吸烟和β3-肾上腺素能受体基因Trp64Arg、锰超氧化物歧化酶9Ala/Val基因多态性与非酒精性脂肪性肝病的相关性  

Correlation of cigarette smoking and the polymorphisms of β3-adrenergic receptor gene Trp64Arg,MnSOD9Ala/Val genes with nonalcoholic fatty liver disease

作　　者：张超贤[1] 郭李柯[2] 郭晓凤[3] 

机构地区：[1]新乡医学院第一附属医院消化内科,河南卫辉453100 [2]新乡医学院第一附属医院口腔科,河南卫辉453100 [3]杭州市第六人民医院肝病科,浙江杭州310014

出　　处：《西安交通大学学报（医学版）》2015年第1期106-111,120,共7页Journal of Xi’an Jiaotong University（Medical Sciences）

摘　　要：目的探讨吸烟和β3-肾上腺素能受体（β3-AR））基因Trp64Arg、锰超氧化物歧化酶9Ala/Val（MnSOD9Ala/Val）基因多态性与非酒精性脂肪性肝病（NAFLD）发病之间的关系。方法采用病例-对照研究的方法,以720例NAFLD患者及720例健康对照者的外周血白细胞为样本,采用聚合酶链反应（PCR）技术分析β3-AR基因Trp64Arg和MnSOD9Ala/Val基因多态性。结果β3-AR基因Trp64Arg（A/A）基因型和MnSOD9Ala/Val（V/V）基因型频率分布分别为39.4%、71.7%（病例组）和21.1%、43.3%（对照组）,差异有统计学意义（P〈0.01;P〈0.01）。Trp64Arg（A/A）基因型者患NAFLD的风险显著增加（OR=2.434,95%CI=1.816～4.075）。MnSOD9Ala/Val（V/V）基因型者患NAFLD的风险也显著增加（OR=3.308,95%CI=1.913～4.509）。基因突变的协同分析发现,Trp64Arg（A/A）/MnSOD9Ala/Val（V/V）基因型者在NAFLD组和对照组中的分布频率分别为32.8%和6.5%,差异有统计学意义（P〈0.01）。Trp64Arg（A/A）/MnSOD9Ala/Val（V/V）基因型者患NAFLD的风险显著增加（OR=9.753,95%CI=4.292～12.426）。病例组的吸烟率显著高于对照组（OR=2.623,95%CI=1.425～4.957）,Trp64Arg（A/A）/MnSOD9Ala/Val（V/V）基因型与吸烟有协同作用（OR=33.764,95%CI=18.907～61.582）。结论 Trp64Arg（A/A）/MnSOD9Ala/Val（V/V）基因型和吸烟是NAFLD的易患因素,三者的联合在NAFLD的发生中起着协同的作用。Objective To investigate the correlation of cigarette smoking and the combination of polymorphisms of β3-adrenergic receptor （β3-AR） gene Trp64Arg and manganese superoxide dismutascgAla/Val （MnSODgAIa/Val） genes with nonalcoholic fatty liver disease （NAFLD）. Methods The genetic polymorphisms of β3-AR gone Trp64Arg and MnSODgAIa/Val were analyzed by polyrnorphism-polymerase chain reaction （PCR） technique in peripheral blood leukocytes of 720 NAFLD patients and 720 healthy persons. Results The frequency of β3-AR gene Trp64Arg （A/A） and MnSOD9AIa/Val （V/V） was 39.4% and 71.7% in NAFLD patients and 2%. 1% and 43.3% in healthy controls, respectively. Statistical tests showed significant differences in the frequency betwcen the two groups （P〈0.01）. The risk of NAFLD in patients carrying Trp64Arg（A/A） was significantly higher than that in the controls （ OR = 2. 434, 95 % CI = 1. 816-- 4. 076）. The individuals carrying MnSODgAIa/Val （V/V） had a higher risk of NAFLD （OR = 3. 308, 95% CI = 1. 913- 4. 509）. Combined analysis of the polymorphisms showed that the percentage of Trp64Arg （A/A）/MnSOD9AIa/Val （V/V） in NAFLD and control groups was 32.8% and 6.5%, respectively （P〈0. 01）. The patients carrying Trp64Arg（A/A）/ MnSODgAIa/Val （V/V） had a higher risk of NAFLD （OR-9. 753, 95% CI= 4. 292-12. 426）. The smoking rate of the case group was significantly higher than that in the control group （0R=2.623, 95% CI=1. 425-- 4. 957, P〈0.01）, and statistic analysis suggested an interaction between cigarette smoking and Trp64Arg（A/A）/MnSODgAla/Val（V/V） which increased the risk of NAFLD （OR：33.764, 95% CI=18.907--61.582）. Conclusion Trp64Arg（A/A）, MnSODgAIa/Val （V/V） and cigarette smoking are the risk factors for NAFLD, and they can play a synergetic role in NAFLD.

关 键 词：非酒精性脂肪性肝病 β3-肾上腺素能受体基因Trp64Arg 锰超氧化物歧化酶9Ala/Val 多态现象 吸烟 

分 类 号：R575.5[医药卫生—消化系统]