Journal article
β2‑Adrenergic Receptor Gene Polymorphisms in
Normal and in Patients with Myocardial Infarction in
the Eastern Province of Saudi Arabia



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Publication Details
Author list: Abdullah Al‑Rubaish, Fahd Al‑Muhanna, Abdullah Al‑Shehri, Awatif Al‑Nafaie, Mohammed Shakil,
Abdullah Al‑Ali4, Khalid Al‑Faraidy, Emmanuel Larbi, Folkert Asselberg6, Amein Al‑Ali

Publisher: Medknow Publications
Publication year: 2013
Journal: Saudi Journal of Medicine and Medical Sciences
Volume number: 1
Issue number: 1
Start page: 25
End page: 29
Number of pages: 5
ISSN: 1658-631X
Web of Science ID:
PubMed ID:
Scopus ID:


Introduction: Single nucleotide polymorphisms (SNPs) of the β2‑adrenergic receptor (β2‑AR) gene have been implicated in the pathogenesis of cardiovascular diseases. This study evaluated two β2‑AR SNPs in association with myocardial infarction (MI), namely arginine‑glycine (G16R) substitution at codon 16 and glutamine‑glutamic (Q27E) substitution at condon 27.

Objectives: Therefore, our main objective was to determine the association of these two SNPs among patients with MI with and without type 2 diabetes (T2D).

Materials and Methods: Blood samples were collected from 201 MI patients with and without diabetes and from 115 controls and the β2‑AR gene polymorphisms at codon 16 and codon 27 were assessed by restriction fragment length polymorphism. The χ2 test was used to compare differences between groups.

Results: The SNPs did not deviate significantly from Hardy‑Weinberg equilibrium in the control population. The allele and genotype frequencies of the β2‑AR gene polymorphism at codon 16 (G16R) was significantly different between MI cases and controls (χ2 = 10.495, P < 0.05 and χ2 = 8.849, P < 0.05, respectively). No significant difference in genotype and allele frequencies at codon 27 was shown between these two groups (χ2 = 2.661, P ≥ 0.05 and χ2 = 1.587, P ≥ 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 (χ2 = 4.631, P = 0.099) and codon 27 (χ2 = 7.247, P = 0.027). However, no significant differences were found in allele frequencies for codon 16 and codon 27 between the two groups (χ2 = 0.628, P = 0.428; χ2 = 0.33, P = 0.565, respectively).

Conclusion: Our findings indicate a moderate association of the β2‑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 β2‑AR G16R gene polymorphism with diabetic patients with MI.

Key words: Adrenergic receptor, cardiovascular diseases, mutation, polymorphism



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Last updated on 2018-06-02 at 16:19