The Relationship Between eNOS (G894T ) Gene Polymorphism and Arterial Stiffness in Patients with Metabolic Syndrome

Abstract

Metabolic syndrome (MS) is a clustering entity characterized by obesity, hypertension, hyperglycemia, dyslipidemia, and insulin resistance. Atherosclerotic lesions may be a complication of MS, arising from endothelial dysfunction and induced by decreased nitric oxide (NO) production. NO is synthesized by nitric oxide synthase (eNOS), encoded by the NOS3 gene, and displays anti-inflammatory, vasodilatory, and antiproliferative effects.We aimed to investigate the relationship between the G894T polymorphism of the eNOS gene and metabolic syndrome (including its components) and the association of this polymorphism with arterial function, assessed by determining pulse wave velocity and the augmentation index.The study included 100 consecutive patients, 55% with metabolic syndrome (based on IDF criteria -study group), 45% without MS (control group). Arterial stiffness was measured using TensioMedTMArteriograph. The presence of the homozygous (TT) or heterozygous (GT) state was associated, compared to subjects without the mutation (GG), with an increased prevalence of arterial hypertension, diabetes mellitus, with an increase of abdominal circumference, an increase of triglycerides, without significantly influencing the level of HDL. No significant differences were found between patients with G894T polymorphism compared to those without the mutation regarding the arterial stiffness. The eNOS gene polymorphism: 894G]T was significantly associated with the presence of MS; the polymorphism in homozygous and heterozygous state was associated with an increased risk of metabolic syndrome. G894T polymorphism did not significantly influence the values of the studied arterial parameters (pulse wave velocity, aortic and brachial augmentation index).