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Plasma Lecithin: Cholesterol Acyltransferase Activity in Liver Disease *
Author(s) -
Calandra S.,
Martin M. J.,
McIntyre N.
Publication year - 1971
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1111/j.1365-2362.1971.tb00642.x
Subject(s) - lecithin , sterol o acyltransferase , cholesterol , enzyme , medicine , acyltransferase , in vivo , endocrinology , chemistry , enzyme assay , reverse cholesterol transport , in vitro , lecithin—cholesterol acyltransferase , biochemistry , biology , lipoprotein , microbiology and biotechnology
. In liver disease the proportion of plasma cholesterol present in the form of ester is lower than that found in normal subjects. Recent work has suggested that a plasma enzyme, lecithin: cholesterol acyltransferase (LCAT), may be a major f actorin the physiological regulation of plasma cholesterol ester levels. In patients with a variety of hepatobiliary disorders LCAT activity was found to be reduced and a study of the effects of interaction between normal and jaundiced plasmas supported the hypothesis that the low LCAT activity was due mainly to a reduction in the plasma concentration of the enzyme. When bile salts were added to an in vitro system clear evidence of inhibition of LCAT was produced only with concentrations higher than those normally found in the plasma of patients with liver disease. This casts doubt on the suggested role of bile salts as in vivo inhibitors of the enzyme. The cholesterol ester concentration of plasma showed good correlation with its LCAT activity when this was measured in a standard substrate. Our results suggest that reduction in LCAT activity may be an important factor in the production of the low ester: free ratio found in almost all hepatic disorders.