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PubMed1995

Glycaemia and body mass as determinants of plasma lecithin: cholesterol acyltransferase activity in Nigerian patients with non-insulin dependent diabetes mellitus.

There is an inverse correlation between plasma high density lipoprotein (HDL) concentrations and atherogenic vascular morbidity risk. An important pathway for modulating circulating HDL levels is the reaction catalysed by the plasma enzyme, lecithin:cholesterol acyltransferase (LCAT). Thus, determinants of LCAT activity should influence plasma HDL levels and be accessible targets for intervention. We therefore assessed such determinants in Nigerian patients with non-insulin dependent diabetes mellitus (NIDDM), classified into age- and sex-matched groups of obese (body mass index, BMI, > 25 kg/m2) and non-obese (BMI < 25 kg/m2). Our results indicated that 10 obese diabetic patients had significantly reduced plasma LCAT activity and HDL levels and increased plasma triglyceride (TG) levels, in comparison with the observations in 9 non-obese diabetic patients (all P < 0.05). Furthermore, worsening of glycaemic control, when oral hypoglycaemic treatment was discontinued for 1 week in 10 diabetic (5 obese) patients, further reduced fasting levels of HDL and plasma LCAT activity (both P < 0.05). Although plasma HDL concentrations and LCAT activity levels did not correlate significantly, the latter nonetheless had a significant inverse relationship with fasting plasma glucose levels in the obese diabetic subjects (r -0.51, P < 0.05). These results indicate that glycaemia and body mass are important determinants of plasma LCAT activity. Both variables are subject to pharmacological and dietary intervention with the objective of increasing circulating HDL levels.

Blood Glucose↗
PubMed1993

Effects of probucol and pravastatin on plasma lipids, activities of postheparin lipoprotein lipase, and lecithin cholesterol acyltransferase and apo A-I containing lipoproteins with and without apo A-II in patients with moderate hypercholesterolemia.

In this study, plasma HDL fractions were separated by ultracentrifugation and apo A-I containing lipoproteins (A-I Lp) were then isolated using anti-apo A-I immunoaffinity chromatography. The A-I Lp were further separated into two fractions with the use of anti-apo A-II immunoaffinity chromatography. One fraction, Lp A-I, contained apo A-I without apo A-II, while the other, Lp A-I/A-II, contained both apo A-I and apo A-II. These techniques were applied to investigate the changes in HDL apoprotein composition in hypercholesterolemic subjects treated with either probucol or pravastatin. Treatment with probucol (500 mg/day) or pravastatin (10 mg/day) reduced mean plasma total cholesterol concentrations by 24% (p < 0.01) and 16% (p < 0.05), respectively. Both drugs caused some reduction in lipoprotein lipase activity, but neither had any influence on the activity of hepatic triglyceride lipase or lecithin cholesterol acyltransferase. Their effects on HDL-cholesterol levels and apoprotein composition differed markedly. Probucol significantly decreased the HDL-cholesterol concentration, the plasma apo A-I/apo A-II ratio, and the number of large particles of diameter greater than 10.4 nm. When the ratios of Lp A-I and Lp A-I/A-II for the probucol-treated subjects were compared with those in the normolipidemic controls, and with the ratios before and after administration of probucol, a remarkable decrease in the level of Lp A-I was apparent. It is presumed that the decrease in HLD-cholesterol by prolonged probucol administration reflects the decrease of Lp A-I more than the decrease of Lp A-I/A-II.(ABSTRACT TRUNCATED AT 250 WORDS)

Apolipoprotein A-I↗
PubMed1986

Lecithin: cholesterol acyltransferase and lysolecithin in coronary atherosclerosis.

Of 100 arteriographically examined, hospitalized, male patients, those without myocardial infarctions were divided into the following categories: zero-, one-, two-, and three-vessel disease; patients diagnosed with myocardial infarction were classified separately. The fasting plasma samples from these patients were examined for concentrations of triglycerides and total cholesterol, lipoprotein profile, lecithin: cholesterol acyltransferase (LCAT) activity, and lysolecithin (LPC) concentration. Those parameters in this group which are commonly determined were consistent with the clinical classification of these patients. Of those remaining parameters, the LCAT activity was increased as the severity of coronary atherosclerosis increased and the changes in the activity of this enzyme were appropriately reflected by increases in LPC concentration and decreases in the proportion of the plasma cholesterol unesterified. The results of this study suggest that increased, rather than decreased, plasma LCAT activity and increased LPC concentrations are characteristic of coronary atherogenesis. The plasma concentrations of LPC observed in these atherosclerotic patients are more than sufficient to qualify this substance for its previously proposed roles of mediator of transmembrane diffusion of LDL and as an inhibitor of platelet aggregation.

