Document Detail


Effect of ethanol on lecithin:cholesterol acyltransferase (LCAT) activity.
MedLine Citation:
PMID:  3992006     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The effect of variable doses of ethanol on plasma lecithin: cholesterol acyltransferase (LCAT) activity was examined in male, atherosclerosis-susceptible squirrel monkeys over a 12-month period. Primates were divided into three groups: 1) Controls fed isocaloric liquid diet; 2) Low Ethanol monkeys given liquid diet with vodka substituted isocalorically for carbohydrate at 12% of calories; and 3) High Ethanol animals fed diet plus vodka at 24% of calories. There were no significant differences between the treatments in serum glutamate oxaloacetate transaminase (SGOT), a measure of liver function. However, plasma LCAT activity (% esterification/min) measured in vitro was significantly reduced in High Ethanol monkeys while cholesterol esterification was elevated in the Low Ethanol group and intermediate in Controls. Similarly, the in vivo appearance of radiolabeled cholesteryl ester in high density lipoproteins (HDL) following the intravenous injection of 3H mevalonolactone was highest in the Low Ethanol primates, intermediate in Controls and significantly lower in monkeys fed the high alcohol diet. In vitro measurement of LCAT enzyme efficiency was similar for the three groups while substrate efficiency was lower in the High Ethanol treatment. Although LCAT activator (apoprotein A-I) was not markedly altered by dietary ethanol and the concentration of LCAT substrates (HDL free cholesterol and phosphatidyl choline) was significantly elevated in the High Ethanol group, subtle modifications in substrate-product composition may account for the observed reduction in cholesterol esterification. These include potential substrate and/or product LCAT inhibition resulting from increased concentrations of plasma free cholesterol, HDL lysophosphatidyl choline, and higher HDL2/HDL3 subfraction ratios, as well as alterations in HDL phospholipid fatty acid profiles in the High Ethanol group. Results from this study provide the first evidence of an anomalous enhancement in LCAT activity in nonhuman primates fed ethanol at 12% of calories and a marked depression in cholesterol esterification at the 24% dose which may be due to substrate alterations and product inhibition prior to overt biochemical evidence of liver dysfunction.
Authors:
J J Mulligan; J E Cluette-Brown; R Noring; F D Igoe; J Chong; J L Hojnacki
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Research communications in chemical pathology and pharmacology     Volume:  47     ISSN:  0034-5164     ISO Abbreviation:  Res. Commun. Chem. Pathol. Pharmacol.     Publication Date:  1985 Feb 
Date Detail:
Created Date:  1985-06-10     Completed Date:  1985-06-10     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0244734     Medline TA:  Res Commun Chem Pathol Pharmacol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  181-202     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Animals
Cholesterol Esters / analysis
Cholesterol, HDL / analysis
Ethanol / pharmacology*
Lipoproteins, HDL / analysis
Lysophosphatidylcholines / metabolism
Male
Phosphatidylcholine-Sterol O-Acyltransferase / analysis*
Phospholipids / analysis
Saimiri
Grant Support
ID/Acronym/Agency:
RR-00168/RR/NCRR NIH HHS
Chemical
Reg. No./Substance:
0/Cholesterol Esters; 0/Cholesterol, HDL; 0/Lipoproteins, HDL; 0/Lysophosphatidylcholines; 0/Phospholipids; 64-17-5/Ethanol; EC 2.3.1.43/Phosphatidylcholine-Sterol O-Acyltransferase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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