Analysis of the association Hind III Polymorphism of Lipoprotein Lipase gene on the risk of coronary artery disease

Abstract

Background: Coronary artery disease (CAD) is one of the leading causes of death and disability around the world. Interaction between genetic and environmental factors determines susceptibility of an individual to develop coronary artery disease. Lipoprotein lipase (LPL) plays an important role in the metabolism of HDL-C (High Density Lipoprotein Cholesterol), LDL-C (Low Density Lipoprotein Cholesterol) and triglycerides (TG). Dysfunction of LPL as a result of genetic variants of lipoprotein 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 controls participated 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, the genotypes are described H+/+, H-/respectively. Results: In this survey, a significant association between the frequent H+/+ genotype and unfavorable TG levels 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-/+ genotype in 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 no significant difference between the distribution of LPL-Hind III genotypes and the healthy subjects and the patients with CAD (P<0.05, 0. 645). The study of LPL genotypes confirms the existence of interrelations between TG levels (P<0.05), but this polymorphisms were not detected as independent risk factors for CAD (P<0.05).

Lipoprotein Lipase/Apolipoprotein Cll Gene Polymorphism in Kurdish Patients With Severe Hypertriglyceridemia

“…According to our statistical analysis, the H+H+ LPL-Hind lll polymorphism was the strongest genetic marker of susceptibility to severe hypertriglyceridemia, which was similar to the results of other studies [17]. The effect of the LPL-Hind III polymorphism on lipid parameters has not demonstrated the same consistency across other populations.…”

Dyslipidemia: Genetics, lipoprotein lipase and HindIII polymorphism

“…In a more recent study, it was established that the presence of homozygous genotype for the common allele (H+/H+) of the LPL gene is a risk factor for a first episode of myocardial infarction 65 . Conversely, studies by Imeni et al 78 in an Iranian population, showed no statistically significant associations between CAD and genotypic distributions of HindIII polymorphism. 80 .…”

Dyslipidemia: Genetics, lipoprotein lipase and HindIII polymorphism

“…Conversely, studies by Imeni et al . 78 in an Iranian population, showed no statistically significant associations between CAD and genotypic distributions of HindIII polymorphism.…”