Document Detail


Monounsaturated fatty acyl-coenzyme A is predictive of atherosclerosis in human apoB-100 transgenic, LDLr-/- mice.
MedLine Citation:
PMID:  17277381     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
ACAT2, the enzyme responsible for the formation of cholesteryl esters incorporated into apolipoprotein B-containing lipoproteins by the small intestine and liver, forms predominantly cholesteryl oleate from acyl-CoA and free cholesterol. The accumulation of cholesteryl oleate in plasma lipoproteins has been found to be predictive of atherosclerosis. Accordingly, a method was developed in which fatty acyl-CoA subspecies could be extracted from mouse liver and quantified. Analyses were performed on liver tissue from mice fed one of four diets enriched with one particular type of dietary fatty acid: saturated, monounsaturated, n-3 polyunsaturated, or n-6 polyunsaturated. We found that the hepatic fatty acyl-CoA pools reflected the fatty acid composition of the diet fed. The highest percentage of fatty acyl-CoAs across all diet groups was in monoacyl-CoAs, and values were 36% and 46% for the n-3 and n-6 polyunsaturated diet groups and 55% and 62% in the saturated and monounsaturated diet groups, respectively. The percentage of hepatic acyl-CoA as oleoyl-CoA was also highly correlated to liver cholesteryl ester, plasma cholesterol, LDL molecular weight, and atherosclerosis extent. These data suggest that replacing monounsaturated with polyunsaturated fat can benefit coronary heart disease by reducing the availability of oleoyl-CoA in the substrate pool of hepatic ACAT2, thereby reducing cholesteryl oleate secretion and accumulation in plasma lipoproteins.
Authors:
Thomas A Bell; Martha D Wilson; Kathryn Kelley; Janet K Sawyer; Lawrence L Rudel
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2007-02-04
Journal Detail:
Title:  Journal of lipid research     Volume:  48     ISSN:  0022-2275     ISO Abbreviation:  J. Lipid Res.     Publication Date:  2007 May 
Date Detail:
Created Date:  2007-05-02     Completed Date:  2007-06-22     Revised Date:  2007-12-03    
Medline Journal Info:
Nlm Unique ID:  0376606     Medline TA:  J Lipid Res     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1122-31     Citation Subset:  IM    
Affiliation:
Department of Pathology, Section on Lipid Sciences, Wake Forest University School of Medicine, Winston-Salem, NC 27157, USA.
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MeSH Terms
Descriptor/Qualifier:
Acyl Coenzyme A / metabolism*
Animal Feed
Animals
Apolipoprotein B-100 / genetics,  metabolism*
Atherosclerosis / genetics,  metabolism*,  pathology*
Biological Markers
Cholesterol / blood
Cholesterol Esters / metabolism
Coenzyme A Ligases / metabolism
Fatty Acids / metabolism
Humans
Lipid Metabolism
Liver / drug effects,  metabolism
Mice
Mice, Transgenic
RNA, Messenger / genetics
Receptors, LDL / deficiency*,  genetics,  metabolism*
Grant Support
ID/Acronym/Agency:
AT-0027820/AT/NCCAM NIH HHS; HL-24736/HL/NHLBI NIH HHS; HL-49373/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Acyl Coenzyme A; 0/Apolipoprotein B-100; 0/Biological Markers; 0/Cholesterol Esters; 0/Fatty Acids; 0/RNA, Messenger; 0/Receptors, LDL; 57-88-5/Cholesterol; EC 6.2.1.-/Coenzyme A Ligases

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


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