Adult↗
PubMed1990

Distribution of lecithin-retinol acyltransferase activity in different types of rat liver cells and subcellular fractions.

It is now well documented that lecithin-retinol acyltransferase (LRAT) is the physiologically important enzyme activity involved in the esterification of retinol in the liver. However, no information regarding the cellular distribution of this enzyme in the liver is presently available. This study characterizes the distribution of LRAT activity in the different types of rat liver cells. Purified preparations of isolated parenchymal, fat-storing, and Kupffer + endothelial cells were isolated from rat livers and the LRAT activity present in microsomes prepared from each of these cell fractions was determined. The fat-storing cells were found to contain the highest level of LRAT specific activity (383 +/- 54 pmol retinyl ester formed min-1.mg-1 versus 163 +/- 22 pmol retinyl ester formed min-1.mg-1 for whole liver microsomes). The level of LRAT specific activity in parenchymal cell microsomes (158 +/- 53 pmol retinyl ester formed min-1.mg-1) was very similar to LRAT levels in whole liver microsomes. The Kuppfer + endothelial cell microsome fractions were found to contain LRAT, at low levels of activity. These results indicate that the fat-storing cells are very enriched in LRAT but the parenchymal cells also posses significant levels of LRAT activity.

Acyltransferases↗
PubMed1991

The induction of lamellar stacking by cholesterol in lecithin-bile salt model systems and human bile studied by synchrotron X-radiation.

Small angle X-ray scattering (SAXS) with synchroton radiation was used to investigate interactions among lipid particles in lecithin-bile salt model systems and in native gallbladder biles. In model systems in the absence of cholesterol, isotropic, continuous spectra were found, indicating the absence of periodic structures. In the presence of excess cholesterol, interaction in the form of lamellar stacking was detected by the appearance of discrete diffraction peaks. In the supersaturated cholesterol region of the commonly accepted phase diagram [1], where cholesterol crystals were expected, we found lamellar stacking. The high proportion of cholesterol to bile salts seems to be the common denominator of these models. The lamellar stacking was also found in native unprocessed bile. This effect of cholesterol on lipid structure has not been previously described. Lamellar stacking may contribute to cholesterol solubilization. Its influence on the kinetics of cholesterol crystallization is presently unknown.

Bile↗
PubMed1983

Carnitine esters: novel inhibitors of plasma lecithin: cholesterol acyltransferase in experimental animals but not in man (Homo sapiens).

1. Long-chain fatty acid esters of carnitine were observed to inhibit lecithin: cholesterol acyltransferase (LCAT, EC 2.3.1.43) in plasma from the rat (Rattus sativa) and rabbit (Oryctolagus cuniculus) but not in man (Homo sapiens). At a level of 500 nmol/ml of plasma, L-palmitoylcarnitine, L-stearoylcarnitine, and L-oleoylcarnitine inhibit the formation of cholesteryl esters by LCAT by 25-30%. 2. The inhibition is concentration-dependent and is observed only with acylcarnitine esters with acyl chains of 12C or greater. 3. Equipotent activity is obtained using either the DL-acylcarnitine esters or the L-acylcarnitine esters. 4. Inhibition of LCAT by carnitine esters is greater than that achievable with sodium dodecylsulfate on a mol:mol basis and is not reversible with albumin. 5. The failure of the carnitine esters to inhibit plasma LCAT from man suggests the possibility of subtle differences in the structure of human LCAT compared with that in other species.

Adult↗
PubMed1993

Interaction of N-methyl-anthraniloyl-labelled porcine apolipoprotein A-I with porcine lecithin: cholesterol acyltransferase: an energy transfer study.

