Résumé
Type 2 diabetes mellitus results from an inadequate adaptation of the functional pancreatic beta cell mass in the face of insulin resistance. Apoptosis is programmed cell death or cell suicide, it is an energy-requiring process that involves de novo protein synthesis. Apoptotic mechanisms could explain insulin deficiency through a reduction in absolute beta cell mass. This study was conducted on 49 patients with type 2 diabetes mellitus from Internal Medicine Department, Kasr- El Aini hospital. They were classified into group A [10 patients] without micro vascular complications, group B [39 patients]with micro vascular complication [peripheral neuropathy, retinopathy and nephropathy] and 10 healthy persons served as control group[group C].All subjects were subjected to full Clinical assessment and routine laboratory investigations, 24 hours urinary albumin, ECG, fundus examination and quantitative assay of proapoptotic markers [Fas, FasL, and Bcl2 proteins] There was significant correlation behveen fasting blood glucose and Fas, FasL, and Bcl2 [P value = 0.01].The serum levels of proapoptotic markers were significantly higher in non complicated and complicated groups [A and B] as compared to control group [C] [p<0.05]. However their levels were significantly higher in complicated group than uncomplicated group [p<0.05]. In hyperglycemia in type 2 diabetes may induce apoptosis in beta cells and this indicated by elevated serum levels of proapoptotic markers [Fas, FasL, and Bcl2 proteins] and these proapoptotic markers increased with microvascular affection [neuropathy, retinopathy and nephropathy] which suggest the role of apoptosis in the pathogenesis of diabetic microvascular complications