Stancáková A, Baldaufová L, Javorský M, Kozárová M, Salagovic J, Tkác I
Department of Internal Medicine IV, Faculty of Medicine, Safárik University, Kosice, Slovak Republic.
Physiol Res. 2006;55(5):483-490. doi: 10.33549/physiolres.930836. Epub 2005 Dec 12.
Dyslipidemia in the metabolic syndrome (MS) is considered to be one of the most important risk factors for atherosclerosis. It is characterized by hypertriglyceridemia, low concentration of plasma HDL-cholesterol, predominance of small dense LDL particles and an increased concentration of plasma apolipoprotein B (apoB). The pathogenesis of this type of dyslipidemia is partially explained, but its genetic background is still unknown. To evaluate the influence of cholesterol ester transfer protein (CETP) TaqIB polymorphism, lipoprotein lipase (LPL) PvuII and HindIII polymorphisms, hepatic lipase (LIPC) G-250A polymorphism and apolipoprotein C-III (APOC3) SstI gene polymorphism on lipid levels in dyslipidemia of the metabolic syndrome, 150 patients with dyslipidemia of metabolic syndrome were included. 96 % of patients had type 2 diabetes. The patients did not take any lipid lowering treatment. The exclusion criterion was the presence of any disease that could affect lipid levels, such as thyroid disorder, liver disease, proteinuria or renal failure. Gene polymorphisms were determined using the polymerase chain reaction and restriction fragment length polymorphisms. The genotype subgroups of patients divided according to examined polymorphisms did not differ in plasma lipid levels with the exception of apoB. The apoB level was significantly higher in patients with S1S1 genotype of APOC3 SstI polymorphism when compared with S1S2 group (1.10+/-0.26 vs. 0.98+/-0.21 g/l, p=0.02). Similarly, patients with H-H- genotype of LPL HindIII polymorphism had significantly higher mean apoB, compared with H+H- and H+H+ group (1.35+/-0.30 vs. 1.10+/-0.26 g/l, p=0.02). In the multiple stepwise linear regression analysis, apoB level seemed to be influenced by APOC3 SstI genotype, which explained 6 % of its variance. The present study has shown that the S1 allele of APOC3 SstI polymorphism and the H- allele of LPL HindIII polymorphism might have a small effect on apoB levels in the Central European Caucasian population with dyslipidemia of metabolic syndrome.
代谢综合征（MS）中的血脂异常被认为是动脉粥样硬化最重要的危险因素之一。其特征为高甘油三酯血症、血浆高密度脂蛋白胆固醇浓度降低、小而密低密度脂蛋白颗粒占主导以及血浆载脂蛋白B（apoB）浓度升高。这种类型血脂异常的发病机制已部分得到解释，但其遗传背景仍不清楚。为评估胆固醇酯转运蛋白（CETP）TaqIB多态性、脂蛋白脂肪酶（LPL）PvuII和HindIII多态性、肝脂肪酶（LIPC）G - 250A多态性以及载脂蛋白C - III（APOC3）SstI基因多态性对代谢综合征血脂异常患者血脂水平的影响，纳入了150例代谢综合征血脂异常患者。96%的患者患有2型糖尿病。这些患者未接受任何降脂治疗。排除标准为存在任何可能影响血脂水平的疾病，如甲状腺疾病、肝脏疾病、蛋白尿或肾衰竭。采用聚合酶链反应和限制性片段长度多态性方法测定基因多态性。除apoB外，根据检测的多态性划分的患者基因型亚组在血浆脂质水平上无差异。与S1S2组相比，APOC3 SstI多态性S1S1基因型患者的apoB水平显著更高（1.10±0.26 vs. 0.98±0.21 g/l，p = 0.02）。同样，与H + H - 和H + H + 组相比，LPL HindIII多态性H - H - 基因型患者的平均apoB显著更高（1.35±0.30 vs. 1.10±0.26 g/l，p = 0.02）。在多元逐步线性回归分析中，apoB水平似乎受APOC3 SstI基因型影响，该基因型解释了其6%的变异。本研究表明，在患有代谢综合征血脂异常的中欧白种人群中，APOC3 SstI多态性的S1等位基因和LPL HindIII多态性的H - 等位基因可能对apoB水平有较小影响。
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