Department of Biochemistry, Faculty of Medicine, University of Kufa, Najaf, Iraq.
Department of Basic Science, College of Dentistry, University of Kufa, Najaf, Iraq.
Clin Biochem. 2022 Feb;100:29-34. doi: 10.1016/j.clinbiochem.2021.11.005. Epub 2021 Nov 14.
Coronary artery disease (CAD) is the primary cause of death worldwide. It is mainly caused by atherosclerosis that initiates from a genetic-environmental interaction. Studies highlighted the association of numerous gene polymorphisms with CAD. Omentin-1 is secreted from visceral adipose tissues, intestine, and others; it has anti-inflammatory and insulin sensitivity improving roles.
To explore the association of the omentin-1 gene polymorphisms (rs2274907 and rs2274908) with serum lipid concentrations and CAD in a sample of the Iraqi population.
A case-control study was followed, in which CAD patients were analyzed versus a group of healthy persons. Serum lipid concentrations were measured by enzymatic methods. Genotyping of the omentin-1 gene for rs2274907 SNP was achieved by ARMS-PCR, while for rs2274908 SNP by allele-specific PCR (AS-PCR) techniques.
Atherogenic serum lipid concentrations increased significantly in CAD patients relative to the control group. Genotyping of the omentin-1 gene for rs2274907 SNP revealed a significant (OR = 4.11, P = 0.035) elevation of the AT genotype carriers in CAD versus the control groups. The genotype analysis of the rs2274908 SNP failed to exhibit a significant variation. The two analyzed SNPs were indicated to be in linkage disequilibrium (r = 0.772, P < 0.0001). The global haplotype association of the 2 SNPs was demonstrated to be significant (P = 0.006). Serum lipid concentrations were found to be independent of the genotype distribution of the rs2274907 SNP.
Carriers of the AT genotype of rs2274907 SNP in the omentin-1gene may have a four-fold risk of developing CAD compared to those of the wild genotype. Alterations of serum lipid concentrations may do not depend on the genotypes of this SNP.
冠心病（CAD）是全球范围内主要的死亡原因。它主要由起始于遗传-环境相互作用的动脉粥样硬化引起。研究强调了许多基因多态性与 CAD 的关联。网膜素-1 由内脏脂肪组织、肠道和其他组织分泌，具有抗炎和改善胰岛素敏感性的作用。
探讨网膜素-1 基因多态性（rs2274907 和 rs2274908）与伊拉克人群血清脂质浓度和 CAD 的关系。
采用病例对照研究，分析 CAD 患者与健康对照组。采用酶法测定血清脂质浓度。采用 ARMS-PCR 检测网膜素-1 基因 rs2274907 单核苷酸多态性，采用等位基因特异性 PCR（AS-PCR）技术检测 rs2274908 单核苷酸多态性。
与对照组相比，CAD 患者的致动脉粥样硬化血清脂质浓度显著升高。rs2274907 SNP 的基因分型显示，与对照组相比，CAD 患者中 AT 基因型携带者的风险显著升高（OR=4.11，P=0.035）。rs2274908 SNP 的基因型分析未显示出显著差异。两个分析的 SNP 显示出连锁不平衡（r=0.772，P<0.0001）。2 个 SNP 的全球单体型关联具有显著性（P=0.006）。血清脂质浓度与 rs2274907 SNP 的基因型分布无关。
与野生基因型相比，网膜素-1 基因 rs2274907 SNP 的 AT 基因型携带者发生 CAD 的风险可能增加四倍。血清脂质浓度的改变可能不依赖于该 SNP 的基因型。
