吸烟量和多巴胺受体基因多态性与向心性肥胖的关联及交互作用

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目的探讨多巴胺受体(DRD1)基因多态性和吸烟量与向心性肥胖的关系,分析DRD1基因型对吸烟量和肥胖的关联是否存在修饰作用。方法以多级随机抽样方法,选择519名现在吸烟男性为调查对象,其中向心性肥胖者240名为病例组,腰围正常者279名为正常对照组,并调查两组人群的人口学特征及吸烟行为等信息,采集静脉血并采用改进的多重高温连接酶检测反应技术(improved multiple ligase detection reaction,IMLDR)单核苷酸多态性(SNP)分型技术对DRD1上SNP位点rs4867798、rs265981和rs4532进行多态性检测。采用logistic回归模型控制混杂因素后,分析吸烟量和DRD1基因多态性对向心性肥胖的主效应及相乘交互作用;基于相加模型进一步采用在线Excel计算相加交互作用指标,分析吸烟量和DRD1基因多态性对向心性肥胖的相加交互作用。结果单因素分析发现,职业、文化程度、喝茶、规律运动和体质指数(BMI)在腰围正常组和向心性肥胖组的分布差异有统计学意义(P<0.05)。经logistic回归模型控制混杂因素后分析发现,吸烟量>15支/d者与向心性肥胖呈显著正关联(OR=2.57,95%CI:1.25~5.26),未发现有相乘交互作用。用相加模型分析发现,与每天吸烟量1~15支者且携带3个基因位点的突变型相比,每天吸烟量大于15支且基因型为野生型者与向心性肥胖显著正关联(OR=3.04,95%CI:1.01~9.17;OR=4.48,95%CI:1.27~15.83;OR=3.63,95%CI:1.13~11.74),每天吸烟量大于15支且携带rs4867798突变型者与向心性肥胖显著正关联(OR=2.40,95%CI:1.01~5.66)。根据相加模型的交互作用指标交互作用指数(S)、交互作用归因比(AP)和交互作用超额相对危险度(RERI)分析,未发现每日吸烟量与DRD1基因3个位点的多态性对向心性肥胖有相加交互效应。结论吸烟量和DRD1基因与向心性肥胖有一定的关联。 Objective To investigate the association of DRD1 gene polymorphism and smoking with central obesity, and to explore whether DRD1 genotypes may be involved in the association between smoking and obesity. Methods A total of 240 smokers with obsessive-compulsive obesity were enrolled in this study. A total of 279 patients with concentric obesity were enrolled in this study. 279 normal persons with normal waist circumference were enrolled in this study. Demographic characteristics and smoking Behavior and other information were collected, venous blood was collected and the SNP genotypes of rs4867798, rs265981 and rs265981 on DRD1 were detected by using improved multiple ligase detection reaction (IMLDR) single nucleotide polymorphism (SNP) rs4532 for polymorphism detection. After using the logistic regression model to control confounding factors, the main effects and multiplying interactions of smoking and DRD1 gene polymorphism on central obesity were analyzed. Based on the additive model, the online interaction calculation was used to calculate the additive interaction and smoking consumption The additive interaction between DRD1 gene polymorphism and central obesity. Results Univariate analysis showed that the distribution of occupational, educational level, drinking tea, regular exercise and body mass index (BMI) in the normal waist circumference group and the central obesity group were statistically different (P <0.05). Logistic regression analysis showed that there was a significant positive correlation between central obesity and obesity (OR = 2.57, 95% CI: 1.25-5.26). However, no cross-interaction was found. By using the additive model, it was found that there was a significant positive correlation between smoking more than 15 cigarettes per day and genotypes of wild type with central obesity, compared with those with 1-15 cigarettes per day and carrying 3 loci OR = 3.04, 95% CI: 1.01-9.19; OR = 4.48, 95% CI: 1.27-15.83; OR = 3.63,95% CI: 1.13-11.74) with more than 15 cigarettes per day and rs4867798 mutant Significant positive correlation was observed with central obesity (OR = 2.40, 95% CI: 1.01-5.66). According to the interaction model interaction index (S), interaction attribution ratio (AP) and interaction overrelated risk (RERI) analysis, we did not find that the daily cigarette smoking and DRD1 gene more than three sites There is additive and reciprocal effect on attitude toward obesity. Conclusion There is a certain relationship between smoking and DRD1 gene and central obesity.
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