Lipid apheresis in an animal model causes in vivo changes in lipoprotein electrophoretic patterns

Abstract

Lipid apheresis, a new extracorporeal procedure based on plasma delipidation and showing promise as a possible treatment for atherosclerosis, was recently reported for the first time from this laboratory [Cham et al., J Clin Apheresis 10:61–69. 1995]. In the present study lipid apheresis was applied to hypercholesterolemic and normocholesterolemic roosters to examine its effect on plasma lipoprotein particles. This procedure resulted in conspicuous changes in electrophoretic patterns of plasma lipoproteins. The electrophoretic mobilities of all the lipoprotein fractions had changed considerably. Lipid stainable material was present in at least three bands in the α‐globulin area. In particular, changes in the electrophoretic region of high‐density lipoproteins were observed. Lipid apheresis markedly induced the anti‐atherogenic pre‐β‐high‐density lipoproteins. The observed changes induced by lipid apheresis were more pronounced in the hyperlipidemic animals compared with the normocholesterolemic controls. A novel pre‐α‐lipoprotein band was observed soon after lipid apheresis. This lipoprotein band had a density larger than 1.21. At approximately 150 minutes after lipid apheresis, the electrophoretic pattern had almost returned to its original base pattern. Lipid apheresis results in plasma lipoprotein changes which may induce reverse cholesterol transport and shows promise as a possible treatment of atherosclerosis. © 1996 Wiley‐Liss, Inc.

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

“…LA may also increase reverse cholesterol transport by removing cholesterol from the body by way of extracting cholesterol directly from plasma which is the essence of the LA procedure [6,7,12,21].…”

“…To date, it has been shown that LA may modulate reverse cholesterol transport by increasing cholesterol efflux. This is achieved because LA results in the formation of apolipoprotein A-1 [12,21], discoidal HDL [22] and pre-beta HDL particles [7]. These HDL particles are regarded as good cholesterol acceptors from cellular cholesterol and may be important components of reverse cholesterol transport [19,20,[23][24][25].…”

“…The activity of LCAT depends on the structure apo A-1 at the interface with lipid [28]. Most recent studies have shown that LA induces changes in HDL to pre-beta-like HDL particles [7], and the latter particles are regarded as good acceptors of unesterified cholesterol of cellular origin and the preferred substrates for LCAT. This cascade of events may be of considerable importance in the overall regulation of cholesterol transport from peripheral tissues to the plasma.…”

“…This effect lasts much longer in normocholesterolaemic animals than in hypercholesterolaemic animals. It has been suggested that this differential response is due to extraplasmatic (outside the plasma compartment) cholesterol pools that are dynamically mobilizable by the apolipoproteins in the treated plasma [6,7]. Following LA, conspicuous changes in the high-density lipoprotein (HDL) and very high-density lipoprotein (VHDL) fractions have also been observed [7].…”

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

“…At approximately 150 minutes after LA, the changes in the HDL pattern had almost returned to the original pre-LA treatment patterns. 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].…”