瘦素受体基因Gln223Arg、锰超氧化物歧化酶9Ala/Val基因多态性与吸烟的交互作用和非酒精性脂肪性肝病关系  

Interaction of polymorphisms of Leptin receptor gene Gln223Arg,MnSOD9Ala /Val genes and smoking in 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 [3]杭州市第六人民医院

出　　处：《卫生研究》2014年第5期724-731,共8页Journal of Hygiene Research

摘　　要：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 of polymorphisms of leptin receptor （LR） gene Gln223Arg, manganese superoxide dismutase9Ala/Val （ MnSOD9Ala/ Val） genes and smoking in nonalcoholic fatty liver disease. Methods The genetic polymorphisms of LEPR gene Gln223Arg and MnSOD9Ala/Val were analyzed bypolymorphism-polymerase chain reaction （PCR） technique in peripheral blood leukocytes of 600 NAFLD cases and 600 healthy persons. Results The frequencies of LR gene GIn223Arg （G/G） and MnSOD9Ala/Val （V/V） were 48.67% and 50. 17% in NAFLD cases and 21.17% and 21.50% in healthy controls respectively. Statistical tests showed significant difference in the frequencies between the two groups （P 〈 0.01 ）. The risk of NAFLD with Gln223Arg （G/G）was significantly higher than those of controls（ OR = 3. 5309, 95% CI = 1. 8165 -5. 0724）. The individuals who carried with MnSOD9Ala/Val （V/V） had a high risk of NAFLD （OR = 3. 6756,95% CI = 1.9137 - 5.5496）. Combined analysis of the polymorphisms showed that percentage of Gln223Arg （G/G）/ MnSOD9Ala/Val （V/V） in NAFLD and control groups was40.33%% and 7.50% respectively（ P 〈0.01 ）. The people who carried with Gln223Arg（ G/G）/ MnSOD9Ala/ Val （V/V） had a high risk of NAFLD （ OR = 8. 4014,95% CI =4. 2926 - 12. 4238）. The smoking rate of the case group was significantly higher than which in the control group （ OR = 3. 6754,95% CI = 1. 4193 - 4. 9581 ,P 〈 0.01 ）, and statistic analysis suggested an interaction between smoking and Gln223Arg （ G/G）/ MnSOD9Ala/Val （V/V） which increase risk of NAFLD （OR = 9. 8665; OR = 8. 5476 ）. Conclusion Gln223Arg （G/G）, MnSOD9Ala/Val （V/V） and smoking are the risk factors in NAFLD, and the significant interactions between genetiepolymorphisms of Gln223Arg, MnSOD9Ala/Val and smoking added the risk of NAFLD.

关 键 词：非酒精性脂肪性肝病 瘦素受体基因Gln223Arg 锰超氧化物歧化酶9Ala/Val 多态性 吸烟 

分 类 号：R575.4[医药卫生—消化系统] R195.4[医药卫生—内科学]