Abstract

BackgroundCoronary artery disease (CAD) is a group of diseases caused by plaque formation in the wall of arteries supplying blood to the heart. Adiponectin (ADIPOQ) is an adipocytokine that controls carbohydrate and lipid metabolism, has anti-diabetic properties, and correlates well with cardio-metabolic risk. ADIPOQ gene polymorphism is reported to be associated with CAD in numerous populations. ObjectiveTo explore the impact of adiponectin gene polymorphism, rs2241766 T > G, rs1501299 G > T, rs17300539 G > A, rs266729 G > A, and rs822395 A > C SNPs, on the CAD in the Iraqi population. MethodsA case-control study of 317 healthy individuals and 302 CAD patients was conducted. Standard protocols for measuring serum lipid profile levels were followed. ADIPOQ and insulin levels were estimated using the ELISA method. Genotyping of ADIPOQ gene was carried out using the RFLP technique. ResultsGenotype assessment of rs2241766, rs1501299, rs266729, and rs17300539 SNPs under several inheritance models pointed out significant (P = 0.012–10−4) elevations of the variant alleles in CAD patients in comparison to the control group. The haplotype analysis of the five analyzed SNPs exhibited five disease-susceptible haplotypes; they were GTCGA (OR: 7.6, 95 % CI: 2.55–21.76), TGCAA (P = 0.013), TGGGA (P = 0.046), TGGAA (P = 0.017), and GGGGA (P = 0.032). The linkage disequilibrium (LD) analysis of the five SNPs in the control versus the patient groups revealed significant LD. The variant genotype of the rs2241766 SNP was found to significantly increase the atherogenic lipids and HOMA values and decrease the ADIPOQ and high-density cholesterol (HDL-c) levels. Those of the rs1501299, rs17300539, and rs266729 SNPs were indicated to increase the metabolic parameter values except ADIPOQ and HDL-c magnitudes, which are reduced in the variant carriers. ConclusionThe rs2241766, rs1501299, rs266729, and rs17300539 SNPs of the ADIPOQ gene are risk factors for CAD in Iraqi individuals. Both single nucleotide and haplotype analyses suggested the implication of the ADIPOQ gene in the pathogenesis of the disease. This implication has occurred through lowering ADIPOQ levels and increasing atherogenic lipids.

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