Srinivasan S R, Ehnholm C, Elkasabany A, Berenson G S
Tulane Center for Cardiovascular Health, New Orleans, LA 70112, USA.
Metabolism. 2001 Jun;50(6):696-702. doi: 10.1053/meta.2001.23299.
To elucidate to what extent apolipoprotein (apo) E polymorphism modulates obesity-induced dyslipidemias during young adulthood, longitudinal data on 759 individuals (72% white/28% black; initial and follow-up mean age, 25.9 and 32.7 years) were examined. Among both races and the total sample, the apo E2 group (with E2/2 or E2/3 phenotype) had significantly lower and the apo E4 (with E4/4 or E3/4 phenotype) group higher low-density lipoprotein (LDL) cholesterol than the apo E3 (with E3/3 phenotype) group at both examinations. In addition, the apo E2 group displayed higher high-density lipoprotein (HDL) cholesterol in the total sample. No allele-specific effect was noted for the longitudinal changes (Delta). An increase in Delta adiposity, measured as Delta body mass index (BMI), was accompanied by higher increase in Delta LDL cholesterol in the e4 carriers than the e2 carriers among the whites (P <.05) and the total sample (P <.01); an increase in Delta triglycerides and decrease in Delta HDL cholesterol in the e2 carriers than the e4 carriers among all the groups (P <.05 to.001). Among the apo E phenotype groups, the incidence of high (>75th percentile specific for race and sex) LDL cholesterol at follow-up was in the order E4 > E3 > E2 both in the obese (BMI > 30; P for trend =.033) and the nonobese (BMI < 25; P for trend =.035) groups. Although the increase of low (<25th percentile specific for race and sex) HDL cholesterol or high triglycerides showed no apo E phenotype-specific trend, the incidence of high triglycerides without high LDL cholesterol was in the order E2 > E3 > E4 only in the obese group (P for trend =.025). The prevalence trend for dyslipidemias at follow-up among the persistently obese and nonobese groups also gave similar results. Thus, apo E gene locus influences not only the levels of certain lipoprotein variables during young adulthood, but also modulates the association between obesity and dyslipidemias.
为了阐明载脂蛋白（apo）E多态性在多大程度上调节青年期肥胖诱导的血脂异常，我们研究了759名个体（72%为白人/28%为黑人；初始和随访平均年龄分别为25.9岁和32.7岁）的纵向数据。在两个种族以及总样本中，apo E2组（具有E2/2或E2/3表型）在两次检查时的低密度脂蛋白（LDL）胆固醇均显著低于apo E3组（具有E3/3表型），而apo E4组（具有E4/4或E3/4表型）的LDL胆固醇则高于apo E3组。此外，在总样本中，apo E2组的高密度脂蛋白（HDL）胆固醇较高。未观察到纵向变化（Delta）的等位基因特异性效应。以Delta体重指数（BMI）衡量的Delta肥胖增加，在白人（P<.05）和总样本（P<.01）中，e4携带者的Delta LDL胆固醇增加幅度高于e2携带者；在所有组中，e2携带者的Delta甘油三酯增加幅度和Delta HDL胆固醇降低幅度高于e4携带者（P<.05至.001）。在apo E表型组中，随访时高（>第75百分位数，根据种族和性别特定）LDL胆固醇的发生率在肥胖组（BMI>30；趋势P=.033）和非肥胖组（BMI<25；趋势P=.035）中均为E4>E3>E2。虽然低（<第25百分位数，根据种族和性别特定）HDL胆固醇升高或高甘油三酯升高未显示出apo E表型特异性趋势，但仅在肥胖组中，无高LDL胆固醇的高甘油三酯发生率为E2>E3>E4（趋势P=.025）。持续肥胖组和非肥胖组随访时血脂异常的患病率趋势也得出了类似结果。因此，apo E基因位点不仅影响青年期某些脂蛋白变量的水平，还调节肥胖与血脂异常之间的关联。
