The impact of omentin-1 gene polymorphisms (rs2274907 and rs2274908) on serum lipid concentrations and coronary artery disease in a sample of Iraqi individuals (A pilot study)

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, int...

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Veröffentlicht in:Clinical biochemistry 2022-02, Vol.100, p.29-34
Hauptverfasser: Al-Barqaawi, Muna Abdulridha, Al-Kashwan, Thekra A., Mahdi, Abeer Ghassan, Mirza, Teba Jabir, Amber, Khalid Ibrahim, Hussain, Majid Kadhum
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Sprache:eng
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Zusammenfassung: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 
ISSN:0009-9120
1873-2933
DOI:10.1016/j.clinbiochem.2021.11.005