Insight into adiponectin gene impact on coronary artery disease from a polymorphism case-control study in Iraqi individuals

IF 1 Q4 GENETICS & HEREDITY

Gene Reports Pub Date : 2024-07-30 DOI:10.1016/j.genrep.2024.101996

Majid Kadhum Hussain , Ibrahem Rahem J. Al-Aadily , Alhan Abdulmohsin A. Al-Rashid , Abdol Hussein A. Algenabi , Ahmed Naseer Kaftan , Muna Abdulridha Al-Barqaawi , Layth Ahmed A. Al-Fahham , Teba Jaber Merza , Iman Jabbar Kadhim , Mohammed Ali Abdulameer Khikani

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Abstract

Background

Coronary 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.

Objective

To 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.

Methods

A 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.

Results

Genotype 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.

Conclusion

The 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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伊拉克人多态性病例对照研究揭示脂肪连通素基因对冠心病的影响

背景冠状动脉疾病（CAD）是由向心脏供血的动脉壁上形成的斑块引起的一组疾病。脂联素（ADIPOQ）是一种控制碳水化合物和脂质代谢的脂肪细胞因子，具有抗糖尿病特性，与心血管代谢风险密切相关。目的探讨伊拉克人群中脂联素基因多态性 rs2241766 T > G、rs1501299 G > T、rs17300539 G > A、rs266729 G > A 和 rs822395 A > C SNPs 对 CAD 的影响。研究采用标准方案测量血清脂质概况水平。ADIPOQ 和胰岛素水平采用 ELISA 方法进行估算。结果在几种遗传模型下对 rs2241766、rs1501299、rs266729 和 rs17300539 SNP 进行基因型评估后发现，与对照组相比，CAD 患者的变异等位基因显著升高（P = 0.012-10-4）。对所分析的五个 SNP 的单倍型分析显示出五个疾病易感单倍型，它们分别是 GTCGA（OR：7.6，95 % CI：2.55-21.76）、TGCAA（P = 0.013）、TGGGA（P = 0.046）、TGGAA（P = 0.017）和 GGGGA（P = 0.032）。对照组与患者组中五个 SNP 的连锁不平衡（LD）分析显示出显著的 LD。研究发现，rs2241766 SNP 的变异基因型会显著增加致动脉粥样硬化血脂和 HOMA 值，降低 ADIPOQ 和高密度胆固醇（HDL-c）水平。结论 ADIPOQ 基因的 rs2241766、rs1501299、rs266729 和 rs17300539 SNPs 是伊拉克人患 CAD 的危险因素。单核苷酸和单倍型分析表明，ADIPOQ 基因与该病的发病机制有关。这种影响是通过降低 ADIPOQ 水平和增加致动脉粥样硬化脂质而产生的。

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来源期刊

Gene Reports Biochemistry, Genetics and Molecular Biology-Genetics

CiteScore

3.30

自引率

7.70%

发文量

246

审稿时长

49 days

期刊介绍： Gene Reports publishes papers that focus on the regulation, expression, function and evolution of genes in all biological contexts, including all prokaryotic and eukaryotic organisms, as well as viruses. Gene Reports strives to be a very diverse journal and topics in all fields will be considered for publication. Although not limited to the following, some general topics include: DNA Organization, Replication & Evolution -Focus on genomic DNA (chromosomal organization, comparative genomics, DNA replication, DNA repair, mobile DNA, mitochondrial DNA, chloroplast DNA). Expression & Function - Focus on functional RNAs (microRNAs, tRNAs, rRNAs, mRNA splicing, alternative polyadenylation) Regulation - Focus on processes that mediate gene-read out (epigenetics, chromatin, histone code, transcription, translation, protein degradation). Cell Signaling - Focus on mechanisms that control information flow into the nucleus to control gene expression (kinase and phosphatase pathways controlled by extra-cellular ligands, Wnt, Notch, TGFbeta/BMPs, FGFs, IGFs etc.) Profiling of gene expression and genetic variation - Focus on high throughput approaches (e.g., DeepSeq, ChIP-Seq, Affymetrix microarrays, proteomics) that define gene regulatory circuitry, molecular pathways and protein/protein networks. Genetics - Focus on development in model organisms (e.g., mouse, frog, fruit fly, worm), human genetic variation, population genetics, as well as agricultural and veterinary genetics. Molecular Pathology & Regenerative Medicine - Focus on the deregulation of molecular processes in human diseases and mechanisms supporting regeneration of tissues through pluripotent or multipotent stem cells.