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 > 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 smaller 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 HDL1. 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.
|Number of pages||11|
|Journal||Biochimica et Biophysica Acta (BBA)/Lipids and Lipid Metabolism|
|State||Published - 24 Jul 1981|
- Apolipoprotein E
- VLDL metabolism