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 HindIII 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 HindIII 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 HindIII variant on plasma lipid levels, and the possibility of considering it a risk factor for atherosclerosis leading to CAD and stroke occurrence.

脂蛋白脂肪酶 (LPL) 被认为是脂质代谢的关键酶，特别是在酶促糖蛋白中，它为组织提供不含脂肪酸的物质，并通过循环消除甘油三酯 (TG)。 LPL 突变被证明会导致脂蛋白内成分的改变，导致动脉粥样硬化的发展，从而导致冠状动脉疾病 (CAD) 和中风的恶化。我们研究了 LPL 中的遗传变异Hind III 与脂蛋白分数、中风发生和 CAD 之间的联系。在这项病例对照研究中，我们招募了 315 名 CAD 病例和 205 名年龄匹配的对照。用纯化的PCR产物消化总共520个基因组DNA，用Hind III限制性内切酶进行限制性片段长度多态性。在研究的 CAD 组中，基因型分布按降序排列为 TT、148 (47%)、GT 135 (42.9%) 和 GG 32 (10.2%)，而对照组的模式为 GT 91 (44.4%)、TT 86 (42%) 和 GG 28 (13.7%)。在我们的研究中，所有等位基因或基因型频率均未发现显着性（p 大于 0.05），而与对照组相比，CAD 患者的 TG 和 LDL-c 生化水平则更容易升高。此外，CAD 组中风的发生率高于对照组：72 例 (22.9%) 比 7 例 (3.4%) [p < 0.000]。这可能表明Hind III 变异对血浆脂质水平的影响，并有可能将其视为动脉粥样硬化导致 CAD 和中风发生的危险因素。