Metabolic fate of VLDL apolipoproteins B and E in hepatectomized rats

Roger A. Davis, Arthur D. Hartman, Ladislav Dory, Brian J. Van Lenten, Paul S. Roheim

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)154-164
Number of pages11
JournalBiochimica et Biophysica Acta (BBA)/Lipids and Lipid Metabolism
Volume665
Issue number1
DOIs
StatePublished - 24 Jul 1981

Fingerprint

Apolipoproteins B
Apolipoproteins E
Rats
Hepatectomy
Apolipoproteins
Cholesterol
Apolipoprotein B-48
Selegiline
Ultracentrifugation
Distillation columns
HDL Lipoproteins
Fractionation
Serum
Metabolism
Liver
Sepharose
Proteins
Lipids

Keywords

  • Apolipoprotein E
  • Hepatectomy
  • VLDL metabolism

Cite this

Davis, Roger A. ; Hartman, Arthur D. ; Dory, Ladislav ; Van Lenten, Brian J. ; Roheim, Paul S. / Metabolic fate of VLDL apolipoproteins B and E in hepatectomized rats. In: Biochimica et Biophysica Acta (BBA)/Lipids and Lipid Metabolism. 1981 ; Vol. 665, No. 1. pp. 154-164.
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abstract = "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.",
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Metabolic fate of VLDL apolipoproteins B and E in hepatectomized rats. / Davis, Roger A.; Hartman, Arthur D.; Dory, Ladislav; Van Lenten, Brian J.; Roheim, Paul S.

In: Biochimica et Biophysica Acta (BBA)/Lipids and Lipid Metabolism, Vol. 665, No. 1, 24.07.1981, p. 154-164.

Research output: Contribution to journalArticle

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AB - 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.

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