Abstract. Lipoprotein lipase (LPL) plays a central role in lipoprotein metabolism by hydrolyzing the core triglycerides (TGs) of circulating chylomicrons and very-low-density lipoprotein (VLDL). The effects of LPL polymorphisms on lipid levels and coronary artery disease (CAD) have been inconsistent among studies and populations. To assess the lipid profiles and distributions of three LPL gene polymorphisms in Saudi patients with CAD, the HindIII, PvuII and Ser447Ter polymorphisms in the LPL gene were analyzed in 226 patients with CAD and 110 controls. Polymerase chain reaction-restriction fragment length polymorphism was used to detect LPL gene polymorphisms. The plasma lipid profiles of the patients were determined using standard enzymatic methods. Patients in the CAD group had significantly higher triglyceride (TG), total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C) levels than controls irrespective of the HindIII, PvuII or Ser447Ter genotype. Compared to the findings in controls, the HindIII TT, PvuII TC and Ser447Ter CC genotypes were associated with significantly reduced high-density lipoprotein cholesterol (HDL-C) levels in patients with CAD (P<0.0001). In summary, there are associations between LPL gene variants and high plasma TG, TC and LDL-C levels as well as low HDL-C levels.

Coronary heart disease (CHD) is a major health problem and a major cause of death in most countries. Evidence has been presented that gene polymorphisms (HindIII, PvuII and Ser447Ter) of lipoprotein lipase (LPL) are risk factors of coronary artery disease (CAD).AimOur objective of the present investigation was to determine whether 3 LPL polymorphisms (LPL-HindIII, LPL-PvuII and LPL-Ser447Ter) can be considered as independent risk factors for CAD in the Saudi population.MethodsWe recruited 120 CAD subjects, confirmed angiographically with identical ethnic backgrounds and 65 control subjects. Polymerase chain reaction-restriction fragment length polymorphisms (RFLP) technique was used to detect the polymorphisms of the LPL gene.Results and conclusionFor the HindIII genotype, within the CAD group, the frequencies of the H+H+ were found in 50.8%, whereas 44.2% carried the H−H+ genotype, and 5% carried the H−H− genotype. Within the control group, the H+H+ genotype was found in 44.6%, whereas 35.4% carried the H−H+ genotype, 20% carried the H−H− genotype. The odds ratio (OR) of HindIII genotype H+H+ vs. H−H− genotype at 95% Confidence Interval (CI) were 4.6 (1.57–13.2) and p < 0.005, hence showing no significant association with CAD. For the PvuII genotype, within the CAD group the frequencies of the P+P+ found in 41.7% whereas 43.3.2% carried the P−P+ genotype, and 15% carried the P−P− genotype. Within the control group the P+P+ was found in 38.5%, 43.0% carried the P−P+ genotype, and 18.5% carried the P−P− genotype. The OR of PvuII genotype P+P+ vs. P−P− genotypes (95% CI) is 1.33 and p = 0.52; hence, it was also insignificant to show association with the disease. For the Ser447Ter genotype, within the CAD group, the frequencies of the C/C found in 83.3%, whereas 16.7% carried the C/G genotype. Within the control group, the C/C was found in 87.7% and 12.3% carried the C/G genotype. We did not get any GG genotypes in control as well as patients for this gene. It can be concluded that C allele of gene masks the presence of G allele in the Saudi population. The OR of CG + GG vs. CC (95% CI) is 1.43 from 0.59 to 3.44 which is insignificant. Hence this gene also has no significant association with CAD in the Saudi population.

BackgroundThe polymorphisms in the components of the renin-angiotensin system (RAS) are important in the development and progression of coronary artery disease (CAD) in some individuals. Our objectives in the present investigation were to determine whether three RAS polymorphisms, angiotensin-converting enzyme insertion/deletion (ACE I/D), angiotensin receptor II (Ang II AT2 - C3123A) and angiotensinogen (AGT-M235T), are associated with CAD in the Saudi population. We recruited 225 subjects with angiographically confirmed CAD who had identical ethnic backgrounds and 110 control subjects. The polymerase chain reaction-restriction fragment length polymorphisms (RFLP) technique was used to detect polymorphisms in the RAS gene.ResultsWithin the CAD group, for the ACE I/D genotype, DD was found in 64.4%, 26.3% carried the ID genotype, and 9.3% carried the II genotype. Within the control group, the DD genotype was found in 56.4%, 23.6% carried the ID genotype, and 20% carried the II genotype. The odds ratio (OR) of the ACE DD vs II genotype with a 95% confidence interval (CI) was 2.45 (1.26-4.78), with p = 0.008. For the Ang II AT2 receptor C3123A genotype, within the CAD group, CC was found in 39.6%, 17.8% carried the CA genotype, and 42.6% carried the AA genotype. Within the control group, CC was found in 39.1%, 60.9% carried the CA genotype, and there was an absence of the AA genotype. The OR of the Ang II AT2 receptor C3123A CC vs AA genotypes (95% CI) was 0.01, with p = 0.0001. A significant association with CAD was shown. For the AGT-M235T genotype, within the CAD group, MM was found in 24.0%, 43.6% carried the MT genotype and 32.4% carried the TT genotype. Within the control group, MM was found in 26.4%, 45.5% carried the TT genotype and 28.2% carried the MT genotype. The OR of MM vs TT (95% CI) was 0.79 (0.43 to 1.46), which was insignificant.ConclusionsThere is an association between the ACE I/D and Ang II AT2 receptor C3123A polymorphisms and CAD, however, no association was detected between the AGT M235T polymorphism and CAD in the Saudi population.

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