Insulin resistance and increased intimal medial thickness in glucose tolerant offspring of type 2 diabetic subjects carrying the D298D genotype of endothelial nitric oxide synthase.

摘要

Endothelial nitric oxide synthase (eNOS) deficiency was found to affect insulin sensitivity and vascular homeostasis in animal models. Blood flow regulation by endothelial NO was suggested to modulate glucose uptake in the skeletal muscle.Therefore, it is possible that also in human subjects defects in eNOS activation or levels could affect insulin sensitivity. The D298D eNOS variant reduces eNOS protein half-life under stress conditions and it has been associated to increased cardiovascular disease (CVD) risk. The aim of present study was to assess whether among healthy offspring of patients with type 2 diabetes mellitus (T2DM) carriers of the D298D genotype are characterized by insulin resistance and early signs of atherosclerosis.