期刊论文详细信息
Research in Molecular Medicine 卷:1
Analysis of the association Hind III Polymorphism of Lipoprotein Lipase gene on the risk of coronary artery disease
Zahra Hosseini Khah1  Mojgan Babanejad1  Atoosa Madadkar1  Seyed HamidJamaldini1  Mahdieh Imeni1  Tahereh Naji1  Behzad Poopak1  Mandana Hasanzad1  ReyhanehKameli1  Hamid RezaSanati1 
[1] ;
关键词: Coronary artery disease (CAD);    Lipoprotein lipase (LPL);    Hind III Polymorphism;    RFLP;    dyslipidemia;   
DOI  :  
来源: DOAJ
【 摘 要 】

Background: Coronary artery disease (CAD) is one of the leading causes of death and disabilityaroundthe world. Interaction between genetic and environmental factors determines susceptibility of an individual to develop coronary artery disease . Lipoprotein lipase (LPL) play an important role in the metabolismofHDL-C ( High Density Lipoprotein Cholesterol ), LDL-C (Low Density Lipoprotein Cholesterol ) and triglycerides (TG). Dysfunction ofLPL as a result of genetic variants oflipoprotein lipase gene is associated with increased risk of CAD. The aim of the present study was to investigate the relationship between the risk of coronary artery disease and LDL-C, HDL-C and TG(triglycerides) levels by lipoprotein lipase gene Hind III polymorphism.Materials and Methods: A total of 202 subjects including 114 patients with coronary artery disease and 88 controlparticipated in this study. The Hind III polymorphism of the lipoprotein lipase gene was determined by PCR- RFLP (Polymerase Chain Reaction-Restriction Fragment Length Polymorphism) . In the presence and absence of restriction site, thegenotypes are described H+/+ ,H-/-respectively.Results: In this survey, a highly significant association between the frequent H+/+ genotype and unfavorable TGlevels was observed in our population . For the Hind III genotypes, within the healthy subjects (n=88), the H+/+ genotype was found in 67 individuals (58.8%), H-/+ genotypein 38 individuals (33.3%) , and 9 individuals (7.8%) carried the H-/- genotype. Within the CAD group (n=114), 47 individuals (53.4%) with H+/+ genotype, 36 (41%) with H-/+ genotype, and 5 (5.6%) carried the H-/- genotype.Conclusion: There was a significant difference between the distribution ofLPL–Hind III genotypesandthehealthy subjects and the patients with CAD (P<0.05, 0. 645). LPL–Hind III polymorphisms were not detected as independentrisk factors for CAD in this study group, but had significant associations with TG levels (P<0.05).

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