PPARA L162V多态性与血脂水平的关系:Framingham后代研究

E. Tai, S. Demissie, L. Cupples, Dolores Corella, P. W. Wilson, E. J. Schaefer, J. Ordovás
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引用次数: 145

摘要

过氧化物酶体增殖物激活受体(PPAR) α是核受体超家族的一员,可调节脂肪酸氧化、细胞外脂质代谢、止血和炎症等关键蛋白。PPARA位点的L162V多态性与脂质和载脂蛋白浓度的改变有关。我们在Framingham后代研究中研究了2373名参与者(1128名男性和1244名女性)的脂质、脂蛋白和载脂蛋白之间的关系以及L162V多态性的存在。较少见的等位基因(V162)的频率为0.069。V162等位基因与男性血清总胆固醇和低密度脂蛋白胆固醇浓度升高(P =0.0012和P =0.0004)以及男性和女性血清载脂蛋白B浓度升高(P =0.009)和女性血清载脂蛋白B浓度升高(经年龄、体重指数、吸烟、使用β受体阻滞剂、利尿剂或雌激素等因素调整后P =0.03)相关。载脂蛋白(apo) C-III浓度在V162等位基因携带者中较高。在APOE位点携带E2等位基因和APOC3 3238C>G等位基因的人群中,L162V多态性与LDL胆固醇浓度的相关性最大。这表明富含甘油三酯的脂蛋白代谢的改变可能与L162V PPARA多态性观察到的LDL胆固醇增加的产生有关。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Association Between the PPARA L162V Polymorphism and Plasma Lipid Levels: The Framingham Offspring Study
Peroxisome proliferator activated receptor (PPAR) alpha is a member of the nuclear receptor superfamily that regulates key proteins involved in fatty acid oxidation, extracellular lipid metabolism, hemostasis, and inflammation. A L162V polymorphism at the PPARA locus has been associated with alterations in lipid and apolipoprotein concentrations. We studied the association among lipids, lipoproteins, and apolipoproteins and the presence of the L162V polymorphism in 2373 participants (1128 men and 1244 women) in the Framingham Offspring Study. The frequency of the less common allele (V162) was 0.069. The V162 allele was associated with increased serum concentrations of total and LDL cholesterol in men (P =0.0012 and P =0.0004, respectively) and apolipoprotein B in men (P =0.009) and women (P =0.03 after adjustment for age, body mass index, smoking, and use of &bgr;-blockers, diuretics or estrogens). Apolipoprotein (apo) C-III concentrations were higher in carriers of the V162 allele. The association of the L162V polymorphism on LDL cholesterol concentration was greatest in those who also carried the E2 allele at the APOE locus and the G allele at the APOC3 3238C>G polymorphism. This suggests that alterations in triglyceride-rich lipoprotein metabolism may be involved in the generation of the increase LDL cholesterol observed with the L162V PPARA polymorphism.
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