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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2007;27:1228.)
© 2007 American Heart Association, Inc.

Editorials

LDL Cholesteryl Oleate

A Biomarker for Atherosclerosis?

Arthur A. Spector; William G. Haynes

From the Departments of Biochemistry (A.A.S.) and Internal Medicine (A.A.S., W.G.H.), Carver College of Medicine, University of Iowa, Iowa City.

Correspondence to Arthur A. Spector, Department of Biochemistry 4-403 BSB, University of Iowa, Iowa City, IA 52242. E-mail arthur-spector@uiowa.edu

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Cholesteryl esters (CE) are synthesized by 2 enzymes, lecithin:cholesterol acyltransferase (LCAT) and acylCoA:cholesterol acyltransferase (ACAT). LCAT functions in the plasma and forms CE in HDL by transferring polyunsaturated fatty acid from phosphatidylcholine to cholesterol. ACAT, which functions intracellularly, uses fatty acid from acylCoA and forms CE enriched in monounsaturated fatty acid. Two isoforms of ACAT are expressed.¹ ACAT1 is present in many tissues and produces the CE that are stored intracellularly, whereas ACAT2 is expressed in the intestine and liver and produces the CE that are secreted in chylomicrons and VLDL.²

See page 1396

In this issue of Arteriosclerosis, Thrombosis, and Vascular Biology, Bell et al report that ACAT2 gene deletion prevents hypercholesterolemia and atherosclerosis induced by diets containing 10% saturated or monounsaturated fat in a murine model of high LDL apoB100 only, LDL receptor-deleted (LDLr^–/–) mice.³ These mice also had larger LDL particle size and hypertriglyceridemia. They attribute the protection of ACAT2 deficiency to a decrease in LDL particles enriched in CE derived from oleate (monounsaturated). When the diet contains large amounts of monounsaturated fats, ACAT2 activity appears to favor production of VLDL particles containing an excessive amount of cholesteryl oleate,⁴ and these monounsaturated CE remain associated with the lipoprotein particle when it undergoes conversion to LDL. These findings remind us that CE synthesized in the liver can be a source of CE for LDL, a fact that tends to be overlooked because of the current emphasis on the role of the reverse cholesterol transport pathway and . . . [Full Text of this Article]

Related Article:

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

Thomas A. Bell, III, Kathryn Kelley, Martha D. Wilson, Janet K. Sawyer, and Lawrence L. Rudel
Arterioscler Thromb Vasc Biol 2007 27: 1396-1402. [Abstract] [Full Text] [PDF]