Evidence map›Paper›PMID 22729917›Full record

ArticleMolecular biology reports2012

Six lipoprotein lipase gene polymorphisms, lipid profile and coronary stenosis in a Tunisian population.

Lamia Rebhi, Kaouther Kchok, Asma Omezzine, Slim Kacem, Jihène Rejeb, Ibtihel Ben HadjMbarek, Radhia Belkahla, Imen Boumaiza, Amira Moussa, Nabila Ben Rejeb and 4 more

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Article in Molecular biology reports, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

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11citing papers in PubMed
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1 · What the graph read from it

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3 · Its place in the literature

Who cites it

11 citing papers in PubMed.

  1. Article
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  3. Associations betweenBioscience reports · 2018
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4 · The record

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5 · Who and what money

Authors and funding

14 authors.

Lamia RebhiBiochemistry Department, Sahloul University Hospital, 4054 Sousse, Tunisia.
Kaouther Kchok
Asma Omezzine
Slim Kacem
Jihène Rejeb
Ibtihel Ben HadjMbarek
Radhia Belkahla
Imen Boumaiza
Amira Moussa
Nabila Ben Rejeb
Naoufel Nabli
Essia Boughzala
Ahmed Ben Abdelaziz
Ali Bouslama

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lipoprotein lipase (LPL) is the rate-limiting enzyme in the hydrolysis of triglyceride-rich lipoprotein particles (Chylomicrons and very-low-density lipoprotein). LPL polymorphisms' effects on lipids and coronary artery disease are controversial among studies and populations. Our aim was to study the association between six polymorphisms, haplotypes and significant coronary stenosis (SCS), disease severity and lipid parameters in Tunisian patients. LPL PvuII, 93 T/G, 188 G/E, HindIII, N291S and D9N polymorphisms were analyzed in 316 patients who underwent coronary angiography. Assessment of coronary angiograms identified SCS as the presence of stenosis >50 % in at least one major coronary artery. The stenosis severity was determined by using Gensini score and vessels number. A significant association of SCS with TT of the HindIII polymorphism was showed (odds ratio (OR): 2.84, 95 % CI, 1.19-7.40, p = 0.017) and TG (OR: 1.77, 95 % CI, 1.99-2.82, p = 0.033). The mutated HindIII genotype was significantly associated with increased TG and ApoB/ApoA-I ratio and with decreased HDL-C. Haplotype analysis showed that OR of SCS associated with the CTGTAG haplotype was 2.12 (95 % CI 1.05-4.25, p = 0.032) and with CGGGAA was 0.71 (95 % CI 0.26-1.95, p = 0.022) compared to the CTGTAA. Significant difference in Gensini score was observed among HindIII genotype and haplotypes. A significant association between the mutated genotype of HindIII polymorphism and decreased HDL-C level and increased ApoB/ApoA-I ratio and TG level was showed. Our results suggest that HindIII and D9N polymorphisms and CTGTAG haplotype seem to be considered as marker of predisposition to coronary stenosis. In another hand, HindIII and haplotypes were related to stenosis severity.

Indexed as

Polymorphism, GeneticAgedApolipoprotein A-IApolipoproteins BCoronary Artery DiseaseCoronary StenosisFemaleGenetic Predisposition to DiseaseGenotypeHaplotypesHumansLipidsLipoprotein LipaseLipoproteinsMaleMiddle AgedApolipoprotein A-IApolipoproteins BLipidsLipoprotein LipaseLipoproteinsLPL protein, human

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.