Lecithin-cholesterol acyltransferase in newborn infants: Low activity level in preterm infants

Lecithin-cholesterol acyltransferase catalyzes the formation of cholesterol ester by the transesterification of free cholesterol in serum high-density lipoproteins, the fatty acid donor being HDL lecithin, which in the process is converted to lysoleeithin.] The latter leaves the HDL particle and, after binding to serum albumin, is rapidly removed from the circulation by various tissues, chief among them the liver?Thus LCAT, an enzyme synthesized in the liver and acting in the circulation, is the key enzyme that controls the metabolism of lipoprotein phospholipid.3,4 The accumulation of lecithin in a specific low-density lipoprotein (lipoprotein X) in preterm infants maintained on total parenteral nutrition, including lntralipid (a commercial preparation that contains 1.2% lecithin), might be due to impaired clearing of the infused lecithin because of low LCAT activity?Indeed, earlier studies showed that LCAT activity is lower at birth in full-term infants than in adults 6-9 and may be lowest in VLBW infantsJ ~The aim of this study was to evaluate LCAT activity levels at birth (in cord blood) in a large number of infants ranging in gestational age from 25 to 42 weeks, as well as to quantitate concomitantly the concentration of the main serum lipids, triglyceride, cholesterol, and lecithin, in cord blood.