Abstract
Role of acyl-CoA: cholesterol acyltransferase in cellular cholesterol metabolism.
Highlights
In recent years the entry of cholesterol into cells by receptor-mediated endocytosis of plasma lipoproteins and the subsequent intracellular fate of free and esterified cholesterol has received much attention by workers interested in cholesterol metabolism and its role in pathological conditions such as coronary heart disease [1]
Uptake of cholesterol leads to an increase in the amount of cholesteryl ester within the cell that is dependent on the activity of acyl-CoA:cholesterol acyltransferase (ACAT)
This ester can be secreted by the liver in very low density lipoprotein (VLDL)
Summary
In recent years the entry of cholesterol into cells by receptor-mediated endocytosis of plasma lipoproteins and the subsequent intracellular fate of free and esterified cholesterol has received much attention by workers interested in cholesterol metabolism and its role in pathological conditions such as coronary heart disease [1]. As a result of entry of cholesterol, the intracellular rate of its synthesis is reduced and its esterification with fatty acids, catalyzed by the subject of this article acyl-CoA:cholesterol acyltransferase (ACAT), is increased. The prototype for this cellular role for ACAT has been the cultured fibroblast, the model on which the low density lipoprotein (LDL) receptor pathway was originally based [2].
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