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PubMed1981

Mode of action of lecithin in suppressing cholesterol absorption.

In vitro studies were performed to investigate a possible mechanism by which lecithin suppresses intestinal cholesterol absorption. The hypothesis that lecithin acts by retarding the diffusion of micelles across the unstirred water layer (UWL) was tested by measuring cholesterol influxes (Ji) in segments of rat intestine under conditions with no maximal and minimal effective thickness of the UWL. Ji was sharply reduced by lecithin under all conditions with no apparent relationship to the thickness of the UWL. The hypothesis was further tested by determining if lecithin had any effect on the molecular weight of the micelles. Gel filtration studies indicated no change in molecular weight (range, 21,000-24,000). Finally, actual measurements of the coefficients of free diffusion (D) of the micelles revealed that lecithin in the concentration that caused a 42-90% reduction in Ji caused only a 22% reduction in D. The basis for the decrease in D is unknown, but it was sufficient to account for the decrease in Ji. Therefore, except for the small decrease in micellar diffusion coefficient as a possible contributing factor, the data offered little support for the hypothesis and we concluded that lecithin suppresses cholesterol absorption by some other or additional mechanism, such as by a direct effect on cell membrane or by holding the cholesterol absorption by some other or additional mechanism, such as by direct effect on the cell membrane or by holding the cholesterol in micellar form to reduce its partition coefficient.

Animals↗
PubMed1977

Nature of interaction of dextran sulfate with lecithin dispersions and lysolecithin micelles.

Lecithin and lecithin/cholesterol dispersions as well as lysolecithin micelles were used to provide basic information on the mechanism of the interaction of zwitterionic phospholipids with dextran sulfate. The addition of dextran sulfate to lecithin dispersions or lysolecithin micelles in the presence of Ca2+ produced insoluble complexes. At each Ca2+ concentration, the amount of insoluble complex formed was maximal at the equivalence dextran sulfate/phospholipid weight ratio. An increase in CaCl2 concentration up to 10 mM progressively increased the equivalence ratios for the phospholipids. Further increase in Ca2+ concentration did not influence the equivalence ratio for maximal complex formation. The conversion of lecithin dispersions into insoluble complexes was very effective even at low Ca2+ concentrations. Approximately 70% of the lecithin was converted to the insoluble complex at CaCl2 concentrations as low as 0.5 mM and the complete conversion was observed at CaCl2 concentrations above 2.5 mM. In the presence of cholesterol, the precipitation curve for insoluble complex formation became broader than that of lecithin alone, indicating the enhancing effect of cholesterol on the insoluble complex formation both below and above the equivalence ratio. The stoichiometry of the interaction of the zwitterionic phospholipids with dextran sulfate inthe presence of calcium was determined using lysolecithin micelles. At the CaCl2 concentrations above 20 mM, the insoluble complex possessed a ratio of lysolecithin/calcium/sulfate group of approximately 2/1/3 (mol/mol/mol). It appears that the formation of the insoluble complex of lecithin or lysolecithin with dextran sulfate represents the mutually enhancing interactions involving both positive and negative charges of the zwitterionic phospholipids. These are the direct electro static interaction between the phospholipid choline nitrogen and the sulfate groups of dextran sulfate and the calcium cross-linking of the phosphate groups to the sulfate groups or to the phosphate groups of neighboring phospholipids.

Binding Sites↗
PubMed1979

Effects of physostigmine and lecithin on memory in Alzheimer disease.

Because there is evidence that central cholinergic mechanisms are depleted in dementia, we studied the effects of central cholinergic augmentation on the memory of 5 patients with Alzheimer disease. Patients received placebo, lecithin, physostigmine, or lecithin plus physostigmine in a double-blind study using titrated doses of the acetylcholinesterase inhibitor physostigmine. Memory was evaluated with alternate forms of the selective reminding procedure. Compared with lecithin alone, the combination of physostigmine and lecithin consistently enhanced memory storage and retrieval; physostigmine without lecithin produced no memory facilitation. The strategy of combining a cholinergic agonist and precursor holds promise, although a larger clinical trial is needed.

Aged↗
PubMed2004

Phytosterols and lecithin do not have an additive effect in lowering plasma and hepatic cholesterol levels in diet-induced hypercholesterolemic rats.

