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 Gln223 Arg 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 Gln223Arg (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 =21. 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 Gln223 Arg (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 geneticpolymorphisms of Gln223Arg,MnSOD9Ala/Val and smoking added the risk of NAFLD.
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 Gln223 Arg 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 Gln223Arg (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 =21. 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 Gln223 Arg (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 geneticpolymorphisms of Gln223Arg,MnSOD9Ala/Val and smoking added the risk of NAFLD.