Disease relevance of Lcat

• Acquired lecithin-cholesterol acyltransferase deficiency in nephrotic syndrome [1].

High impact information on Lcat

• Stimulation of de novo cholesterogenesis in the mammary gland and depression in circulating LCAT activity levels correlated with the incidence and growth of mammary tumors, suggesting that stimulation of de novo cholesterogenesis plays an important role in mammary cancer development [2].
• In addition, incubation of plasma isolated from human subjects who were deficient in lecithin-cholesterol acyltransferase (LCAT) did not result in increases of either LPC or LPA [3].
• A small fraction, about 14%, of PLPC disappearance was due to removal of linoleate from the sn-2 ester bond to form plasma cholesterol esters, presumably by lecithin-cholesterol acyltransferase [4].
• The results provide strong evidence that retinol-CRBP(II) esterification in the intestine proceeds via a phosphatidylcholine-dependent transacylase mechanism similar to that established for the esterification of cholesterol by lecithin-cholesterol acyltransferase [5].
• Effect of chronic intermittent exercise on biliary lipids, plasma lecithin cholesterol acyltransferase, and red blood cell lipids in rats [6].

Biological context of Lcat

• Effect of hypophysectomy of cholesteryl ester synthesis and hydrolysis in testes and on serum lecithin-cholesterol acyltransferase activity in rats [7].
• In a recent study, we found marked downregulation of hepatic lecithin-cholesterol acyltransferase, or LCAT, expression, which can account for impaired HDL maturation and depressed HDL cholesterol concentration in CRF [8].
• Effect of etiroxate on LCAT activity and on certain energy metabolism enzymes in the rat [9].
• The content of HDL cholesterol, activity of lecithin-cholesterol acyltransferase, and intensity of VLDL lipolysis increased [10].
• A&A improves disorders of lipid metabolism perhaps through up-regulating the expression of hepatic LDL-R gene and through increasing the activities of serum LPL and LCAT [11].

Anatomical context of Lcat

• Adult female lean and obese Zucker rats maintained under standard conditions were used for the estimation of plasma, liver and white adipose tissue (WAT) activity of lipoprotein lipase, plasma and liver hepatic lipase and plasma lecithin-cholesterol acyltransferase [12].
• LCAT did not influence the cholesterol level in red cell membranes because its activity in the plasma was not affected by either splenectomy or the protein content of the diet [13].

Associations of Lcat with chemical compounds

• Although serum LCAT and testicular cholesterol esterase activities were decreased, the overall effect of hypophysectomy produced an increase in the level of serum cholesterol and cholesteryl esters [7].
• Effects of aspirin and salicylic acid on lecithin-cholesterol acyltransferase and cholesterol content in rat serum [14].
• Also, when lecithin-cholesterol acyltransferase (LCAT) (E.C. 2.3.1.43) activity was expressed as the percentage of the total serum that free cholesterol esterified, the acyltransferase activity in rats treated with cupric ions showed a slight decrease while the triglyceride content in rat serum and liver decreased by 54% and 61%, respectively [15].
• Effect of Triton WR-1339 on lecithin-cholesterol acyltransferase in the rat [16].
• Alterations of rat serum lipoproteins and lecithin-cholesterol-acyltransferase activity in praseodymium-induced liver damage [17].

Other interactions of Lcat

• Studies are reported of the effect of hypophysectomy on cholesterol esterase activity of testicular tissue and serum lecithin-cholesterol acyltransferase (LCAT) activity in rats [7].
• No modification in the expression levels of lecithin cholesterol acyltransferase, hepatic lipase, apo A-I and apo E mRNA was observed [18].

Analytical, diagnostic and therapeutic context of Lcat

• LCAT activity was significantly decreased by hypophysectomy compared to that of control animals [7].
• Effect of portacaval shunt on rat serum lipids, lecithin cholesterol acyltransferase, and lipoproteins [19].
• The purified hog lecithin-cholesterol acyltransferase had an apparent molecular weight of 66 000 on SDS-polyacrylamide gel electrophoresis and HPLC and was found to contain about 21.4% (w/w) carbohydrate-hexose, 11.3%; hexosamine, 1.9%; sialic acid, 8.2% [20].
• The relative hepatic LDL receptor, apo B, apo E, lecithin-cholesterol acyltransferase (LCAT) and hepatic triglyceride lipase (HTGL) mRNA levels in the protocatechuic acid group were significantly higher than those in the control group [21].

References