Document Detail


Very low and low density lipoprotein synthesis and secretion by the human hepatoma cell line Hep-G2: effects of free fatty acid.
MedLine Citation:
PMID:  3021884     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The liver is a major source of the plasma lipoproteins; however, direct studies of the regulation of lipoprotein synthesis and secretion by human liver are lacking. Dense monolayers of Hep-G2 cells incorporated radiolabeled precursors into protein ([35S]methionine), cholesterol ([3H]mevalonate and [14C]acetate), triacylglycerol, and phospholipid ([3H]glycerol), and secreted them as lipoproteins. In the absence of free fatty acid in the media, the principal lipoprotein secretory product that accumulated had a density maximum of 1.039 g/ml, similar to serum low density lipoprotein (LDL). ApoB-100 represented greater than 95% of the radiolabeled apoprotein of these particles, with only traces of apoproteins A and E present. Inclusion of 0.8 mM oleic acid in the media resulted in a 54% reduction in radiolabeled triacylglycerol in the LDL fraction and a 324% increase in triacylglycerol in the very low density lipoprotein (VLDL) fraction. Similar changes occurred in the secretion of newly synthesized apoB-100. The VLDL contained apoB-100 as well as apoE. In the absence of exogenous free fatty acid, the radiolabeled cholesterol was recovered in both the LDL and the high density lipoprotein (HDL) regions. Oleic acid caused a 50% decrease in HDL radiolabeled cholesterol and increases of radiolabeled cholesterol in VLDL and LDL. In general, less than 15% of the radiolabeled cholesterol was esterified, despite the presence of cholesteryl ester in the cell. Incubation with oleic acid did not cause an increase in the total amount of radiolabeled lipid or protein secreted. We conclude that human liver-derived cells can secrete distinct VLDL and LDL-like particles, and the relative amounts of these lipoproteins are determined, at least in part, by the availability of free fatty acid.
Authors:
J L Ellsworth; S K Erickson; A D Cooper
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Journal of lipid research     Volume:  27     ISSN:  0022-2275     ISO Abbreviation:  J. Lipid Res.     Publication Date:  1986 Aug 
Date Detail:
Created Date:  1986-12-17     Completed Date:  1986-12-17     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0376606     Medline TA:  J Lipid Res     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  858-74     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Acetates / metabolism
Apolipoproteins B / biosynthesis
Carcinoma, Hepatocellular / metabolism*,  secretion
Cell Line
Humans
Kinetics
Lipoproteins, LDL / biosynthesis*,  secretion
Lipoproteins, VLDL / biosynthesis*,  secretion
Liver / metabolism
Liver Neoplasms / metabolism*,  secretion
Methionine / metabolism
Mevalonic Acid / metabolism
Oleic Acid
Oleic Acids / metabolism
Phospholipids / metabolism
Serum Albumin, Bovine
Triglycerides / metabolism
Grant Support
ID/Acronym/Agency:
AM 18774/AM/NIADDK NIH HHS; AM07294/AM/NIADDK NIH HHS; HL 05360/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Acetates; 0/Apolipoproteins B; 0/Lipoproteins, LDL; 0/Lipoproteins, VLDL; 0/Oleic Acids; 0/Phospholipids; 0/Serum Albumin, Bovine; 0/Triglycerides; 112-80-1/Oleic Acid; 150-97-0/Mevalonic Acid; 63-68-3/Methionine

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