Advanced glycosylation in diabetes mellitus. Occurrence of late complications.

M C Esteves, A M Gonçalves, J L Caldeira

Abstract


Chronic hyperglycaemia contributes to tissue and organ damage retina, kidney and nerves by promoting the formation of advanced glycosylation end products (AGE). The AGE accumulation both in intra and extracellular proteins plays an essential role in the pathogenesis of diabetic complications by production of cross links on extracellular matrix proteins, by interaction with specific cellular receptors and by modification of nucleic acids. Human studies are being conducted to examine the pharmacokinetics efficacy and toxicity of pharmacologic agents that inhibit the AGE formation--aminoguanidine and aminoguandine-like--in order to define its role in the prevention and treatment of retinopathy, nephrology, neuropathy and diabetic atherosclerosis.

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