Abstract

Coronary artery disease (CAD) is a major cause of death all over the world. CAD is caused by atherosclerosis which is induced by the interaction of genetic factors and environmental factors. Genome-wide association studies have revealed the association of certain gene polymorphisms with susceptibility to CAD. Omentin 1 is an adipokine secreted by the visceral adipose tissues and has been reported to have anti-inflammatory, cardioprotective, and enhances insulin sensitivity. In this study, we examined the role of omentin-1 common single nucleotide polymorphisms (SNPs) (rs2274907 A > T and rs2274908 G > A) in CAD. We conclude that the AT genotype and the T allele of the rs2274907 A > T is associated with Cad in the south Indian population. Our results indicated that the rs2274907 SNP may be associated with CAD in this population. This finding needs further validation in well-designed and large-sample size studies before being introduced in clinical settings.

Highlights

  • Thank you very much for your interest in our study by Jha et al, 2019 [1]

  • We suggested that the deviation from HWE observed in our study occurred due to the substructure of this population. In support of this assumption is the recent study by Rathwa et al [6] (Table 1), in which they report 0% AA genotype, 17.6% AT genotype, and more than 80% for the mutant genotype (TT)

  • This indicates a complete shift to the mutant genotype (TT) in this population

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Summary

Introduction

Thank you very much for your interest in our study by Jha et al, 2019 [1]. We acknowledge that no genotyping method is 100% efficient and that genotyping errors can occur. We used the amplification refractory mutation system PCR (ARMS-PCR) and allele-specific PCR to genotype omentin 1 single nucleotide polymorphisms (SNPs) rs2274907 A > T and rs2274908 G > A. Results were repeated several times and once perfection was achieved, the remaining CAD samples were screened. Our genotyping result deviated from HWE and this was probably due to many factors including population structure and/or sample size, purifying selection, copy number variation, inbreeding, or the substructure of this population [4,5].

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