Association between HindIII (rs320) variant in the lipoprotein lipase gene and the presence of coronary artery disease and stroke among the Saudi population

Abstract

Lipoprotein Lipase (LPL) is known to be a key enzyme for lipid metabolism specifically in an enzymatic glycoprotein which provide tissues without fatty-acids and eliminates triglycerides (TG) by the circulation. Mutations in LPL were proven to cause alteration in fractions within lipoprotein, causing the development of atherosclerosis which predispose to weakening coronary artery disease (CAD) and stroke. We examined the linkage between genetic variant Hind III in LPL on lipoprotein fractions, stroke occurrences and CAD. In this case-control study, we have recruited 315 CAD cases and 205 age-matched controls. A total of 520 genomic DNA was digested with the purified PCR products for restriction fragment length polymorphism with Hind III restriction enzyme. The distribution of genotypes in a decreasing order were TT, 148 (47%), GT 135 (42.9%) and GG 32 (10.2%) in CAD groups of the study while the pattern in controls were GT 91 (44.4%), TT 86 (42%) and GG 28 (13.7%). None of all the allele or genotype frequencies were found to be significant in our study (p greater than 0.05), while the biochemical levels for both TG and LDL-c were shown to be prone in CAD patients when compare with the controls. Furthermore, the occurence of strokes were more in CAD groups vs. controls: 72 (22.9%) vs. 7 (3.4%) [p 0.000]. This could indicate the influence of Hind III variant on plasma lipid levels, and the possibility of considering it a risk factor for atherosclerosis leading to CAD and stroke occurrence.

Lipoprotein Lipase/Apolipoprotein Cll Gene Polymorphism in Kurdish Patients With Severe Hypertriglyceridemia

“…Regarding APO Cll-Ava ll, we observed a lower OR for A1A1 vs. A2A2 compared to A1A2 vs. A2A2, indicating that APO Cll-Ava ll gene polymorphism is a less significant genetic marker compared to H+H+ LPL-Hind III polymorphism, as reported elsewhere [4]. Recent evidence supports the association between LPL-Hind III polymorphism and both hemorrhagic stroke risk and high lipid levels in the Chinese Han population [18].…”

Study of Lipoprotein Lipase Gene Variants in Dyslipidemic Type-2 Diabetes Mellitus

“…Similarly, scientists have proposed a link between lipid serum levels and certain interactions between genetic variations and environmental considerations [9] . Results of studies that targeted LPL gene variants and their association with dyslipidemia and so predisposition to cardiac diseases and thrombotic events are conflicting, with no general agreements on the role of certain variants in the development of dyslipidemia [10] One of the most prevalent LPL gene variations is the LPL (rs320) variant at which thymine transition to guanine base occurred at position +495 in intron [4] According to NCBI LPL (rs320) variant has the major allele (T) and minor allele that is either (G) or (A), with worldwide frequencies T=79.785%, A=0.001% and G= 20.21% [12] .…”

Genetic Association of rs10757278 on Chromosome 9p21 and Coronary Artery Disease in a Saudi Population

“…The study was conducted as per the Helsinki Declaration. Our recent publication 20 described the selection of the cases and controls in detail. The inclusion criteria for the CAD cases were selected based on full assessments in the hospital premises.…”