Monounsaturated fatty acyl-CoA is predictive of atherosclerosis in human ApoB100 transgenic, LDLr-/- mice

doi:10.1194/jlr.M600526-JLR200

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A more recent version of this article appeared on May 1, 2007

Papers In Press, published online ahead of print February 4, 2007
J. Lipid Res., doi:10.1194/jlr.M600526-JLR200

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Submitted on December 11, 2006
Revised on January 18, 2007
Accepted on February 3, 2007

Monounsaturated fatty acyl-CoA is predictive of atherosclerosis in human ApoB100 transgenic, LDLr^-/- mice

Thomas A. Bell III, Martha D. Wilson, Kathryn Kelley, Janet K. Sawyer, and Lawrence L. Rudel

Dept. of Pathology / Lipid Sciences, Wake Forest University School of Medicine, Winston-Salem, NC 27157

Corresponding Author: lrudel{at}wfubmc.edu

ACAT2, the enzyme responsible for the formation of cholesteryl esters incorporated into apoB-containing lipoproteins by the small intestine and liver, forms predominately cholesteryl oleate from acyl-CoA and free cholesterol. 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 oleoyl-CoA, and values were 36% and 46% for the n-3 and n-6 polyunsaturated diet groups and 55% and 62% in saturated and monounsaturated diet groups. 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. The 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.

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