascular disease (CVD). In contrast, the exact role of circulating CML in type 2 diabetes (T2DM) remains unclear, because remarkably, so far no consistent data on levels of plasma CML have been described in individuals with vs. without T2DM.
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