In vitro effects of lecithin:cholesterol acyltransferase on apolipoprotein distribution in familial lecithin:cholesterol acyltransferase deficiency

Glomset, J.A.; Mitchell, C.D.; King, W.C.; Applegate, K.A.; Forte, T.; Norum, K.R.; Gjone, E.

Annals of the new York Academy of Sciences 348: 224-243

1980


ISSN/ISBN: 0077-8923
PMID: 6930928
DOI: 10.1111/j.1749-6632.1980.tb21303.x
Accession: 043360227

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Abstract
Action of LCAT on the plasma of patients afflicted with familial LCAT deficiency shifts the distribution of C apolipoproteins from lipoproteins of d less than 1.019 g/ml to lipoproteins of d greater than 1.109 g/ml, and causes an opposite shift in the distribution of apolipoprotein E. The altered distribution of apolipoprotein E appears to depend primarily on enzyme-related effects on HDL. Loss of apolipoprotein E from HDL occurs as cholesteryl esters are formed and transfer to other lipoproteins; disc-shaped HDL, rich in apolipoprotein E, are converted into spherical particles; and the population of HDL as a whole is converted first into particles the size of HDL2 and HDL3 and then into intermediate-sized particles. Transfer of apolipoprotein E to artificially prepared triglyceride-rich particles occurs at a nearly linear rate that is slow than the rates of formation and transfer of cholesteryl esters or the rate of formation of "HDL2" and "HDL3." Transfer of apolipoprotein E is faster, however, when the patients' disc-shaped HDL are incubated with triglyceride-rich particles in the presence of normal plasma lipoproteins of d greater than 1.063 g/ml. Since the disc-shaped HDL, rich in apolipoprotein E, resemble particles reported to be released from perfused rat livers, they may be nascent lipoproteins of hepatic origin. If so, it appears that action of LCAT on these lipoproteins may be one of the factors that regulates the content of apolipoprotein E in VLDL.