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Dietary fat-induced alterations in atherosclerosis are abolished by ACAT2-deficiency in ApoB100 only, LDLr-/- mice. | LitMetric

Dietary fat-induced alterations in atherosclerosis are abolished by ACAT2-deficiency in ApoB100 only, LDLr-/- mice.

Arterioscler Thromb Vasc Biol

Wake Forest University School of Medicine, Department of Pathology/Lipid Sciences, Medical Center Blvd, Winston-Salem, NC 27157, USA.

Published: June 2007

AI Article Synopsis

  • The enzyme ACAT2 in the liver converts cholesterol and fatty acids into cholesteryl esters that are important for the formation of certain lipoproteins involved in the bloodstream.
  • A study with genetically modified mice showed that those lacking ACAT2 had significantly lower cholesterol levels and atherosclerosis, regardless of the type of dietary fat they consumed.
  • The findings suggest that ACAT2 is crucial for the relationship between dietary fats and atherosclerosis development, as it impacts lipoprotein concentration and composition in the body.

Article Abstract

Objectives: The enzyme acyl-coenzymeA (CoA):cholesterol O-acyltransferase 2 (ACAT2) in the liver synthesizes cholesteryl esters (CE) from cholesterol and fatty acyl-CoA, which get incorporated into apoB-containing lipoproteins that are secreted into the bloodstream. Dietary fatty acid composition influences the amount and fatty acid composition of CE within apoB-containing lipoproteins. We hypothesized that when ACAT2 activity is removed by gene deletion, hepatic CE synthesis and secretion would be minimal and, as a result, dietary fat-related differences in atherosclerosis would be eliminated.

Methods And Results: Groups of female apoB100 only, LDLr-/- mice with and without ACAT2 were fed diets enriched in either omega-3 or omega-6 polyunsaturated fat, saturated fat, and cis or trans monounsaturated fat. After 20 weeks on diet, mice fed diets enriched in monounsaturated or saturated fat exhibited significantly higher amounts of plasma cholesterol, larger LDL particles enriched in monounsaturated CE, and more atherosclerosis than mice fed polyunsaturated fat. The dietary fat-induced shifts in plasma cholesterol, LDL size, LDL CE composition, and atherosclerosis were not observed in ACAT2-/- mice. Regardless of the diet fed, the ACAT2-/- mice were protected from atherosclerosis.

Conclusions: The results indicate that in apoB100 only, LDLr-/- mice, ACAT2 plays an essential role in facilitating dietary fat type-specific atherosclerosis through its various effects on plasma lipoprotein concentration and composition.

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Source
http://dx.doi.org/10.1161/ATVBAHA.107.142802DOI Listing

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