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Reverse cholesterol transport: its contribution to cholesterol catabolism in normal and disease states
Objectives:
To review the reverse cholesterol transport (RCT) model and its contribution to cholesterol catabolism in normal and disease states.
Data Sources:
Pertinent articles were identified through a MEDLINE search of the English language literature from 1983 to 1995, followed by a manual search of the bibliographies of pertinent articles.
Study Selection:
Review articles, laboratory and clinical studies and case reports.
Data Extraction:
The physiology of the RCT pathway as well as alterations observed in individuals with diseases or lifestyle changes were reviewed.
Data Synthesis:
Data were derived mainly from laboratory studies and clinical observations. The RCT model is proposed to explain the removal of excess cholesterol from extrahepatic tissues and its delivery to liver for catabolism. This involves several regulated steps mediated by the plasma apolipoproteins and two key enzymes, lecithin:cholesterol acyltransferase (LCAT) and cholesteryl ester transfer protein (CETP). In essence free cholesterol in peripheral tissues is taken up by nascent high density lipoprotein (HDL) particles, converted to cholesteryl esters (by LCAT), and then transferred to apo B-containing lipoproteins (by CETP) for hepatic removal. Altered cholesterol catabolism may occur in individuals with disorders of a genetic or acquired nature as well as lifestyle changes, as a result of alterations in one of several of the putative steps or enzymes involved in RCT.
Conclusions:
The proposed antiatherogenic role of RCT remains to be validated as a review of the possible alterations noted in various disorders showed conflicting results in atherogenic propensity.