Abstract

Diabetes mellitus is the most common metabolic disease, and has late complications that are due to chronic hyperglycaemia. Altered carbohydrate and lipid metabolism together with impaired detoxification of carbonyl substrates and impaired trapping of oxygen radicals are responsible for cell damage in diabetes. Variable functional capacity of detoxifying systems could contribute to differing susceptibility to the development of complications. Identification of genetic variants responsible for modulating relevant intermediate phenotypes in diabetics could help to define individual risk profiles and to modify therapeutic strategy accordingly.

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