Clinical biochemistry · 2021
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).
СтатьяНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Al-Barqaawi Muna Abdulridha, Al-Kashwan Thekra A, Mahdi Abeer Ghassan, Mirza Teba Jabir, Amber Khalid Ibrahim, Hussain Majid Kadhum
Аннотация
BACKGROUND: 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.
AIM: 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.
METHODS: 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.
RESULTS: 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.
CONCLUSION: 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.
AIM: 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.
METHODS: 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.
RESULTS: 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.
CONCLUSION: 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.