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

ABSTRACT: 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 ?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.

SUBMITTER: Shi R

PROVIDER: S-EPMC6966009 | biostudies-literature | 2017

REPOSITORIES: biostudies-literature

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Effect of interactions between <i>LEPR</i> polymorphisms and smoking on coronary artery disease susceptibility.

Shi Ruina R Zhang Min M Wang Wei W Song Xiantao X Liu Hong H Tian Rui R Yang Fuqiang F Ding Mingchao M Lv Shuzheng S

International journal of clinical and experimental pathology 20170901 9

<h4>Objective</h4>This study was designed with the purpose of analyzing the relationship between the interactions of leptin receptor (<i>LEPR</i>) rs1137101, rs1137100 polymorphisms with smoking and the susceptibility to coronary artery disease (CAD).<h4>Methods</h4>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 <i>LEPR</i> polymorphisms were performed by polymerase chain reaction-restriction fra ...[more]

PMID: 31966858

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Project description:Coronary artery disease (CAD) is the principal cause of death in patients with nonalcoholic fatty liver disease (NAFLD). The aim of the present study was to investigate whether NAFLD is causally involved in the pathogenesis of CAD. For this, previously reported NAFLD susceptibility genes were clustered and tested for an association with CAD in the Coronary Artery Disease Genome-Wide Replication and Meta-Analysis plus the Coronary Artery Disease Genetics (CARDIoGRAMplusC4D) Consortium data set. The role of plasma lipids as a potential mediator was explored by using data from the Global Lipids Genetics Consortium. Statistical analyses revealed that the combination of 12 NAFLD genes was not associated with CAD in 60,801 CAD cases and 123,504 controls (odds ratio [OR] per NAFLD risk allele, 1.0; 95% confidence interval [CI], 0.99-1.00). In a subsequent sensitivity analysis, a positive relationship was observed after exclusion of gene variants that are implicated in NAFLD through impaired very low-density lipoprotein secretion (i.e., microsomal triglyceride transfer protein [MTTP], patatin-like phospholipase domain containing 3 [PNPLA3], phosphatidylethanolamine N-methyltransferase [PEMT], and transmembrane 6 superfamily member 2 [TM6SF2]) (OR, 1.01; 95% CI, 1.00-1.02). Clustering of the excluded genes showed a significant negative relationship with CAD (OR, 0.97; 95% CI, 0.96-0.99). A substantial proportion of the observed heterogeneity between the individual NAFLD genes in relation to CAD could be explained by plasma lipids, as reflected by a strong relationship between plasma lipids and CAD risk conferred by the NAFLD susceptibility genes (r = 0.76; P = 0.004 for low-density lipoprotein cholesterol). Conclusion: NAFLD susceptibility genes do not cause CAD per se. The relationship between these genes and CAD appears to depend to a large extent on plasma lipids. These observations strongly suggest taking plasma lipids into account when designing a new drug to target NAFLD.

Dataset Information

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

Publications

Effect of interactions between <i>LEPR</i> polymorphisms and smoking on coronary artery disease susceptibility.

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