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Results for “Sterol O-Acyltransferase”

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At least 19 recordsLinked to original sources
PubMed1975

Synthesis of cholesterol esters in the plasma and liver of sheep.

A study was made with sheep on the formation in vitro of long chain fatty acid esters of cholesterol by the lecithin-cholesterol-acyltransferase system present in the plasma and the acyl CoA-cholesterola cyltransferase system present in the liver. The rate of cholesterol esterification in the plasma was 0.024 mumoles/ml/hr. The relative pattern of fatty acids esterified during incubation of the plasma remained constant over the 8 hr period of incubation and was similar to the fatty acids in the plasma cholesteryl esters before incubation began and to the fatty acids in the 2-position of the plasma lecithin. The predominant cholesteryl esters synthesized contained monoenoic and dienoic fatty acids. Unlike the bovine, there was no apparent discrimination in favor of the 18:2 containing species of plasma lecithin as donors of fatty acids. This difference could be accounted for by the similarity in the 18:2 content of the phospholipids present in the high density (density greater than 1.062 and less than 1.21) and the low density (density greater than 1.006 and less than 1.063) lipoprotein fractions of the sheep plasma. The possibility of some discrimination against 20:4 during cholesterol ester synthesis in the plasma of the sheep cannot be excluded. In the liver, the predominant cholesteryl esters synthesized contained saturated and monoenoic fatty acids; cholesteryl linoleate was synthesized to a very much less extent. There was considerable similarity between the composition of the unesterified fatty acid fraction of the liver before incubation began and the fatty acid composition of the cholesteryl esters synthesized during incubation. Addition of sonicated suspensions of free fatty acidsaltered markedly the fatty acid pattern of the cholesteryl esters synthesized by the liver slices. From the evidence presented it is concluded that the cholesteryl esters in sheep plasma are syntheized mainly by the plasma lecithin-cholesterol-acyltransferase system. The results are discussed in relation to cholesterol esterification systems demonstrated in the plasma and liver of monogastric animals.

Animals↗
PubMed1976

The influence of LP-X and other lipoproteins associated with hepatic dysfunction on the activity of lecithin:cholesterol acyltransferase.

A study was made of the in vitro effects of the abnormal serum lipoproteins associated with liver disease on the activity of the enzyme lecithin:cholesterol acyltransferase. At lipoprotein concentrations equivalent to those found in hepatic disease sera, the results indicate that: (1) LP-X levels greater than 2.5 mg/ml produced total inhibition of enzyme activity. (2) LP-X levels remained constant even up to 36 h incubation, despite active cholesterol esterification in the presence of LP-X concentrations less than 2.5 mg/ml. In addition, the specific activity of radiolabelled LP-X, and its electrophoretic properties remained unchanged after incubation showing that the molecule remained intact. (3) Low density lipoproteins other than LP-X stimulated the enzymes activity, but this effect was overcome by LP-X. (4) Additional concentrations of high density lipoproteins also produced enhancement of enzyme activity, but at higher levels inhibition was seen. LP-X prevented the enhancement of lecithin:cholesterol acyltransferase activity. (5) Small samples of pure LP-X, obtained with the minimum of physical manipulation, showed a complete absence of cholesterol ester and triacylglycerol from the molecule. The implications of these results are discussed, particularly in relation to other reports which have presented evidence that LP-X is a substrate for lecithin:cholesterol acyltransferase.

Acyltransferases↗
PubMed1976

Secretion of lecithin: cholesterol acyltransferase from isolated rat hepatocytes.

1. Lecithin:cholesterol acyltransferase is secreted from isolated rat heptocytes. 2. The secretion is stimulated when serum is added to the incubation medium. 3. Optimal conditions for secretion are: 5-10(6) hepatocytes per ml, 5 h incubation, pH 7.3-7.4 and 25% serum in the incubation medium. 4. Concomitantly with the secretion of lecithin:cholesterol acyltransferase there is a secretion of unesterified cholesterol and triacylglycerol. 5. Colchicine or cycloheximide in the incubation medium inhibits secretion of lecithin:cholesterol acyltransferase.

Acyltransferases↗
PubMed1977

Uptake and degradation of cholesterol ester-labelled rat plasma lipoproteins in purified rat hepatocytes and nonparenchymal liver cells.

1. A new method for isolation and purification of rat liver hepatocytes and nonparenchymal cells by differential centrifugation is described. 2. Cholesterol ester-labelled lipoproteins (prepared by the action of lecithin: cholesterol acyltransferase) intravenously injected were taken up by hepatocytes and nonparenchymal cells. 3. Hepatocytes and nonparenchymal cells in suspension were able to take up and hydrolyse the cholesterol ester portion of lipoproteins. 4. Uptake of cholesterol ester labelled whole rat plasma and high density lipoproteins (HDL) increased with increasing concentrations until a distinct saturation level was reached in hepatocytes. In nonparenchymal cells there was no saturation of lipoprotein uptake. 5. Concanavalin A inhibited cholesterol ester-labelled lipoprotein uptake in hepatocytes, indicating that the uptake at least partially depends on carbohydrate sites on the cell surface. The uptake in nonparenchymal cells was unaffected of concanavalin A. 6. The specific activity of the acid cholesterol ester hydrolase was the same in homogenates from hepatocytes and nonparenchymal cells while acyl-CoA: cholesterol acyltransferase was found almost exclusively in hepatocytes.

Acid Phosphatase↗
PubMed1979

Purification of human plasma lecithin:cholesterol acyltransferase and its specificity towards the acyl acceptor.

