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

Publish Year: 1392
نوع سند: مقاله ژورنالی
زبان: English
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شناسه ملی سند علمی:

JR_REMJ-1-3_004

تاریخ نمایه سازی: 22 دی 1402

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) 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 ۲۰۲ subjects including ۱۱۴ patients with coronary artery disease and ۸۸ 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=۸۸), the H+/+ genotype was found in ۶۷ individuals (۵۸.۸%), H-/+ genotype in ۳۸ individuals (۳۳.۳%) , and ۹ individuals (۷.۸%) carried the H-/- genotype. Within the CAD group (n=۱۱۴), ۴۷ individuals (۵۳.۴%) with H+/+ genotype, ۳۶ (۴۱%) with H-/+ genotype, and ۵ (۵.۶%) 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<۰.۰۵, ۰. ۶۴۵). 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<۰.۰۵).

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Authors

Mahdieh Imeni

Biology Department, Islamic Azad University of pharmaceutical sciences, Tehran, Iran

Mandana Hasanzad

Medical Sciences Research Center, Tehran Medical Branch, Islamic Azad University, Tehran, Iran

Tahereh Naji

Biology Department, Islamic Azad University of pharmaceutical sciences, Tehran, Iran

Behzad Poopak

Medical Sciences Research Center, Tehran Medical Branch, Islamic Azad University, Tehran, Iran

Mojgan Babanejad

Cardiogenetics Research Center, Shahid Rajaie Cardiovascular. Medical & Research Center, Tehran University of Medical Sciences, Tehran, Iran.

Hamid Reza Sanati

Cardiogenetics Research Center, Shahid Rajaie Cardiovascular. Medical & Research Center, Tehran University of Medical Sciences, Tehran, Iran.

Reyhaneh Kameli

Biology Department, Islamic Azad University of pharmaceutical sciences, Tehran, Iran

Atoosa Madadkar

Cardiogenetics Research Center, Shahid Rajaie Cardiovascular. Medical & Research Center, Tehran University of Medical Sciences, Tehran, Iran

Zahra Hosseini Khah

Molecular and Cell Biology Research Center, Mazandaran University of Medical Science, Sari, Mazandaran, Iran

Seyed Hamid Jamaldini

Cardiogenetics Research Center, Shahid Rajaie Cardiovascular. Medical & Research Center, Tehran University of Medical Sciences, Tehran, Iran