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Lecithin: Cholesterol acyltransferase and plasma proteins in liver disease

1974; Elsevier BV; Volume: 53; Issue: 2 Linguagem: Inglês

10.1016/0009-8981(74)90099-0

1873-3492

J. P. Blomhoff, Sverre Skrede, S Ritland,

Drug Transport and Resistance Mechanisms

Lecithin: cholesterol acyltransferase (LCAT) activity has been measured by the method of Stokke and Norum and by the method of Glomset and Wright in plasma from 53 patients with various liver diseases. The results were compared with the concentration of plasma albumin, prealbumin and α-lipoprotein and with Normotest as well as plasma cholesterol. In most cases, the method of Stokke and Norum and the method of Glomset and Wright gave the same results. Therefore, substrate deficiency probably does not contribute much to low activities obtained by the method of Stokke and Norum in liver disease. The activity of LCAT was found to parallel the levels of plasma proteins. In acute hepatitis LCAT activity followed the proteins with short half-life. In chronic liver disease the LCAT activity was also correlated with plasma albumin. LCAT activity was normal in some patients with primary biliary cirrhosis who had subnormal levels of prealbumin, but normal or high levels of α-lipoprotein. The previously reported stimulating effect on LCAT activity with inactivated substrates from patients with primary biliary cirrhosis may be caused by high concentration of α-lipoprotein, either as substrate or as LCAT cofactor. In the total material the activity of LCAT was not correlated with the concentration of free cholesterol, but was correlated with the levels of cholesteryl esters.