Effects of the acute phase response on the concentration and density distribution of plasma lipids and apolipoproteins.

Longitudinal studies were carried out in the rabbit model to determine alterations in the concentration and density distribution of plasma lipids and apolipoproteins during the acute phase response (APR) characterized by elevated levels of C-reactive protein (CRP) and serum amyloid A (SAA). Twelve h...

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Main Authors: V G Cabana, J N Siegel, S M Sabesin
Format: Article
Language:English
Published: Elsevier 1989-01-01
Series:Journal of Lipid Research
Online Access:http://www.sciencedirect.com/science/article/pii/S0022227520383905
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spelling doaj-ca06fd2cc86341ce9df3c3e65329343d2021-04-25T04:18:55ZengElsevierJournal of Lipid Research0022-22751989-01-013013949Effects of the acute phase response on the concentration and density distribution of plasma lipids and apolipoproteins.V G Cabana0J N Siegel1S M Sabesin2Department of Medicine, University of Chicago, IL 60637.Department of Medicine, University of Chicago, IL 60637.Department of Medicine, University of Chicago, IL 60637.Longitudinal studies were carried out in the rabbit model to determine alterations in the concentration and density distribution of plasma lipids and apolipoproteins during the acute phase response (APR) characterized by elevated levels of C-reactive protein (CRP) and serum amyloid A (SAA). Twelve hr after the intramuscular injection of croton oil, SAA was detectable in high density lipoprotein (HDL). At the height of the response (72 hr), HDL decreased while SAA became the major HDL apoprotein, up to 80% of the proteins in the higher density fractions. The SAA-enriched particles became denser (density of HDL3) but larger (size of HDL2), had slower electrophoretic mobility, and were depleted in apoA-I, cholesterol, triglyceride, and phospholipid. HDL-cholesterol decreased and was redistributed to other fractions while apoA-I disappeared from the circulation. During this time plasma triglycerides increased 6- to 10-fold while plasma cholesterol and phospholipids showed minimal changes. ApoB increased 5- to 6-fold while the apoB-containing particles shifted to higher density resulting in elevated IDL and then LDL during recovery. VLDL (d less than 1.006 g/ml) increased and acquired 30-40% of the plasma triglycerides, cholesterol, phospholipid, and apoB. SAA also increased in VLDL while apoE decreased.http://www.sciencedirect.com/science/article/pii/S0022227520383905
collection DOAJ
language English
format Article
sources DOAJ
author V G Cabana
J N Siegel
S M Sabesin
spellingShingle V G Cabana
J N Siegel
S M Sabesin
Effects of the acute phase response on the concentration and density distribution of plasma lipids and apolipoproteins.
Journal of Lipid Research
author_facet V G Cabana
J N Siegel
S M Sabesin
author_sort V G Cabana
title Effects of the acute phase response on the concentration and density distribution of plasma lipids and apolipoproteins.
title_short Effects of the acute phase response on the concentration and density distribution of plasma lipids and apolipoproteins.
title_full Effects of the acute phase response on the concentration and density distribution of plasma lipids and apolipoproteins.
title_fullStr Effects of the acute phase response on the concentration and density distribution of plasma lipids and apolipoproteins.
title_full_unstemmed Effects of the acute phase response on the concentration and density distribution of plasma lipids and apolipoproteins.
title_sort effects of the acute phase response on the concentration and density distribution of plasma lipids and apolipoproteins.
publisher Elsevier
series Journal of Lipid Research
issn 0022-2275
publishDate 1989-01-01
description Longitudinal studies were carried out in the rabbit model to determine alterations in the concentration and density distribution of plasma lipids and apolipoproteins during the acute phase response (APR) characterized by elevated levels of C-reactive protein (CRP) and serum amyloid A (SAA). Twelve hr after the intramuscular injection of croton oil, SAA was detectable in high density lipoprotein (HDL). At the height of the response (72 hr), HDL decreased while SAA became the major HDL apoprotein, up to 80% of the proteins in the higher density fractions. The SAA-enriched particles became denser (density of HDL3) but larger (size of HDL2), had slower electrophoretic mobility, and were depleted in apoA-I, cholesterol, triglyceride, and phospholipid. HDL-cholesterol decreased and was redistributed to other fractions while apoA-I disappeared from the circulation. During this time plasma triglycerides increased 6- to 10-fold while plasma cholesterol and phospholipids showed minimal changes. ApoB increased 5- to 6-fold while the apoB-containing particles shifted to higher density resulting in elevated IDL and then LDL during recovery. VLDL (d less than 1.006 g/ml) increased and acquired 30-40% of the plasma triglycerides, cholesterol, phospholipid, and apoB. SAA also increased in VLDL while apoE decreased.
url http://www.sciencedirect.com/science/article/pii/S0022227520383905
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