The ENOSGlu298Asp polymorphism was associated with hypercholesterolemia (odds ratio 0.658, 95%CI 0.460-0.940; p=0.025) and the ACE D/I variant was associated with hypertriglyceridemia (odds ratio 0.722, 95%CI 0.536-0.973; p=0.033).
Endothelium-derived nitric oxide facilitates skeletal muscle glucose uptake, and data from animal models indicate that endothelial nitric oxide synthase (eNOS) gene-null mice present with a phenotype of insulin resistance, hypertension, and hypertriglyceridemia, much like that observed in humans with metabolic syndrome.