肝切除大鼠中极低密度脂蛋白载脂蛋白B和E的代谢命运

Davis R A, Hartman A D, Dory L, Van Lenten B J, Roheim P S

Biochim Biophys Acta. 1981 Jul 24;665(1):154-64. doi: 10.1016/0005-2760(81)90243-5.

The metabolic fate of VLDL apolipoproteins B and E was examined in functionally hepatectomized rats. 1 h after hepatectomy, there was almost complete absence of ultracentrifugally isolated VLDL lipid and protein, including apolipoproteins B and E. Analysis of apolipoprotein concentrations by electroimmunoassay showed hepatectomy did not affect the total serum concentrations of apolipoproteins B and E; thus, hepatectomy caused a redistribution of these apolipoproteins from VLDL to higher density lipoproteins. In the LDL (d = 1.03--1.063 g/ml) fraction, hepatectomy, increased the concentrations of free cholesterol (40%), esterified cholesterol (57%) and protein (18--67%), due to an increase in apolipoproteins B (22--48%) and E (250--300%). After hepatectomy, the HDL fraction accumulated the greatest total amount of apolipoprotein E. Since the majority of apolipoprotein E was isolated in the d greater than 1.21 g/ml fraction after sequential ultracentrifugation, the redistribution of apolipoproteins B and E was further defined by fractionation of serum on 5 M agarose columns. Electroimmunoassay of the column fractions showed that the apolipoprotein B peak eluted before the apolipoprotein E peak. Although a considerable portion of apolipoprotein E eluted with A-I, the peak of apolipoprotein E eluted before the A-I peak in both groups. These data suggest that a portion of apolipoprotein E is associated with particles which are similar than LDL but are larger than A-I-rich HDL. Hepatectomy caused an accumulation of apolipoprotein B in LDL, and apolipoprotein E and cholesterol in particles which were smaller than LDL and may represent LDL1. It is likely that under normal physiological conditions the liver plays a role in the removal of these apolipoprotein E-rich particles which are derived, at least in part, from the metabolism of VLDL.

在功能性肝切除的大鼠中研究了极低密度脂蛋白（VLDL）载脂蛋白B和E的代谢命运。肝切除术后1小时，通过超速离心分离的VLDL脂质和蛋白质几乎完全消失，包括载脂蛋白B和E。用电免疫测定法分析载脂蛋白浓度表明，肝切除术不影响血清中载脂蛋白B和E的总浓度；因此，肝切除术导致这些载脂蛋白从VLDL重新分布到更高密度的脂蛋白中。在低密度脂蛋白（LDL，d = 1.03 - 1.063 g/ml）组分中，肝切除术使游离胆固醇浓度增加了40%，酯化胆固醇浓度增加了57%，蛋白质浓度增加了18% - 67%，这是由于载脂蛋白B增加了22% - 48%，载脂蛋白E增加了250% - 300%。肝切除术后，高密度脂蛋白（HDL）组分积累了最大总量的载脂蛋白E。由于在连续超速离心后，大部分载脂蛋白E存在于d大于1.21 g/ml的组分中，通过在5M琼脂糖柱上对血清进行分级分离进一步明确了载脂蛋白B和E的重新分布。对柱分级分离物进行电免疫测定表明，载脂蛋白B峰在载脂蛋白E峰之前洗脱。尽管相当一部分载脂蛋白E与载脂蛋白A-I一起洗脱，但两组中载脂蛋白E峰均在载脂蛋白A-I峰之前洗脱。这些数据表明，一部分载脂蛋白E与比LDL相似但比富含载脂蛋白A-I的HDL更大的颗粒相关。肝切除术导致LDL中载脂蛋白B的积累，以及比LDL小且可能代表LDL1的颗粒中载脂蛋白E和胆固醇的积累。在正常生理条件下，肝脏可能至少部分地参与了对这些富含载脂蛋白E的颗粒的清除，这些颗粒至少部分源自VLDL的代谢。