Taskinen M R, Kuusi T, Yki-Järvinen H, Nikkilä E A
Second Department of Medicine, University of Helsinki, Finland.
J Clin Endocrinol Metab. 1988 Aug;67(2):291-9. doi: 10.1210/jcem-67-2-291.
To study the effects of short term low dose prednisone administration on serum lipids and lipoproteins we measured the concentration and composition of serum lipoproteins; serum apoproteins (apo) A-I, A-II, and B; and plasma lipolytic enzymes before and during prednisone administration (30 mg/day for 7 days) in eight normal men. We also measured insulin binding to adipocytes. Serum high density lipoprotein (HDL) cholesterol increased significantly after 2 days of prednisone administration; the maximal increase was 27% (P less than 0.01 after 5 days). The rise of HDL cholesterol was accounted for by that of HDL2 cholesterol. There were marked changes in the distribution of HDL particles; HDL2 increased, whereas HDL3 decreased. These changes were also apparent after 2 days of prednisone administration and were maximal at 5 days [mean, 1.58 +/- 0.12 (+/- SE) vs. 2.00 +/- 0.14 g/L (P less than 0.001) for HDL2; 1.82 +/- 0.11 vs. 1.61 +/- 0.06 g/L (P less than 0.05) for HDL3], and they were due to opposing changes in cholesterol, phospholipids, and proteins in the HDL subfractions. The change in HDL2 protein correlated inversely with that in HDL3 protein (r = -0.73; P less than 0.05). Notably, prednisone did not change the apo A-I concentration, but that of apo A-II decreased (0.32 +/- 0.02 vs. 0.27 +/- 0.01 g/L; P less than 0.05). Consequently, the lipid to protein ratio of HDL increased. Prednisone induced no significant changes in very low density or low density (LDL) lipoproteins. Adipose tissue LPL activity did not increase until after 7 days of prednisone intake (1.10 +/- 0.28 vs. 3.43 +/- 1.02 mumol FFA/g.h; P less than 0.05), and the same was true for muscle LPL (0.49 +/- 0.14 vs. 0.82 +/- 0.11 mumol FFA/g.h; n = 4; P = 0.06). Specific insulin binding was normal, but both basal and maximal insulin-stimulated glucose transport decreased significantly. In summary, prednisone induces changes in serum HDL which are characterized by redistribution of particles within HDL density toward less dense particles and a quantitative rise of lipids in the HDL2 fraction.
为研究短期小剂量泼尼松给药对血清脂质和脂蛋白的影响，我们测定了8名正常男性在服用泼尼松（30毫克/天，共7天）之前及期间的血清脂蛋白浓度和组成、血清载脂蛋白（apo）A-I、A-II和B以及血浆脂解酶。我们还测定了胰岛素与脂肪细胞的结合情况。服用泼尼松2天后，血清高密度脂蛋白（HDL）胆固醇显著升高；最大增幅为27%（5天后P<0.01）。HDL胆固醇的升高是由HDL2胆固醇的升高引起的。HDL颗粒的分布有明显变化；HDL2增加，而HDL3减少。这些变化在服用泼尼松2天后也很明显，并在5天时达到最大[HDL2的平均值，1.58±0.12（±标准误）与2.00±0.14克/升（P<0.001）；HDL3的平均值，1.82±0.11与1.61±0.06克/升（P<0.05）]，这是由于HDL亚组分中胆固醇、磷脂和蛋白质的相反变化所致。HDL2蛋白质的变化与HDL3蛋白质的变化呈负相关（r=-0.73；P<0.05）。值得注意的是，泼尼松没有改变apo A-I的浓度，但apo A-II的浓度降低了（0.32±0.02与0.27±0.01克/升；P<0.05）。因此，HDL的脂质与蛋白质比值增加。泼尼松对极低密度或低密度（LDL）脂蛋白没有显著影响。脂肪组织脂蛋白脂肪酶（LPL）活性直到服用泼尼松7天后才增加（1.10±0.28与3.43±1.02微摩尔游离脂肪酸/克·小时；P<0.05），肌肉LPL也是如此（0.49±0.14与0.82±0.11微摩尔游离脂肪酸/克·小时；n=4；P=0.06）。特异性胰岛素结合正常，但基础和最大胰岛素刺激的葡萄糖转运均显著降低。总之，泼尼松诱导血清HDL发生变化，其特征是HDL密度范围内的颗粒重新分布向密度较低的颗粒，以及HDL2组分中脂质的定量增加。
