Abstract

Objectives: Besides peripheral insulin resistance the decrease in beta-cell mass has been shown to play a crucial role in the pathogenesis of diabetes type 2. Although Cyclosporine A is a powerful immunosuppressive drug its therapeutic use is limited by a number of untoward effects, among them hyperglycemia. Inhibition of stimulated insulin gene transcription leading to beta-cell dysfunction by cyclosporine is likely to contribute to the drug's diabetogenic effect (1, 2). In addition, other mechanisms might exist. In the present study the effect of cyclosporine on beta-cell survival was investigated.

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