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

• Main Authors: Mahdieh Imeni, Mandana Hasanzad, Tahereh Naji, Behzad Poopak, Mojgan Babanejad, Hamid Reza Sanati, Reyhaneh Kameli, Atoosa Madadkar, Zahra Hosseini Khah, Seyed Hamid Jamaldini
• Format: Article
• Language: English
• Published: Mazandaran University of Medical Sciences and Health Services 2013-11-01
• Series: Research in Molecular Medicine
• Subjects: Coronary artery disease (CAD); Lipoprotein lipase (LPL); Hind III Polymorphism; RFLP; dyslipidemia
• Online Access: http://rmm.mazums.ac.ir/browse.php?a_code=A-10-26-18&slc_lang=en&sid=1

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) play 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 control 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 highly 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 a significant difference between the distribution of LPL–Hind III genotypes and the healthy subjects and the patients with CAD (P<0.05, 0. 645). LPL–Hind III polymorphisms were not detected as independent risk factors for CAD in this study group, but had significant associations with TG levels (P<0.05).