Six lipoprotein lipase gene polymorphisms, lipid profile and coronary stenosis in a Tunisian population.
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.
Biochemistry Department, Sahloul University Hospital, 4054 Sousse, Tunisia.
Lamia
L
Rebhi
Kaouther
K
Kchok
Asma
A
Omezzine
Slim
S
Kacem
Jihène
J
Rejeb
Ibtihel
I
Ben HadjMbarek
Radhia
R
Belkahla
Imen
I
Boumaiza
Amira
A
Moussa
Nabila
N
Ben Rejeb
Naoufel
N
Nabli
Essia
E
Boughzala
Ahmed
A
Ben Abdelaziz
Ali
A
Bouslama
D000368:Aged; D016632:Apolipoprotein A-I / Q000235:genetics; D001055:Apolipoproteins B / Q000235:genetics; D003324:Coronary Artery Disease / Q000235:genetics; D023921:Coronary Stenosis / Q000208:ethnology / Q000235:genetics*; D005260:Female; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006239:Haplotypes; D006801:Humans; D008055:Lipids / Q000235:genetics; D008071:Lipoprotein Lipase / Q000097:blood / Q000235:genetics*; D008074:Lipoproteins / Q000097:blood; D008297:Male; D008875:Middle Aged; D011110:Polymorphism, Genetic; D014416:Tunisia
D016632:Apolipoprotein A-I; D001055:Apolipoproteins B; D008055:Lipids; D008074:Lipoproteins; C548261:LPL protein, human; D008071:Lipoprotein Lipase