Premium
A T −786 C polymorphism in 5′‐flanking region of the endothelial nitric oxide synthase gene and endothelium‐dependent arterial dilation in Type 2 diabetes
Author(s) -
Guangda X.,
Qiongshu W.,
Wen J.
Publication year - 2005
Publication title -
diabetic medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.474
H-Index - 145
eISSN - 1464-5491
pISSN - 0742-3071
DOI - 10.1111/j.1464-5491.2005.01713.x
Subject(s) - medicine , enos , endocrinology , endothelium , endothelial dysfunction , brachial artery , type 2 diabetes , allele , population , nitric oxide synthase , nitric oxide , diabetes mellitus , cardiology , blood pressure , genetics , gene , biology , environmental health
Objective Several studies have shown that the T −786 C 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 −786 C 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 −786 C 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 ( R 2 = 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 ( R 2 = 0.258, P = 0.0017) in smokers, but not in non‐smokers. Conclusion The C allele of T −786 C polymorphism of eNOS gene is a genetic risk factor for endothelial dysfunction in Type 2 diabetic patients, especially among smokers.