Literature DB >> 1988004

Net mass transfer of cholesteryl esters from low density lipoproteins to high density lipoproteins in plasma from normolipidemic subjects.

A Van Tol1, L M Scheek, J E Groener.   

Abstract

Net mass transfer of lipids was measured in plasma from fasted, normolipidemic subjects. The plasma was incubated, and lipoproteins were subsequently separated by polyanion precipitation or density gradient ultracentrifugation. Total cholesterol, unesterified cholesterol, and triglycerides were measured in the isolated lipoprotein fractions. The rate of cholesterol esterification was measured simultaneously. All plasma samples showed an increase in high density lipoprotein (HDL) cholesteryl esters during 1-hour incubations. In most cases, this increase was higher than the cholesteryl ester formation in total plasma due to cholesterol esterification. Therefore, we concluded that a net mass transfer of cholesteryl esters occurred from the very low plus low density lipoprotein (VLDL + LDL) fractions to HDL in plasma from most of the subjects studied. Transfer of triglycerides occurred from VLDL + LDL to HDL in plasma from all subjects. The cholesteryl ester transfer (measured after 1 hour) is not related to the activity of cholesteryl ester transfer protein. Inhibition of cholesterol esterification did not change the direction of cholesteryl ester or triglyceride transfer. Ultracentrifugal separation of plasma lipoproteins revealed that both HDL and VLDL are acceptors of cholesteryl esters and that VLDL donates triglycerides to both LDL and HDL. Removal of VLDL from plasma by ultracentrifugation did not affect the cholesteryl ester transfer from LDL to HDL. We conclude that LDL may act as a donor of cholesteryl esters during incubation of normolipidemic plasma.

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Year:  1991        PMID: 1988004     DOI: 10.1161/01.atv.11.1.55

Source DB:  PubMed          Journal:  Arterioscler Thromb        ISSN: 1049-8834


  2 in total

1.  Changes in high density lipoprotein subfraction lipids during neutral lipid transfer in healthy subjects and in patients with insulin-dependent diabetes mellitus.

Authors:  M C Ritter; J D Bagdade
Journal:  Lipids       Date:  1996-01       Impact factor: 1.880

2.  Mechanism of inhibition defines CETP activity: a mathematical model for CETP in vitro.

Authors:  Laura K Potter; Dennis L Sprecher; Max C Walker; Frank L Tobin
Journal:  J Lipid Res       Date:  2009-03-11       Impact factor: 5.922

  2 in total

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