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目的探讨瘦素受体(LEPR)基因Gln223Arg、锰超氧化物歧化酶9Ala/Val(manganese superoxide dismutase9Ala/Val,MnSOD9Ala/Val)基因多态性与吸烟的交互作用与非酒精性脂肪性肝病(NAFLD)的关系。方法采用病例-对照研究的方法,以600例NAFLD患者及600例健康对照者的外周血白细胞为样本,利用PCR分析LR基因Gln223Arg和MnSOD9Ala/Val基因多态性。结果 LR基因LEPR Gln223Arg(G/G)基因型和MnSOD9Ala/Val(V/V)基因型频率分布分别为48.67%、50.17%(病例组)和21.17%、21.50%(对照组),二者经χ2检验差异有显著性(P<0.01;P<0.01)。Gln223Arg(G/G)患NAFLD的风险显著增加(OR=3.5309,95%CI 1.8165~5.0724)。MnSOD9Ala/Val(V/V)基因型者患NAFLD的风险也显著增加(OR=3.6756,95%CI=1.9137~5.5496)。基因突变的协同分析发现Gln223Arg(G/G)/MnSOD9Ala/Val(V/V)基因型者在NAFLD组和对照组中的分布频率分别为40.33%%和7.50%,二者经χ2检验有显著性差异(P<0.01)。Gln223Arg(G/G)/MnSOD9Ala/Val(V/V)基因型者患NAFLD的风险显著增加(OR=8.4014,95%CI 4.2926~12.4238)。病例组的吸烟率显著高于对照组的吸烟率(OR=3.6754,95%CI 1.4193~4.9581,P<0.01),吸烟与Gln223Arg(G/G)和MnSOD9Ala/Val(V/V)基因型均有交互作用(OR=8.5476;OR=8.8665)。结论Gln223Arg(G/G)/MnSOD9Ala/Val(V/V)基因型和吸烟是NAFLD的易患因素,基因多态性与吸烟的交互作用增加了NAFLD的发病风险。
Objective To investigate the interaction between LEPR gene Gln223Arg, manganese superoxide dismutase9Ala / Val (MnSOD9Ala / Val) polymorphism and smoking and non-alcoholic fatty liver disease (NAFLD) )Relationship. Methods Using the case-control study, polymorphisms of the Gln223Arg and MnSOD9Ala / Val LR genes were analyzed by PCR using peripheral blood leukocytes from 600 NAFLD patients and 600 healthy controls. Results The frequency distributions of LEPR Gln223Arg (G / G) genotype and MnSOD9Ala / Val (V / V) genotype were 48.67%, 50.17% (case group) and 21.17%, 21.50% χ2 test showed significant difference (P <0.01; P <0.01). The risk of NAFLD was significantly increased for Gln223Arg (G / G) (OR = 3.5309, 95% CI 1.8165 to 5.0724). Patients with MnSOD9Ala / Val (V / V) also had a significantly increased risk of NAFLD (OR = 3.6756, 95% CI = 1.9137-5.5496). The co-analysis of gene mutations found that the distribution frequencies of Gln223Arg (G / G) / MnSOD9Ala / Val (V / V) genotypes in NAFLD group and control group were 40.33% and 7.50%, respectively, Sex differences (P <0.01). The risk of NAFLD was significantly increased in the Gln223Arg (G / G) / MnSOD9Ala / Val (V / V) genotype (OR = 8.4014,95% CI 4.2926-12.4238). The smoking rates in case group were significantly higher than those in control group (OR = 3.6754,95% CI 1.4193 ~ 4.9581, P <0.01). Both smoking and Gln223Arg (G / G) and MnSOD9Ala / Val (V / V) Interaction (OR = 8.5476; OR = 8.8665). Conclusions Gln223Arg (G / G) / MnSOD9Ala / Val (V / V) genotype and smoking are risk factors for NAFLD. The interaction between genetic polymorphisms and smoking increases the risk of NAFLD.