A simple and convenient method for the purification of human plasma lecithin-cholesterol acyltransferase was developed. The method involves the adsorption of the enzyme from diluted human plasma on DEAE-Sephadex, treatment with 1-butanol in the presence of (NH4)2SO4, DEAE-Sephadex chromatography, treatment with dextran sulfate in the presence of Ca2+, and hydroxyapatite chromatography. The enzyme purified showed a single main band by polyacrylamide gel electrophoresis in the presence and absence of sodium dodecyl sulfate. In addition, the enzyme obtained was stable for more than four weeks, when it was kept at 4 degrees C under N2 in a buffer of low ionic strength. The purified enzyme was used to study its specificity toward the acyl acceptor. This specificity was found to be broad in that not only sterols but also long chain primary alcohols exhibited considerable acceptor activity. Furthermore, in agreement with our previous observations with crude enzyme (Piran, U. and Nishida, T. (1976) J. Biochem. (Tokyo) 80, 887-889), the purified enzyme was found to be capable of hydrolyzing the ester linkage at the carbon-2 position of phosphatidylcholine. The transesterification, as well as the hydrolytic reaction, required the presence of the cofactor polypeptide, apolipoprotein A-I.

Apolipoproteins↗
PubMed1977

Familial hyper-alpha-lipoproteinaemia. Further studies on serum lipoproteins and some serum enzymes.

Some new data are given concerning a family whose members are characterized by high levels of alpha-(HDL)-cholesterol. Data from the new members of the family, not previously studied, confirm that the defect is not associated with any cardiac or neurological defect nor with xanthomata. Studies performed to assess the polypeptide composition of HDL of the affected members resulted in completely normal results. The post-heparin lipolytic activity (PHLA), the liver lipase and the lecithin-cholesterol acyltransferase (LCAT) activities also proved to be within the normal limits.

Acyltransferases↗
PubMed1978

Apolipoprotein A-1 in cholestatic liver diseases.

The apolipoprotein A-1 in cholestatic liver diseases was determined by rocket immunoelectrophoresis. A decrease in the serum apo A-1 was generally observed in LP-X positive liver disease, particularly in the patients with extrahepatic biliary obstruction. With reference to LP-X levels and LCAT activity, the results indicated that not only hepatocellular damage but also cholestasis contribute to the decrease of apo A-1 concentration in patients with liver disease.

Adult↗
PubMed1978

Triglyceride lipase activity in postheparin plasma and plasma lipoproteins in liver disease.

Hepatic lipase activity and lipoprotein lipase activity were studied in postheparin plasma from 14 patients with various liver disorders. Plasma lecithin: cholesterol acyltransferase (LCAT) activity and lipoprotein composition and structure were also estimated. Five patients had lower hepatic lipase activity than the lowest control value, and in three of these no hepatic lipase activity was detected. Lipoprotein lipase was low in 5 patients, but in only one of them was hepatic lipase activity also low. Hepatic lipase was not significantly correlated to the concentration of plasma triglycerides, either in controls or in patients, whereas lipoprotein lipase was negatively correlated with plasma triglycerides both in controls and patients. Lipoprotein lipase and LCAT activity, but not hepatic lipase, was negatively correlated to the triglyceride content of the low density lipoproteins (density 1.019-1.063 g/ml) from the patients. No specific lipid or lipoprotein pattern was found in plasma from the patients with a low or without any hepatic lipase activity. The results suggest an important role of lipoprotein lipase and LCAT, for the increased content of triglycerides in the low density lipoproteins in patients with liver disease. The role of hepatic lipase remains unclear.

Adult↗
PubMed1977

Lecithin: cholesterol acyl transfer rate in plasma and its relation to lipid and lipoprotein concentrations in primary hyperlipidemia.

Plasma lecithin: cholesterol acyl transfer (LCAT) rate and concentrations of lipids in plasma and lipoproteins were studied in 107 hyperlipidemic subjects. In all types of hyperlipoproteinemia LCAT rates were higher than in a normolipidemic reference group. LCAT rates were highest in type IV and V. There was a considerable overlap of LCAT rates between type IIa, IIb and reference subjects. The LCAT rate correlated positively with very low density lipoprotein concentration, body mass and excess body mass. Low density lipoprotein concentration correlated positively with the LCAT rate only in the reference group. The high density lipoprotein concentration correlated negatively with the LCAT rate. It was suggested that the LCAT rate in vitro reflects the in vivo turnover of cholesteryl esters as a part of the turnover of apoprotein-B containing lipoprotein complexes in plasma. The results might then indicate an inflow rate of lipoproteins in plasma that is increased in most type IV cases but normal or only moderately increased in type IIa and IIb subjects. Analysing the relations between the LCAT rate and the concentrations of lipids in plasma by multiple regression indicated hypothetically deficiencies of lipoprotein removal from plasma in half of type IIa and one third of type IIb subjects.

Acyltransferases↗
PubMed1978

Lipoprotein composition in diabetes mellitus.

Lipoprotein cholesterol and triglyceride levels have been determined in normal and diabetic Pima Indian women aged 20-35, HDL cholesterol levels were lower, LDL cholesterol levels were higher, and the ratio of HDL cholesterol/LDL cholesterol, a reflection of lipoprotein cholesterol distribution, was lower in the diabetics compared to the normals. VLDL triglyceride levels were also elevated in the diabetics. An analysis of lipoprotein composition suggested that these changes primarily reflect changes in numbers of particles, since lipid composition and lipid/protein ratios were similar in lipoproteins isolated from normals and diabetics. The ratio of ester/free cholesterol in LDL and HDL was lower in normal Pima Indians than in a comparable group of Caucasians, although plasma LCAT activity was not significantly different. The data indicate that diabetes may be associated with shifts in distribution of LDL and HDL, as well as with increases in VLDL.

Adult↗