Lipopolysaccharide toxin can directly stimulate the intracellular accumulation of lipids and their secretion into medium in the primary culture of rabbit hepatocytes

Low doses (0.1–0.3 μg ml per 10 6 cells) of the lipopolysaccharide toxin (LPS) from Salmonella typhimurium were shown to increase (after an 18 h incubation) the intracellular content of free cholesterol (CH), esterified cholesterol (EC) and triglycerides (TG) by 30–40% in the primary culture of rabb...

Full description

Saved in:
Bibliographic Details
Published in:FEBS letters Vol. 256; no. 1; pp. 155 - 158
Main Authors: Victorov, A.V., Gladkaya, E.M., Novikov, D.K., Kosykh, V.A., Yurkiv, V.A.
Format: Journal Article
Language:English
Published: Amsterdam Elsevier B.V 09-10-1989
Elsevier
Subjects:
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Low doses (0.1–0.3 μg ml per 10 6 cells) of the lipopolysaccharide toxin (LPS) from Salmonella typhimurium were shown to increase (after an 18 h incubation) the intracellular content of free cholesterol (CH), esterified cholesterol (EC) and triglycerides (TG) by 30–40% in the primary culture of rabbit hepatocytes. A similar increase was found for the incorporation of [ 14C]acetate into these lipids. The concentration of lipids in cultural medium, under these conditions, was also augmented: by 30–40% for CH; by 50–60% for TG and by 60–80% for EC. Higher doses (up to 50 μg ml ) of LPS hardly affected the lipid content in hepatocytes but strongly (by two-fold) inhibited the secretion of lipids. It is suggested that in vivo low concentrations of LPS in bloodstream (in the absence of conspicuous pathology) might induce hyperlipidemia directly influencing on hepatic cells, while, under the higher concentrations of LPS, hyperlipidemia caused by cachectin (or tumor necrosis factor) is probably observed. Lipopolysaccharide toxin; Hyperlipidemia; (Rabbit hepatocyte)
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:0014-5793
1873-3468
DOI:10.1016/0014-5793(89)81738-7