| Part 1: Genetic variant in visfatin gene promoter is associated with the decreased risk of coronary artery disease in a Chinese populationVisfatin is a newly identified pro-inflammatory adipokine expressed predominantly in visceral fat. Previous studies have suggested a role for visfatin in low-grade inflammation and regulation of lipid metabolism. Most recently, a genetic polymorphism -1535C>T located in visfatin gene promoter has been identified, and suggested to be associated with the regulation of visfatin expression, lipid and glucose levels. However, it is unclear whether this polymorphism has a linkage with CAD.1.The distribution of genotypic characteristics in the cases and controls for the genetic polymorphism -1535C>TThe frequencies of the CC, CT, and TT genotypes in cases were significantly different from those of controls (χ2=6.223, P=0.045). Subjects with the variant genotypes (CT+TT) had a 40% decreased risk of CAD relative to CC carriers (adjusted OR=0.60, 95%CI=0.40-0.89). Furthermore, the adjusted OR of TT genotype for CAD was 0.52 (95%CI=0.31-0.87).2.Association of -1535C>T polymorphism with lipid metabolismThere was a significant association between visfatin-1535C>T polymorphism and triglyceride levels in both CAD patients and controls (P=0.003, 0.018, respectively).3.Stratified analysesIn stratified analyses, the T allele was significantly associated with reduced risk of CAD in males, subjects with age <59 years, and non-smokers.4.Association of polymorphism with the severity of CAD among cases A borderline statistical significance (P = 0.058 for trend) was observed between the variant genotypes and severity of CAD.Part 2: A polymorphism in the visfatin gene promoter is related to decreased plasma levels of inflammatory markers in patients with coronary artery diseaseVisfatin, a newly identified proinflammatory adipokine, has been linked to coronary artery disease (CAD). The–1535C>T polymorphism located in the visfatin gene promoter is reportedly associated with proinflammatory status. However, it is unclear whether this polymorphism correlates with plasma levels of inflammatory markers including visfatin, hs-CRP, IL-6 and TNF-αin CAD patients. 1. Plasma visfatin levelsPlasma visfatin levels were markedly different between patients with stable angina pectoris (SAP, 11.91±0.70 ng/L) and those with unstable angina pectoris (UAP, 17.49±0.20 ng/L) or acute myocardial infarction (AMI, 16.63±0.22 ng/L; SAP versus UAP or AMI, P<0.05).2. Association of polymorphism with Plasma levels of inflammatory mediatorsCompared with the CC genotype, variant genotypes CT and TT correlated with significantly lower levels of visfatin, hs-CRP, IL-6 and TNF-αin the SAP group (P<0.05), with lower levels of hs-CRP and IL-6 in the UAP group (P<0.05), and with lower levels of visfatin in the AMI group (P<0.05) after adjustment for age, gender, smoking, hypertension, diabetes, dyslipidemia and medication. |