[Glycation and protein crosslinking in the diabetes and ageing pathogenesis]

Long exposition to hyperglycemia is associated with development of vascular diseases in diabetic patients. Many of these effects are mediated by non-enzymatic glycosylation (glycation) of proteins and formation of advanced glycation end-products (AGEs). This phenomenon is accelerated in conditions where glucose concentration is chronically high, as it happens in diabetes mellitus. AGE formation is associated with structure-function alterations of proteins such as collagen, and particularly in tissues where these products are accumulated. A number of studies have demonstrated that AGEs can act as mediators, not only for the development of chronic complications of diabetes, but also in those related to ageing, nephropathy, Alzheimer's disease and erectile dysfunction, among others. In this paper, information generated about formation and accumulation of AGEs, including its biological effects and their participation in the development of complications in diabetes mellitus and other process such as ageing is revised. In addition, therapeutic strategies and a new methodology to measure glycation products are also considered.