抵抗素基因启动子-420C/G、细胞色素P4501A1-MspI多态性与吸烟的交互作用对非酒精性脂肪性肝病的影响

Interaction of polymorphisms in resistin gene promoter-420C/G,cytochromes P4501A1 gene MspI and cigarette smoking on nonalcoholic fatty liver disease

目的:探讨抵抗素基因启动子-420C/G、细胞色素P4501A1-Msp I(CYP1A1-Msp I)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1 200例NAFLD患者及1 200例健康对照者的外周血白细胞为样本,利用聚合酶链反应(polymerase chain reaction,PCR)技术分析了抵抗素基因启动子-420C/G和CYP1A1-Msp I基因多态性。结果:-420C/G(GG)基因型和CYP1A1-Msp I(m2/m2)基因型频率分布分别为49.75%、50.08%(病例组)和24.00%、24.25%(对照组),两者经χ2检验差异显著(P<0.01)。-420C/G(GG)基因型者患NAFLD的风险显著增加。CYP1A1-Msp I(m2/m2)基因型者患NAFLD的风险也显著增加。基因突变的协同分析发现-420C/G(GG)/CYP1A1-Msp I(m2/m2)基因型者在NAFLD组和对照组中的分布频率分别为39.83%和12.83%,两者经χ2检验有显著差异(P<0.01)。-420C/G(GG)/CYP1A1-Msp I(m2/m2)基因型者患NAFLD的风险显著增加。病例组的吸烟率显著高于对照组的吸烟率(P<0.01),吸烟与-420C/G(GG)和CYP1A1-Msp I(m2/m2)基因型均有交互作用。结论:-420C/G(GG)、CYP1A1-Msp I(m2/m2)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。

AIM：To investigate the interaction of polymorphisms of resistin gene promoter -420C/G, cyto-chromes P4501A1-MspI and cigarette smoking in nonalcoholic fatty liver disease （NAFLD）.METHODS： The genetic polymorphisms in resistin gene promoter -420C/G and CYP1A1-MspI were analyzed by the technique of polymerase chain reaction （ PCR） in peripheral blood leukocytes of 900 NAFLD cases and 900 healthy persons.RESULTS：The frequencies of -420C/G （GG） and CYP1A1-MspI （m2/m2） were 49.75%and 50.08%in NAFLD cases and 24.00%and 24.25%in healthy controls, respectively.Statistical tests showed a significant difference in the frequencies between the 2 groups （ P〈0.01）.The risk of NAFLD with -420C/G （GG） was significantly higher than that of controls.Individuals who carried with CYP1A1-MspI （m2/m2） had a high risk of NAFLD.Combined analysis of the polymorphisms showed that the per-centages of -420C/G （GG）/CYP1A1-MspI （m2/m2） in NAFLD and control groups were 39.83% and 12.83%, re-spectively （P〈0.01）.The people who carried with -420C/G （GG）/CYP1A1-MspI（m2/m2） had a high risk in NAFLD group.The cigarette smoking rate in NAFLD group was signi-ficantly higher than that in control group （ P〈0.01） , and the statistic analysis suggested an interaction between cigarette smoking and -420C/G （GG） and CYP1A1-MspI （m2/m2）, which increased the risk of NAFLD.CONCLUSION： -420C/G （GG）, CYP1A1-MspI （m2/m2） and cigarette smoking ＆ nbsp;are the risk factors in NAFLD.The interactions between genetic polymorphisms in -420C/G, CYP1A1-MspI （ m2/m2） and cigarette smoking increase the risk of NAFLD.