Prematurity and lecithin-cholesterol acyltransferase deficiency in newborn infants.
The occurrence of hyperlipidemia and fat accumulation in certain tissues of premature newborn infants is known. Lecithin-cholesterol acyltransferase (LCAT) catalyzes esterification of free cholesterol and is important in the transport and disposal of lipids. Cord plasma LCAT activity of full-term newborn infants is nearly one-half of that present in the adult plasma. The present study also has found a significant positive correlation between cord plasma LCAT activity and gestational age of the newborn. The ratio of circulating cholesterol ester to free cholesterol was significantly lower only in newborn infants with gestational age less than 32 wk, in comparison to full-term newborn infants or adults. LCAT deficiency and decreased cholesterol ester formation may be responsible for the inadequate lipid clearance in premature newborn infants.
D000328:Adult; D002784:Cholesterol / Q000097:blood; D002788:Cholesterol Esters / Q000097:blood; D008076:Cholesterol, HDL / Q000097:blood; D005865:Gestational Age; D006801:Humans; D007009:Hypolipoproteinemias / Q000201:enzymology*; D007231:Infant, Newborn; D007235:Infant, Premature, Diseases / Q000201:enzymology*; D007863:Lecithin Cholesterol Acyltransferase Deficiency / Q000201:enzymology*; D008079:Lipoproteins, VLDL / Q000097:blood; D007862:Phosphatidylcholine-Sterol O-Acyltransferase / Q000097:blood*; D014280:Triglycerides / Q000097:blood
D002788:Cholesterol Esters; D008076:Cholesterol, HDL; D008079:Lipoproteins, VLDL; D014280:Triglycerides; D002784:Cholesterol; D007862:Phosphatidylcholine-Sterol O-Acyltransferase