Alvarez J J, Montelongo A, Iglesias A, Lasunción M A, Herrera E
Departamento de Investigación, Hospital Ramón y Cajal, Madrid, Spain.
J Lipid Res. 1996 Feb;37(2):299-308.
To understand the mechanism responsible for maternal hyperlipidemia, 25 healthy pregnant women were studied longitudinally during the three trimesters of gestation and at post-partum, and 11 were studied again at post-lactation. Triglyceride and cholesterol levels increased with gestation in all the lipoprotein fractions. However, the greatest change appeared in low density (LDL) and high density (HDL) lipoproteins, both of which showed an increase in their triglyceride/cholesterol ratio. The proportional distribution of HDL subfractions showed that the HDL2b fraction was the only one that increased with gestation, whereas both HDL3a and HDL3b had the greatest decrease. Cholesteryl ester transfer protein activity increased during the second trimester of gestation. While postheparin lipoprotein lipase activity decreased during the third trimester, postheparin hepatic lipase activity progressively decreased from the first trimester. The 17 beta-estradiol, progesterone, and prolactin hormones progressively increased from the first trimester of gestation. The lipoprotein-triglyceride values correlated linearly and negatively with the logarithm of either postheparin lipase activities, HDL-triglycerides showing the highest correlation coefficient when plotted against the hepatic lipase values (r = -0.757). It appeared that the highest correlation between any of the HDL subclasses and the activity of the enzymes was for hepatic lipase activity versus HDL2b (r = 0.456) or HDL3a (r = 0.519). A significant lineal correlation also appeared between the postheparin hepatic lipase activity and the logarithm of any of the sex hormones studied, the highest value corresponding to estradiol (r = -0.783). Therefore, during gestation, the effect of estrogen in enhancing very low density lipoprotein (VLDL) production and decreasing hepatic lipase activity plays a key role in the accumulation of triglycerides in lipoproteins of density higher than VLDL.
为了解孕产妇高脂血症的发病机制，对25名健康孕妇在妊娠三期及产后进行了纵向研究，11名孕妇在哺乳期后再次接受研究。所有脂蛋白组分中的甘油三酯和胆固醇水平均随妊娠进展而升高。然而，最大的变化出现在低密度脂蛋白（LDL）和高密度脂蛋白（HDL）中，二者的甘油三酯/胆固醇比值均升高。HDL亚组分的比例分布显示，HDL2b亚组分是唯一随妊娠增加的，而HDL3a和HDL3b亚组分下降最为明显。胆固醇酯转运蛋白活性在妊娠中期增加。虽然肝素后脂蛋白脂肪酶活性在妊娠晚期降低，但肝素后肝脂肪酶活性从妊娠早期开始逐渐下降。17β-雌二醇、孕酮和催乳素激素从妊娠早期开始逐渐升高。脂蛋白甘油三酯值与肝素后脂肪酶活性的对数呈线性负相关，当以肝脂肪酶值作图时，HDL甘油三酯显示出最高的相关系数（r = -0.757）。似乎任何HDL亚类与酶活性之间的最高相关性是肝脂肪酶活性与HDL2b（r = 0.456）或HDL3a（r = 0.519）之间的相关性。肝素后肝脂肪酶活性与所研究的任何一种性激素的对数之间也出现了显著的线性相关性，最高值对应于雌二醇（r = -0.783）。因此，在妊娠期间，雌激素增强极低密度脂蛋白（VLDL）生成并降低肝脂肪酶活性的作用在高于VLDL密度的脂蛋白中甘油三酯的蓄积中起关键作用。
