Liu Jun, Zhao Dong, Liu Jing, Liu Sa, Qin Lan-ping, Wu Zhao-su
Department of Epidemiology, Beijing Institute of Heart, Lung and Blood Vessel Diseases, Beijing 100029, China.
Zhonghua Yi Xue Za Zhi. 2005 May 25;85(19):1339-43.
To study the effect of lipoprotein lipase (LPL)-HindIII and PvuII polymorphisms on preheparin plasma LPL concentration and triglyceride.
A cross-sectional study was carried out in a general population of Beijing in 1999, using stratified-random sampling method. LPL-HindIII and PvuII polymorphism and preheparin plasma LPL concentration were determined in 670 individuals aged 45 - 64.
(1) The frequencies of H1H1, H1H2, and H2H2 genotypes were 0.646, 0.322, and 0.031 respectively; and the frequencies of P1P1, P1P2, and P2P2 genotypes were 0.410, 0.472, and 0.118 respectively. The distribution of genotypes and that of alleles were homogeneous in both sexes. (2) The plasma LPL concentrations of the 12 type heterozygotes (H1H2 and P1P2) and those of the 22 type (H2H2 and P2P2) homozygotes were all higher than that of the 11 type homozygotes (H1H1 and P1P1) (all P < 0.01). And the LPL concentration varied greatly among different individuals of the same genotype. (3) Smoking, alcohol consumption, BMI, and waist level influenced LPL concentration more significantly in the H1H1 and P1P1 homozygotes and P1P2 heterozygotes. Multivariate analysis showed that smoking and obesity were independent influencing factors of serum LPL concentration (both P < 0.01). (4) The prevalence rate of hypertriglyceridemia was significantly different among different genotypes, the 11 type homozygotes having the highest rate, and the 22 type homozygotes having the lowest. In the same genotype, along with the increase of the serum LPL concentration the prevalence of hypertriglyceridemia decreased (P < 0.05).
LPL-HindIII and PvuII polymorphisms are determinants of plasma LPL concentration. This genetic effect can be modified by some environmental factors, such as smoking and obesity.
研究脂蛋白脂肪酶(LPL)-HindIII和PvuII基因多态性对肝素化前血浆LPL浓度及甘油三酯的影响。
1999年采用分层随机抽样方法,对北京市普通人群进行横断面研究。测定了670名45 - 64岁个体的LPL-HindIII和PvuII基因多态性以及肝素化前血浆LPL浓度。
(1)H1H1、H1H2和H2H2基因型频率分别为0.646、0.322和0.031;P1P1、P1P2和P2P2基因型频率分别为0.410、0.472和0.118。基因型和等位基因分布在两性中均呈均匀分布。(2)12型杂合子(H1H2和P1P2)和22型纯合子(H2H2和P2P2)的血浆LPL浓度均高于11型纯合子(H1H1和P1P1)(均P < 0.01)。且同一基因型的不同个体间LPL浓度差异很大。(3)吸烟、饮酒、BMI和腰围对H1H1和P1P1纯合子以及P1P2杂合子的LPL浓度影响更显著。多因素分析显示吸烟和肥胖是血清LPL浓度的独立影响因素(均P < 0.01)。(4)高甘油三酯血症患病率在不同基因型间有显著差异,11型纯合子患病率最高,22型纯合子患病率最低。在同一基因型中,随着血清LPL浓度升高,高甘油三酯血症患病率降低(P < 0.05)。
LPL-HindIII和PvuII基因多态性是血浆LPL浓度的决定因素。这种遗传效应可被一些环境因素如吸烟和肥胖所改变。