Lecithin–cholesterol acyltransferase activity in normocholesterolaemic and hypercholesterolaemic roosters: modulation by lipid apheresis

Abstract

Abstract. Lipid apheresis, a recently described procedure for the elimination of lipid but not apolipoproteins from plasma, was applied to normocholesterolaemic and hypercholesterolaemic roosters. Lipid apheresis resulted in an immediate reduction in plasma unesterified cholesterol concentration, which was sustained for 150 min. The reduction in unesterified cholesterol concentration was higher in the normocholesterolaemic animals than in the hypercholesterolaemic animals. Lipid apheresis induced changes in the ratio of plasma unesterified to total cholesterol in normocholesterolaemic animals but not in hypercholesterolaemic animals. In hypercholesterolaemic animals, lecithin-cholesterol acyltransferase (LCAT) activity was not affected by lipid apheresis, whereas in normocholesterolaemic animals LCAT activity was acutely reduced for 150 min after lipid apheresis. Saturated LCAT kinetics occurred in the hypercholesterolaemic 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 a treatment for atherosclerosis.

Not All “BAD” Cholesterol Carriers Are Necessarily Bad and Not All “GOOD” Cholesterol Carriers Are as Good as Can Be: Plasma Delipidation, a Non-Pharmacological Treatment for Atherosclerosis

“…Concomitant to the changes in the HDL pattern was the immediate reduction in plasma cholesterol concentrations, which was sustained also for 150 minutes [17]. Saturated LCAT kinetics was observed for 150 minutes after reinfusion of delipidated plasma in the hypercholesterolemic animals but not normocholesterolemic animals, suggesting that a larger pool of FC was being mobilized in the hypercholesterolemic animals [18].…”

“…Whereas, with the rooster, bovine and porcine models, all the lipoprotein classes in the plasma were delipidated. Efficacious mobilization of endogenous lipid stores including regression of atherosclerosis were obtained when plasma delipidation resulted in the removal of over 90% of cholesterols and triglycerides but retaining over 50% of phospholipids [7] [9] [16]- [18] [20]- [22]. Regression was also related to the delipidated plasma volume and frequency of LA treatment.…”

Plasma delipidation process induces rapid regression of atherosclerosis and mobilisation of adipose tissue

“…A multifunctional plasma delipidation process (PDP) for the extracorporeal removal of lipids but not apolipoproteins from plasma previously termed lipid apheresis has been reported [21][22][23][24][25][26][27][28][29][30][31]. Essentially, PDP results in acute removal of plasma lipid but the apolipoproteins and other biochemical and haematological parameters remain unaltered in the delipidated plasma [29][30][31]. PDP has been applied to cell culture studies and it was shown that there is a decrease in cholesterol supply to cells when exposed to delipidated plasma even though the cells do recognize and bind to cholesterol-free LDL [32].…”

“…Apo HDL present in the delipidated plasma removes cholesterol from cells and this activates cellular cholesteryl ester hydrolase [33][34][35]. PDP does not affect CETP [36,37] or LCAT activity in vitro [31].…”

“…In vivo studies have shown that following PDP, conspicuous changes in newly lipid containing HDL particles occurred and a relatively large pool of pre-b-HDL was formed [30]. In the PDP-treated hypercholesterolemic animals, LCAT activity was maximal whereas in PDP-treated normocholesterolemic animals, LCAT activity was reduced [31]. It was further shown that PDP in hypercholesterolemic animals resulted in quantitative removal of lipid from the liver and aorta [38].…”