1. To investigate whether a direct protein-protein interaction between apoA-I and lecithin:cholesterol acyltransferase (LCAT) is necessary for the activation of the enzyme, apoA-I was labelled with N-methylisatoic anhydride at lysine residues. The intermolecular resonance energy transfer from tryptophan residues of LCAT (donor) to N-methyl-anthraniloyl (NMA)-labelled apoA-I (NMA-apoA-I) (acceptor) was used as a sensitive fluorescence method for studying molecular interactions. 2. In the absence of lipids no fluorescence energy transfer was measurable. 3. Fluorescence energy transfer occurred from LCAT to NMA-apoA-I in the presence of liposomes with phospholipid/cholesterol ratios ranging from 5:1 to 18:1 and regardless whether only 1 or up to 5 NMA-apoA-I molecules resided at the liposome surface. 4. This indicates a preferred binding of the enzyme directly to or in spatial proximity to the activator protein NMA-apoA-I even if enough space at the liposome surface is available to allow LCAT binding at a distance, where no energy transfer is measurable.

Anhydrides↗
PubMed1989

Effect of fetal sex and race on amniotic fluid lecithin concentration.

Amniotic fluid lecithin phosphorus concentration (AF-Lec) was measured in 209 healthy women at 31.7-42.7 weeks gestation. The patients were divided into four groups according to race and fetal sex. No differences in AF-Lec between black and white nor between male and female fetuses were found. The relationship of AF-Lec to gestational age and the incidence of "mature" AF-Lec was not different among the four groups. We conclude that there is no effect of fetal sex, race, or the interaction between them on fetal lung development as measured by AF-Lec.

Adult↗
PubMed1977

Lecithin: cholesterol acyl transferase activity in the serum of rats fed saturated and unsaturated fats.

Groups of rats were fed diets containing either butter, beef, fat or safflower oil. After 20 or 70 days of feeding, blood was taken from the animals in a postabsorptive state. Serum lipid levels and lecithin: cholesterol acyl transferase activity were measured. Feeding the different fats did not alter serum total cholesterol levels but free cholesterol and triglycerides were significantly lower in the safflower oil-fed group. Net cholesterol esterification in vitro was also significantly depressed in the safflower oil-fed group and this was shown to be due to the inability of the lipoprotein substrate to support the reaction rather than because of low LCAT enzyme activity.

Acyltransferases↗
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↗
PubMed1979

Cholesteryl ester distribution in lecithin bilayer membranes.

The saturated cholesteryl ester, cholesteryl 16-doxylstearate, is shown to incorporate into hydrated egg yolk lecithin multilayers in two distinct forms as visualized by electron spin resonance (ESR) spectroscopy. At concentrations less than 1 mole%, the ester is uniformly distributed in the membrane while at higher concentrations, patches of solid ester are formed.

Cholesterol Esters↗
PubMed1983

Serum lecithin:cholesterol acyltransferase activities of cynomolgus monkeys fed different carbohydrate diets.

Although serum lecithin:cholesterol acyltransferase (LCAT) activity is known to be modulated by nutritional factors, little is known about the effects of dietary carbohydrate on this enzyme. Therefore, LCAT activities were assessed in cynomolgus monkeys fed diets for 6 weeks on 4 diets containing 77% of calories as sucrose or starch and cholesterol at 0 and 1 mg/kcal. Three different assay conditions were used in order to measure the overall LCAT activity and to differentiate enzyme activity from the effect of serum substrate and end-product lipoprotein alterations by diet on this enzyme. Molar rate of serum total LCAT activity was higher in sucrose than starch diets (P less than 0.01). Use of sera from sucrose-fed animals, either as substrate or enzyme source, increased the fractional rate of cholesterol esterification (P less than 0.01). Exogenous cholesterol lowered serum total LCAT activity only in sucrose diet (P less than 0.01). Use of sera from sucrose + cholesterol-fed animals as substrate significantly lowered the fractional rate of cholesterol esterification (P less than 0.01); whereas no such alterations were noted when this serum was used as enzyme source. The differential effect of starch and sucrose diets on LCAT activity suggests that the nature of dietary carbohydrates may affect LCAT activity in association with triglyceride metabolism by altering the amount of enzyme in terms of its activity and/or the nature of substrate and cholesterol ester acceptor lipoproteins.

Animals↗
PubMed1987

Alterations in molecular species of cholesterol esters formed via plasma lecithin-cholesterol acyltransferase in human subjects consuming fish oil.

