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. Cyclosporin A is a powerful immunosuppressive drug but its therapeutic use is limited by a number of untoward effects, among them hyperglycemia. Blocking of calcineurin phosphatase activity leading to an inhibition of stimulated insulin gene transcription is likely to contribute to the diabetogenic action of cyclosporin A. Previous results indicated that the dual leucine zipper bearing kinase is a calcineurin-sensitive kinase. In the present study the effect of cyclosporin A and of DLK on beta-cell survival was investigated.
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