Effect of interactions between LEPR polymorphisms and smoking on coronary artery disease susceptibility.

Objective: This study was designed with the purpose of analyzing the relationship between the interactions of leptin receptor ( LEPR ) rs1137101, rs1137100 polymorphisms with smoking and the susceptibility to coronary artery disease (CAD).
Methods: The subjects of this study consisted of 101 CAD patients and 110 healthy people frequency-matched with the former in age and sex. The genotyping of LEPR polymorphisms were performed by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method. The distribution differences of genotype and allele between two groups was estimated by χ ² test. The relative risk of CAD was showed by odds ratio (OR) with 95% confidence interval (95% CI). Crossover analysis was applied in the studying of gene-environment interactions.
Results: LEPR rs1137101 polymorphism showed significant difference between CAD patients and healthy controls neither genotypes nor alleles in this study population ( P >0.05). Fortunately, we detected that AA genotype of LEPR rs1137100 polymorphism had frequency difference between two study groups with a significant level, compared with the common genotype GG ( P =0.03), which showed that this polymorphism had an independent association with CAD (OR=3.07, 95% CI=1.08-8.73). So was A allele of rs1137100 (OR=1.58, 95% CI=1.04-2.39). Furthermore, we observed the interaction of smoking and rs1137100 polymorphism in CAD occurrence (OR=2.69, P =0.01).
Conclusions: Not only is LEPR rs1137100 polymorphism an independent risk factor for CAD, but it exists the interaction with smoking in the onset of CAD in this Chinese population.
Competing Interests: None.
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