Lack of association between endothelial nitric oxide synthase glu298Asp variation, visceral obesity and insulin related phenotypes in Turkish type 2 diabetic patients

Nitric oxide (NO) is an endothelium derived relaxing factor (EDRF) important in regulating heart-vessel physiology. The objective of this study was to investigate whether the eNOS gene Glu298Asp variation influenced the lipid parameters, visceral obesity, insulin related phenotypes and type 2 diabetes mellitus (T2DM) development, for the first time in a Turkish study group. We analyzed the the eNOS gene Glu298Asp genotype frequencies in 115 type 2 diabetic and 68 healthy control subjects. Serum lipids and insulin-related phenotypes were also analyzed. No significant difference for genotypic frequencies was observed for the Ban II (Eco241) restriction site in T2DM patients as compared to controls. eNOS Glu298Asp polymorphism was not found to affect visceral obesity and insulin related phenotypes. However, T2DM patients with Asp/Asp genotype were found to have lower hepatic insulin sensitivity (HIS) in comparison to Glu/Glu. In healthy controls, the insulin and HOMA levels were found to be lower in Glu/Asp genotype with respect to Glu/Glu genotype carriers (p>0.05). In T2DM patients, visceral obesity was observed in higher frequencies with Asp/Asp genotype, in comparison to Glu/Glu genotype. eNOS Glu298Asp polymorphism was not found to affect serum lipid levels in the T2DM group. However in the control group, lower serum apoB levels were observed in Asp/Asp genotype carriers in comparison to Glu/Glu genotype (p ≤ 0.05). The eNOS gene Glu298Asp polymorphism was not found to be associated with T2DM in the present study group. Although not significant, since the eNOS Glu298Asp genotypes were found to be related to HIS, insulin, HOMA and visceral obesity in the present study, further studies on larger samples are needed to explore the exact role of eNOS Glu298Asp polymorphism in insulin related phenotypes and visceral obesity