Abstract
Lecithin–cholesterol acyltransferase (LCAT) generates the major part of cholesteryl esters in human plasma from lipoprotein lecithin and unesterified cholesterol. As a practical matter, isolated LCAT is reactive to a significant extent only with the high-density lipoprotein (HDL) class of human plasma lipoproteins. The mechanism of action of LCAT under physiological conditions is quite different from that determined with a fully defined system of synthetic lipids. Because information is insufficient at this point to fully integrate the data that have been obtained with synthetic and physiological substrates, these will first be considered separately. A comparison of the types of data will be made. The most effective direct substrate for LCAT would therefore be one containing phospholipid, apoA-I only, and little cholesteryl ester or free cholesterol. Such a particle has been identified in normal plasma by immunoaffinity chromatography and accumulates in congenital LCAT deficiency. This is the primary substrate for LCAT in vivo , acting as the recipient of free cholesterol from cell membranes, very low-density lipoproteins (VLDL), and low-density lipoproteins (LDL), and the source of the cholesteryl esters are transferred away to the major lipoprotein classes of the plasma.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.