engleski

The role of uric acid in the etiology of diabetes mellitus

Diabetes mellitus results from either absolute or relative insulin deficiency. Despite well-known differences in the pathogenesis of type 1 and type 2 diabetes, the central event in the development of diabetes is a final destruction of the insulin-producing pancreatic b-cells via autoimmune (type 1) or toxic-degenerative (type 2) mechanisms. Biogenetic hypothesis of the aetiology of diabetes, postulating a possible production of highly selective b-cytotoxins, alloxan and/or alloxan-like compounds from uric acid, became apparent as a plausible experimental model in searching for the unique b-specific mechanisms, particularly with respect to the recently recognised antioxidant action of urate and production of reactive oxidation and/or nitrosation products. The aim of this study was to reinvestigate the biogenetic hypothesis by evaluating the influence of urate and a range of its derived chemical models on the glucose-stimulated insulin release in vitro. The results of the study on isolated rat islets of Langerhans revealed a pronounced, so far unknown inhibitory effect of urate and its NO-adducts, on the glucose stimulated insulin release.

uric acid ; uricolysis ; reactive oxygen and nitrogen species ; insulin-release

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