The influence of a dietary supplement of n-3 polyunsaturated fatty acids containing eicosapentaenoic acid (EPA, 20:5n-3) and docosahexaenoic acid (DHA, 22:6n-3) on the molecular species of cholesteryl esters (CE) formed via the plasma lecithin (phosphatidylcholine)-cholesterol acyltransferase (LCAT; EC 2.3.1.43) reaction was evaluated. For this purpose, one group of eight subjects received an encapsulated fish lipid concentrate (MaxEPA) and another group of eight volunteers in the control group received encapsulated olive oil for 22 days. Plasma lipid profiles and fatty acid compositions of plasma phosphatidylcholine (PC) and CE were measured at day 0 and day 22 in all subjects. A decrease in plasma triglyceride (by 34%) and a moderate rise in high-density lipoprotein (HDL)-cholesterol (by 13%) was observed in the MaxEPA group. For characterization of the plasma LCAT-derived reaction products formed in vitro, [14C]cholesterol was used as the substrate and the newly formed molecular species of [14C]CE were separated by argentation thin-layer chromatography. Marked shifts were found in the abundance of the various classes of LCAT-derived products in the MaxEPA group whereas no significant changes were observed in the controls. The proportion of the [14C]CE as pentaenoic (EPA) species rose by 9-fold (from 1.5% at day 0 to 14.4% at day 22) as the dienoic (linoleate) species fell (from 50.6 to 39.2%); a moderate rise in the hexaenoic (DHA) species (from 1.7 to 2.4%) with no significant change in the tetraenoic (arachidonate) (AA) species was observed. The LCAT results were in the order of the observed shifts in the fatty acid patterns of the plasma CE.(ABSTRACT TRUNCATED AT 250 WORDS)

Chemical Phenomena↗
PubMed1988

Relationship of high density lipoprotein composition to plasma lecithin:cholesterol acyltransferase concentration in men.

The epidemiological associations between the plasma concentrations of several components of high density lipoprotein (HDL) and plasma lecithin:cholesterol acyltransferase (LCAT) concentration have been studied in 101 men aged 52-67 years. Subjects were apparently healthy, and had been selected to provide a wide range of HDL-cholesterol levels. A weak positive correlation was observed between plasma total HDL-cholesterol concentration and LCAT concentration (r = 0.24, P less than 0.02). This reflected an association between HDL3-cholesterol (measured by precipitation) and enzyme concentration (r = 0.21, P less than 0.05). Apoprotein (apo) A-II concentration was also positively correlated with LCAT (r = 0.27, P less than 0.01). HDL2-cholesterol and apo A-I concentration were unrelated to LCAT concentration, as also were the HDL2/HDL3 and HDL-cholesterol/apo A-I ratios. The associations of HDL3 cholesterol and apo A-II with LCAT were strengthened when allowance was made by multiple regression for the effect of log plasma triglyceride; under these circumstances variation in LCAT explained statistically 8% of the variance in HDL3-cholesterol, and 10% of that in apo A-II.

Aged↗
PubMed1988

Variations in the apolipoprotein AI-CIII-AIV gene region and in lecithin:cholesterol acyltransferase concentration are determinants of plasma cholesterol concentrations.

We have examined the effects of variation in the region of the apolipoprotein (apo) AI-CII-AIV genes, and in plasma lecithin: cholesterol acyltransferase (LCAT) concentration, on plasma cholesterol concentration in 109 unrelated men aged 52-67 yrs. Restriction fragment length polymorphisms (RFLPs) were detected using the restriction enzymes XmnI, PstI and SstI and individuals were divided into groups using information from all three RFLPs in conjunction. Mean plasma concentrations of both total cholesterol and estimated low density lipoprotein-cholesterol differed significantly (P less than 0.0125) among groups of men with different genotypes. Thus, variation in this gene region may be one of the polygenetic factors involved in determining cholesterol levels in the normal population. In the same subjects, plasma cholesterol was also positively correlated with plasma LCAT concentration (r = 0.55, P less than 0.001), due mainly to an increase in the cholesteryl ester content of apo B-containing lipoproteins with increasing LCAT concentration. Since apolipoproteins AI, CIII and AIV have each been shown to modify the activity of LCAT in vitro, the associations of the RFLPs with plasma cholesterol concentration may reflect changes in LCAT activity secondary to qualitative or quantitative changes in one or more of these apolipoproteins.

Aged↗
PubMed1989

Lecithin: cholesterol acyltransferase activity in children and young adults.

