Key result
The T/C or C/C genotype of the eNOS T-786C polymorphism was associated with lower flow-mediated arterial dilation compared to the T/T genotype (3.73% vs 4.15%, P=0.000).
Why the study?
Is the T-786C polymorphism of the eNOS gene associated with reduced endothelium-dependent arterial dilation in Type 2 diabetic men?
Cross-Sectional (n=162)
Is the T-786C polymorphism of the eNOS gene associated with reduced endothelium-dependent arterial dilation in Type 2 diabetic men?
Absolute Event Rate: 3.73% vs 4.15%
p-value: p=0.000
The C allele of the T-786C polymorphism in the eNOS gene is associated with reduced endothelium-dependent arterial dilation in Type 2 diabetic men, particularly among smokers.
Supports hypothesis of genetic influence on endothelial dysfunction in T2DM; leaves open whether genotyping aids risk stratification or management.
OBJECTIVE: Several studies have shown that the T-786C polymorphism in 5'-flanking region of the endothelial nitric oxide synthase (eNOS) gene is associated with coronary artery disease in non-diabetic population. In the present study, we attempted to assess whether the T-786C polymorphism of eNOS gene is associated with endothelial dysfunction Type 2 diabetes. RESEARCH DESIGN AND METHODS: A total of 162 Type 2 diabetic men were studied. PCR/allele-specific probes were used to analyse the T-786C polymorphism of eNOS gene, and high resolution ultrasound was used to measure brachial artery diameter at rest, after reactive hyperaemia and after sublingual glyceryltrinitrate. RESULTS: The flow-mediated arterial dilation among subjects with T/C or C/C was 3.73+/-0.50%, which was significantly lower than that in subjects with T/T (4.15+/-0.49%) (P=0.000). On multiple linear regression analysis, the presence of C allele, mean blood pressure, low-density lipoprotein (LDL) and serum lipoprotein (a) [Lp(a)] were independent determinants for reduced endothelium-dependent arterial dilation (R2=0.175, P=0.0021). The flow-mediated arterial dilation in smokers with T/C or C/C was significantly lower than that in smokers with T/T (P<0.001), but not in non-smokers. In addition, the presence of C allele, LDL and Lp(a) were independent determinants for reduced endothelium-dependent arterial dilation (R2=0.258, P=0.0017) in smokers, but not in non-smokers. CONCLUSION: The C allele of T-786C polymorphism of eNOS gene is a genetic risk factor for endothelial dysfunction in Type 2 diabetic patients, especially among smokers.
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Xiang Guang-da (2005) conducted a cross-sectional in Type 2 diabetes (n=162). T/C or C/C genotype of the eNOS T-786C polymorphism vs. T/T genotype was evaluated on flow-mediated arterial dilation (p=0.000). The T/C or C/C genotype of the eNOS T-786C polymorphism was associated with lower flow-mediated arterial dilation compared to the T/T genotype (3.73% vs 4.15%, P=0.000).
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