Author/Authors :
Imeni، Mahdieh نويسنده Biology Department , Islamic Azad University of pharmaceutical sciences, Tehran ,Iran , , Hasanzad، Mandana نويسنده Tehran Medical Branch, Islamic Azad University, Tehran , , Naji، Tahere نويسنده Biology Department , Islamic Azad University of pharmaceutical sciences, Tehran ,Iran , , Poopak، Behzad نويسنده Hematology Department, Islamic Azad University, Tehran Medical Branch, Tehran, Iran , , Babanejad، Mojgan نويسنده Cardiogenetics Research Center , Shahid Rajaie Cardiovascular Medical & Research Center, Tehran University of Medical Sciences , Tehran, Iran , , Sanati، Hamid Reza نويسنده Cardiovascular Intervention Research Center, Shaheed Rajaei Cardiovascular Medical and Research Center, Iran University of Medical Sciences, Tehran, , , Kameli، Reyhaneh نويسنده Biology Department , Islamic Azad University of pharmaceutical sciences, Tehran ,Iran , , Madadkar، Atoosa نويسنده Cardiogenetics Research Center , Shahid Rajaie Cardiovascular Medical & Research Center, Tehran University of Medical Sciences , Tehran, Iran , , Hosseini-khah، Zahra نويسنده Molecular and cell biology cente , Faculty of medicine, Mazandaran University of Medical Sciences, Sari, Iran Hosseini-khah, Zahra , Jamaldini، Seyed Hamid نويسنده Genetics Research Center, University of Social Welfare and Rehabilitation Sciences, Tehran ,
Abstract :
Background and Aim: 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.
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 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).
