Abstract
BackgroundThe C242T polymorphism of the CYBA gene that encodes p22phox, a component of NADPH oxidase, has been found to modulate superoxide production. Oxidase is a major source of the superoxide anion that contributes to individual components of metabolic syndrome. We examined the relationship of the C242T polymorphism with the prevalence of metabolic syndrome in a Chinese population, taking account of consumed cigarette amounts.Methodology/Principal FindingsIn 870 participants, we collected biomarkers related to metabolic syndrome and detailed history of smoking and genotyped the C242T polymorphisms. After adjustment for covariates, the CT/TT genotypes were associated with a lower risk of metabolic syndrome (P = 0.0008). The odds of having metabolic syndrome in the CT/TT participants were 0.439 (95%CI: 0.265, 0.726), while for CC participants the odds were 1.110 (95%CI: 0.904, 1.362). There was significant (P = 0.014) interaction between the C242T polymorphism and smoking status in relation to the prevalence of metabolic syndrome. For smokers who smoke no less than 25 pack-years, those with CT/TT genotypes had lower risk of metabolic syndrome as compared with CC polymorphism carriers (P = 0.015). In the multiple regression analysis, the CT/TT genotypes were significantly associated with lower serum concentration of triglycerides both in all subjects and smokers; furthermore, the CT/TT genotypes were also related to smaller waist circumference in smokers.ConclusionsOur study suggests that the C242T gene polymorphism is indeed related to the prevalence of metabolic syndrome and smoking dose might modify this association.
Highlights
Metabolic syndrome is defined as a cluster of metabolic abnormalities that increases the risk for type 2 diabetic mellitus, coronary artery disease (CAD) and other cardiovascular diseases
Our study suggests that the C242T gene polymorphism is related to the prevalence of metabolic syndrome and smoking dose might modify this association
As smoking may influence vascular Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activation [8,9,10,11], we further examined whether smoking dose could modify the genetic effect in a Chinese population
Summary
Metabolic syndrome is defined as a cluster of metabolic abnormalities that increases the risk for type 2 diabetic mellitus, coronary artery disease (CAD) and other cardiovascular diseases. The core components of metabolic syndrome are high blood pressure, central obesity, impaired fasting glucose and dyslipidemia [1]. Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, a multisubunit protein complex consisting of membranebound and cytosolic subunits, is a major source of superoxide anion in the vasculature [3]. The p22phox subunit is essential for activation of the NADPH oxidase system [4]. Several polymorphisms of the CYBA gene have been identified. The functional significance of the C242T polymorphism has been related to NADPH oxidase activity with subsequent production of the superoxide anion [6,7]. The C242T polymorphism of the CYBA gene that encodes p22phox, a component of NADPH oxidase, has been found to modulate superoxide production. Oxidase is a major source of the superoxide anion that contributes to individual components of metabolic syndrome. We examined the relationship of the C242T polymorphism with the prevalence of metabolic syndrome in a Chinese population, taking account of consumed cigarette amounts
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