J. Lipid Res.
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Journal of Lipid Research, Vol. 20, 399-407, March 1979
Copyright © 1979 by Lipid Research, Inc.

Regulation of plasma lecithin:cholesterol acyltransferase in man. III. Role of high density lipoprotein cholesteryl esters in the activating effect of a high-fat test meal

Herbert G. Rose and Joseph Juliano

Lipid Research Laboratory, Bronx VA Hospital, Bronx, NY 10468 and the Department of Medicine, Mt. Sinai School of Medicine, City University of New York, NY

Plasma lecithin:cholesterol acyltransferase (LCAT) activity is increased during the clearance phase of alimentary lipemia induced by a high-fat test meal in normal subjects. Ultracentrifugal fractionation of high density lipoproteins (HDL) into HDL2, HDL3, and very high density (VHD) subfractions followed by analyses of lipid and protein components has been accomplished at intervals during alimentary lipemia to seek associations with enzyme changes. HDL2 lipids and protein increased substantially, characterized primarily by enrichment with lecithin. HDL3, which contain the main LCAT substrates, revealed increased triglycerides and generally reduced cholesteryl esters which were reciprocally correlated, demonstrating a phenomenon previously observed in vitro by others. Both changes correlated with LCAT activation, but partial correlation analysis indicated that ester content is primarily related to triglycerides rather than LCAT activity. The VHD cholesteryl esters and lysolecithin were also reduced. Plasma incubation experiments with inactivated LCAT showed that alimentary lipemic very low density lipoproteins (VLDL) could reduce levels of cholesteryl esters in HDL by a nonenzymatic mechanism. In vitro substitution of lipemic VLDL for postabsorptive VLDL resulted in enhanced reduction of cholesteryl esters in HDL3 and VDH, but not in HDL2, during incubation. Nevertheless, augmentation of LCAT activity did not result, indicating that cholesteryl ester removal from substrate lipoproteins is an unlikely explanation for activation. Since VHD and HDL3, which contain the most active LCAT substrates, were also most clearly involved in transfers of esters to VLDL and low density lipoproteins, the suggestion that LCAT product lipoproteins are preferentially involved in nonenzymatic transfer and exchange is made. The main determinant of ester transfer, however, appears to be the level of VLDL, both in vitro and in vivo. Rose, H. G., and J. Juliano. Regulation of plasma lecithin: cholesteryl acyltransferase in man. III. Role of high density lipoprotein cholesteryl esters in the activating effect of a high-fat test meal.

Supplementary key words triglyceride:cholesteryl ester exchange • lysolecithin • primary hypertriglyceridemia • cholesterol ester equilibrium • HDL3 • HDL2 • very high density lipoprotein (VHDL)

Submitted on November 29, 1977
Revised on March 28, 1978
Accepted on October 4, 1978


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