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• W2076981708 abstract "Background . Extensive evidence, arising from models of endothelial nitric oxide synthase gene ( NOS3 )-knockout mice supports the role of endothelial malfunction in the pathogenesis of the metabolic syndrome (MS). Aims . The aim of this study was to evaluate the role of −786T/C polymorphism in the etiology of MS and assess previously reported interaction with cigarette smoking. Methods . Based on International Diabetes Federation 2005 criteria, we recruited randomly 152 subjects with MS and 75 subjects without MS. Results . Allelic and genotype frequencies did not differ significantly between both groups. Total cholesterol level (CHOLT) and intima-media thickness of carotid arteries were significantly higher in −786CC homozygotes, in comparison with −786TC and −786TT patients. Regarding current smoking status, −786C allele was associated with higher CHOLT than −786T allele. Conclusion . Our study indicates the putative role of −786T/C polymorphism in the development of hypercholesterolemia, in patients with MS, which might be enhanced by cigarette smoking." @default.
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• W2076981708 date "2011-01-01" @default.
• W2076981708 modified "2023-09-30" @default.
• W2076981708 title "The Role of −786T/C Polymorphism in the Endothelial Nitric Oxide Synthase Gene in Males with Clinical and Biochemical Features of the Metabolic Syndrome" @default.
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• W2076981708 doi "https://doi.org/10.1155/2011/458750" @default.
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