LECITHIN-CHOLESTEROL ACYLTRANSFERASE ACTIVITY IN NORMOCHOLESTEROLEMICAND HYPERCHOLESTEROLEMIC ROOSTERS - MODULATION BY LIPID APHERESIS

Citation
Km. Kostner et al., LECITHIN-CHOLESTEROL ACYLTRANSFERASE ACTIVITY IN NORMOCHOLESTEROLEMICAND HYPERCHOLESTEROLEMIC ROOSTERS - MODULATION BY LIPID APHERESIS, European journal of clinical investigation, 27(3), 1997, pp. 212-218
Citations number
28
Categorie Soggetti
Medicine, Research & Experimental","Medicine, General & Internal
ISSN journal
00142972
Volume
27
Issue
3
Year of publication
1997
Pages
212 - 218
Database
ISI
SICI code
0014-2972(1997)27:3<212:LAAIN>2.0.ZU;2-R
Abstract
Lipid apheresis, a recently described procedure for the elimination of lipid but not apolipoproteins from plasma, was applied to normocholes terolaemic and hypercholesterolaemic roosters. Lipid apheresis resulte d in an immediate reduction in plasma unesterified cholesterol concent ration, which was sustained for 150 min. The reduction in unesterified cholesterol concentration was higher in the normocholesterolaemic ani mals than in the hypercholesterolaemic animals. Lipid apheresis induce d changes in the ratio of plasma unesterified to total cholesterol in normocholesterolaemic animals but not in hypercholesterolaemic animals . In hypercholesterolaemic animals, lecithin-cholesterol acyltransfera se (LCAT) activity was not affected by lipid apheresis, whereas in nor mocholesterolaemic animals LCAT activity was acutely reduced for 150 m in after lipid apheresis. Saturated LCAT kinetics occurred in the hype rcholesterolaemic animals but not in the normocholesterolaemic animals . LCAT obeyed Michaelis-Menten kinetics. After lipid apheresis, there was a pool of unesterified cholesterol that was available as substrate for LCAT to a greater extent in hypercholesterolaemic animals than in normocholesterolaemic animals. These observations may have important implications for lipid apheresis as It treatment for atherosclerosis.