Dietary Fat–Induced Alterations in Atherosclerosis Are Abolished by ACAT2-Deficiency in ApoB100 Only, LDLr −/− Mice | Zendy

Thomas A. Bell | Zendy; Kathryn L. Kelley | Zendy; Martha D. Wilson | Zendy; Janet K. Sawyer | Zendy; Lawrence L. Rudel | Zendy

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Dietary Fat–Induced Alterations in Atherosclerosis Are Abolished by ACAT2-Deficiency in ApoB100 Only, LDLr ^−/− Mice

Author(s) -

Thomas A. Bell,

Kathryn L. Kelley,

Martha D. Wilson,

Janet K. Sawyer,

Lawrence L. Rudel

Publication year - 2007

Publication title -

arteriosclerosis thrombosis and vascular biology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 3.007

H-Index - 270

eISSN - 1524-4636

pISSN - 1079-5642

DOI - 10.1161/atvbaha.107.142802

Subject(s) - apolipoprotein b , chemistry , ldl receptor , medicine , endocrinology , polyunsaturated fatty acid , cholesterol , cholesteryl ester , lipoprotein , intermediate density lipoprotein , fatty acid , saturated fat , biochemistry , biology , very low density lipoprotein

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.

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