Advances in understanding of the role of lecithin cholesterol acyltransferase (LCAT) in cholesterol transport

We review the structure and function of lecithin cholesterol acyl transfera se (LCAT), the advances in the studies of molecular genetics of LCAT and it s deficiency states as well as the developments in assessment of LCAT activ ity particularly the concept of measurement of fractional esterification ra te of plasma cholesterol in the absence of apoB lipoproteins (FERHDL) as an indication of atherogenic risk. We discuss LCAT reaction from two points o f view: one that is consistent with the general belief in LCAT antiatheroge nic potential and another, namely, a proposed concept of potentially opposi ng roles of LCAT in normal and dyslipidemic plasmas. While other plasma lip oproteins can (in addition to HDL) provide unesterified cholesterol (UC) fo r LCAT reaction, HDL may play an unique role in trafficking of newly formed cholesteryl esters (CE) rather than as a primary acceptor of cellular chol esterol. Thus, the plasma HDL, specifically the larger (HDL2b) particles, d irect the efflux of most of (LCAT produced) CE to its specific catabolic si tes rather than to potentially atherogenic VLDLs and back to LDLs. (C) 1999 Elsevier Science B.V. All rights reserved.