The association between serum lecithin: cholesterol acyltransferase (LCAT) activity and demographic and environmental factors, and the correlation of LCAT activity with serum lipids and lipoproteins were studied in a representative series of 1071 9-24-year-old subjects from East and West Finland. LCAT activity was determined by a method involving the use of exogenous substrate. Males had higher LCAT activity than females and subjects from East Finland had significantly higher activity than those from West Finland. LCAT activity tended to be lowest shortly after puberty. Women using oral contraceptives had significantly lower LCAT activity than women not using them. Serum LCAT activity was not associated with body mass index, physical activity index or smoking. Serum LCAT activity correlated positively with most serum lipid and lipoprotein variables. The highest correlation coefficients were found between LCAT activity and total cholesterol. LCAT activity correlated positively with the change in serum total cholesterol which had occurred during the preceding 3 and 6 years in men. Our results suggest that sex hormonal factors are associated with serum LCAT activity. The results are also in accordance with the idea that activity of LCAT increases in response to enhanced demands for cholesterol esterification in plasma.

Adolescent↗
PubMed1990

Associations of lecithin: cholesterol acyltransferase (LCAT) mass concentrations with exercise, weight loss, and plasma lipoprotein subfraction concentrations in men.

The relationships between plasma lecithin:cholesterol acyltransferase (LCAT) mass concentrations and lipids, apolipoprotein, and lipoprotein subfraction concentrations were studied in men assigned at random to a one-year exercise program (n = 48) and to a sedentary control condition (n = 31). Exercise training did not significantly affect mean concentrations of LCAT-mass. Moreover changes in LCAT within the exercise group were unrelated to distance run and weight loss. The baseline data and the one-year change data showed consistent positive correlations between LCAT concentrations and total cholesterol, low density lipoprotein cholesterol, very low density lipoprotein cholesterol, and apolipoprotein B concentrations, and consistently weak correlations between LCAT concentrations and high density lipoprotein (HDL)-cholesterol, HDL2, and apolipoprotein A-I concentrations. The strong correlation between LCAT and total cholesterol may account for LCAT's relationships with lipoprotein subfractions, apolipoprotein B and other lipoprotein cholesterol concentrations.

Adult↗
PubMed1991

An investigation of the role of lecithin:cholesterol acyltransferase and triglyceride-rich lipoproteins in the metabolism of pre-beta high density lipoproteins.

Small high density lipoproteins (HDL) with pre-beta electrophoretic mobility (pre-beta HDL) have recently been shown to be the primary acceptor of cholesterol from cultured cells. We studied the metabolism of these particles by incubating serum at 37 degrees C in the presence and absence of active lecithin: cholesterol acyltransferase (LCAT). We found that the serum pre-beta HDL concentration decreased in the presence of LCAT, but when LCAT was inhibited the concentration remained constant, or increased, depending on the method of inhibition. This suggests that pre-beta HDL are a substrate for LCAT. We also found a significant negative correlation between levels of LCAT activity and pre-beta HDL in 28 fasting healthy subjects, this provides evidence that the activity of LCAT regulates, at least in part the concentration of these particles in vivo. During the early phase of incubation there was a more rapid decrease in pre-beta HDL concentration which was greater in the post-prandial than fasting state. When we infused a triglyceride emulsion into 6 subjects or added this to serum in vitro we observed an immediate fall in pre-beta HDL concentration. These findings suggest that pre-beta HDL interact with triglyceride rich particles. We investigated the origin of pre-beta HDL from blood lipoproteins during their lipolysis, in vivo and in vitro and found that they were produced from both triglyceride-rich and high-density lipoproteins. Formation from triglyceride-rich lipoproteins was evident by the rise in pre-beta HDL concentration during heparin-induced lipolysis when fasting and post-prandially. The rise was greater post-prandially and particularly marked in 4 hypertriglyceridaemic patients following a fat load. Generation from alpha-HDL was evident when we prolonged the action of the heparin-released lipases by incubation of post-heparin sera at 37 degrees C. Continued formation of pre-beta HDL occurred at an equal rate in the fasting and post-prandial samples suggesting release by lipolysis of alpha-HDL. This was supported by the action of lipases on serum and isolated HDL in vitro, where triglyceride lipase rather than phospholipase activity appeared more effective at releasing pre-beta HDL. These findings suggest binding and release of pre-beta HDL by triglyceride-rich lipoproteins depending on the prandial state and production from alpha-HDL through the action of lipases.

Adolescent↗