β 2 adrenergic receptor gene polymorphisms in normal and in patients with myocardial infarction in the eastern province of Saudi Arabia

Abstract

Single nucleotide polymorphisms (SNPs) of the ?₂ -adrenergic receptor (?₂ -AR) gene have been implicated in the pathogenesis of cardiovascular diseases. This study evaluated two ?₂ -AR SNPs in association with myocardial infarction (MI), namely arginine-glycine (G16R) substitution at codon 16 and glutamine-glutamic (Q27E) substitution at condon 27. bjectives:</b> Therefore, our main objective was to determine the association of these two SNPs among patients with MI with and without type 2 diabetes (T2D). <b>Materials and Methods:</b> Blood samples were collected from 201 MI patients with and without diabetes and from 115 controls and the ?₂ -AR gene polymorphisms at codon 16 and codon 27 were assessed by restriction fragment length polymorphism. The ?² test was used to compare differences between groups. <b>Results:</b> The SNPs did not deviate significantly from Hardy-Weinberg equilibrium in the control population. The allele and genotype frequencies of the ?₂ -AR gene polymorphism at codon 16 (G16R) was significantly different between MI cases and controls (?² = 10.495, <i>P</i> &lt; 0.05 and ?² = 8.849, <i>P</i> &lt; 0.05, respectively). No significant difference in genotype and allele frequencies at codon 27 was shown between these two groups (?² = 2.661, <i>P</i> ? 0.05 and ?² = 1.587, <i>P</i> ? 0.05, respectively). When the MI patients with and without T2D were pooled together, genotype distribution was different between cases and controls at codon 16 (?² = 4.631, <i>P</i> = 0.099) and codon 27 (?² = 7.247, <i>P</i> = 0.027). However, no significant differences were found in allele frequencies for codon 16 and codon 27 between the two groups (?² = 0.628, <i>P</i> = 0.428; ?² = 0.33, <i>P</i> = 0.565, respectively). <b>Conclusion:</b> Our findings indicate a moderate association of the ?₂ -AR G16R gene polymorphism with MI suggesting that this gene plays a universal role in the development of MI across ethnicities. However, there was no association of ?₂ -AR G16R gene polymorphism with diabetic patients with MI.