Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.1.8 (cholinesterase)
12,691 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To elucidate the role of the liver in the metabolism of HDL subfractions, the levels of HDL2 and HDL3 were determined in the sera obtained from patients with liver disease. The determinations were carried out either by zonal ultracentrifugation or by gradient gel electrophoresis combined with HDL cholesterol measurement. Mean HDL3 cholesterol level in patients with liver cirrhosis was about one third of the normal controls whereas no significant changes were observed in HDL2 cholesterol concentration. HDL3 cholesterol levels in patients with chronic hepatitis were about a half of the controls. The levels of HDL3 cholesterol correlated significantly to the levels of serum albumin and to choline esterase activities. The results suggest either that HDL3 is synthesized in the liver or that there is a metabolic defect in the conversion of HDL2 to HDL3 in liver disease.
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PMID:Quantitative determinations of HDL2 and HDL3 in patients with liver disease. 683 48

Lipids of HDL (high density lipoproteins) and their subfractions (HDL2 and HDL3), and LCAT activity (lecithin: cholesterol acyltransferase) were determined in hepatobiliary diseases without severe hyperbilirubinemia (less than 10 mg/dl). The decrease in major lipid constituents (cholesterol and phospholipids) of HDL was mainly attributable to the decrease in those of HDL3, except in some liver diseases of acute or severe stage (acute hepatitis in an acute stage and hepatoma) which were accompanied with a simultaneous moderate decrease in those of HDL2 and in fatty liver which showed a preferential decrease in those of HDL2. The LCAT activity also decreased in several diseases. Some of the hepatobiliary diseases, on the contrary, showed an increase in HDL-triglycerides (mostly in HDL3 and in some diseases also in HDL2) which might participate to some extent in secondary hyperlipidemia in the liver parenchymal diseases, although they were the minor lipid constituents of HDL. From results that HDL3- but not HDL2-cholesterol levels significantly correlated with serum total protein, albumin and choline esterase, it was suggested that the decrease in large constituents of HDL, particularly of HDL3, is caused by hepatocellular dysfunction which causes inhibition of protein and lipid syntheses in the liver in most of the hepatobiliary diseases except for fatty liver which has a preferential decrease in HDL2 lipids.
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PMID:Changes in high density lipoproteins in patients with hepatobiliary diseases. Levels and lipid composition of HDL2 and HDL3 and LCAT reaction. 685 43