Lipoprotein lipase gene variants: Association with acute myocardial infarction and lipid profiles

Akram Eydi,Mohammad Mehdi Jahani,Mahyar Bahrami,Sadegh Alipoor,Taghi Golmohammadi,Hamzeh Barati,Ahmad Fatemi,Zohre Sharifi

doi:10.1016/j.ejmhg.2015.04.001

Abstract

BackgroundStudies showed that lipid metabolism disorders are significant risk factors for myocardial infarction and coronary artery disease (CAD). Therefore, genes involved in lipid and lipoprotein metabolism pathways such as lipoprotein lipase (LPL), are proper candidates for susceptibility to CAD. AimTo investigate the possible association between LPL gene variants (HindIII (rs320) and PvuII (rs285)), acute myocardial infarction (AMI) and serum lipid levels. Subjects and methodsThe study population consisted of 211 patients with a diagnosis of premature AMI, and 203 age-matched individuals with normal coronary angiograms as controls. Genotyping of HindIII and PvuII polymorphisms was done by the PCR-RFLP technique. ResultsAlthough the H+ and P+ alleles were more observed among the patients, there were no significant differences in genotype distributions and allele frequencies of HindIII and PvuII polymorphisms between patient and control subjects (P>0.05). Triglyceride levels were found to be significantly elevated in H+H+ and P+P+ genotypes compared to others (P<0.05). However, there was no association between HindIII and PvuII genotypes and HDL-C, LDL-C and cholesterol levels. ConclusionOur findings indicate that LPL-HindIII and PvuII polymorphisms are not associated with acute myocardial infarction but with triglyceride levels.

Highlights

Results: the H+ and P+ alleles were more observed among the patients, there were no significant differences in genotype distributions and allele frequencies of HindIII and PvuII polymorphisms between patient and control subjects (P > 0.05)
There was no association between HindIII and PvuII genotypes and high-density lipoprotein cholesterol (HDL-C), low density lipoprotein-cholesterol (LDL-C) and cholesterol levels
Our findings indicate that lipoprotein lipase (LPL)-HindIII and PvuII polymorphisms are not associated with acute myocardial infarction but with triglyceride levels

Summary

Introduction

Epidemiological and clinical studies showed that lipid metabolism disorders such as elevated levels of total cholesterol (TC), triglycerides (TGs), low density lipoprotein cholesterol (LDLC) and low levels of high-density lipoprotein cholesterol (HDL-C) are significant risk factors for myocardial infarction and coronary artery disease [1,2]. Genes involved in lipid and lipoprotein metabolism pathways including lipoprotein lipase (LPL), are proper candidates for susceptibility to CAD [3]. The association between several polymorphic sites of LPL gene including the T-93G (rs1800590), D9N (rs1801177), G188E, N291S (rs268), PvuII (rs285), HindIII (rs320), and S447X (rs328) and CAD risk was investigated in several studies [8,9,10]. The HindIII polymorphism (rs320) is located in position 495 of LPL gene’s intron 8th In this single nucleotide polymorphism (SNP) the ancestral allele (T) is substituted by (G) allele [11]. Genes involved in lipid and lipoprotein metabolism pathways such as lipoprotein lipase (LPL), are proper candidates for susceptibility to CAD

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Conclusion