Both plant sterols and lecithin are used as dietary supplements for lowering blood cholesterol in Western countries. This study evaluated the possibility of an additive effect of these ingredients on the regulation of lipid concentrations and cholesterol metabolism. Male Sprague-Dawley rats were randomly divided into three groups, and fed one of the following diets for 5 weeks; high cholesterol diet (HCD), phytosterol mixture-supplemented diet (PD, HCD+0.25% phytosterols), or phytosterol mixture and lecithin-supplemented diet (PLD, PD+0.15% lecithin). Feeding the PD for 5 weeks resulted in a 34% and 41% decrease in plasma total- and VLDL+LDL-cholesterol levels, respectively, and a 23% decrease in hepatic cholesterol content compared to those for the HCD rats (p < 0.05). These cholesterol-lowering properties of the phytosterol mixture were also associated with the down-regulation of hepatic acyl CoA:cholesterol acytransferase (ACAT) activity (p < 0.05). Addition of lecithin plus phytosterol mixture to the hypercholesterolemic diet did not significantly affect blood and hepatic lipid concentrations (with the exception of 36% decrease in hepatic triglyceride level, p < 0.05) as well as hepatic ACAT activity compared to feeding the hypercholesterolemic diet supplemented with phytosterol alone. These results indicate that combining lecithin, at a 0.15% level, with a phytosterol mixture-supplemented diet does not exhibit an additive effect in regulating hepatic ACAT activity or lowering blood cholesterol in hypercholesterolemic rats.

Animals↗
PubMed1985

Effects of a commercial soy lecithin preparation on development of sensorimotor behavior and brain biochemistry in the rat.

Pregnant rat dams and offspring were exposed to a 5 or 2% soy lecithin preparation or a control diet. Enrichment was either lifelong beginning at gestation, limited to the time preceding, or the time following weaning, or absent (constituting a "pure" control group). The most marked early sensorimotor deficits (reflex righting and swimming development) were seen in the 5% soy lecithin preparation group, although all soy lecithin preparation-exposed offspring had elevated brain/body weight ratios and choline acetyltransferase levels. Later, animals exposed to lifelong 5 or 2% soy lecithin preparations were hypoactive, had poor postural reflexes, and showed attenuated morphine analgesia. The results indicate that dietary soy lecithin preparation enrichment during development leads to behavioral and neurochemical abnormalities in the exposed offspring.

Animals↗
PubMed1980

Adsorption of lecithin by cholesterol.

Egg lecithin was adsorbed significantly by cholesterol monohydrate crystals. Adsorption data obtained at initial concentrations of less than 1.1 mM lecithin fitted the Langmuir equation. The calculated adsorption capacity suggested formation of a lecithin bilayer or a mixed bilayer of lecithin and cholesterol. The amount of lecithin adsorbed was highly dependent on the cholate concentration in the incubation medium. Minimal adsorption was observed at approximately 5 mM cholate. The presence of quaternary ammonium slats and dioctyl sodium sulfosuccinate caused desorption. The finding of an adsorptive layer supported the existence of an interfacial barrier than controls cholesterol dissolution.

Adsorption↗
PubMed1992

Lecithin organogel as matrix for transdermal transport of drugs.

Organogels obtained by adding small amounts of water to a solution of lecithin in organic solvents were studied as matrices for the transdermal transport of drugs. Gels obtained from isopropyl palmitate and cyclooctane were used (molar ratios of water to lecithin of 3 and 12, respectively). Preliminarily histological studies showed that the gels have no harmful effect when applied to the skin for prolonged periods. Data relative to the stability of the organogels with time are also presented. Scopolamine and broxaterol were used as model drugs, and the transdermal experiments were done with a Franz diffusion cell and human skin obtained from plastic surgery. The transport rate of scopolamine obtained with the lecithin gels was about one order of magnitude higher than that obtained with an aqueous solution of the drug at the same concentration. In contrast, the transport rates of scopolamine obtained with the microemulsion solution prior to gelation (molar ratio of water to lecithin, 0) were not different from those obtained with the gel. The same variations in transport rates were observed for broxaterol, in which case the flux through the skin was directly proportional to the concentration of drug in the gel. At a concentration of broxaterol of 75 mg/mL in the donor gel, the flux was 47 micrograms.h-1.cm-2. Because preliminary results showed that transdermal transport is successful with amino acids and peptides also, it is concluded that lecithin gels may be efficient vehicles for the transdermal transport of various drugs.

Adult↗
PubMed1998

The Effects of Caseinate Submicelles and Lecithin on the Thin Film Drainage and Behavior of Commercial Caseinate.

The drainage behaviour (stratification, thickness, and mobility) of thin foam films stabilized by commercial caseinate was studied in 10 mM phosphate buffer at pH 7.0. Thin films of commercial caseinate drained in a stepwise manner, with steps of similar thickness. The drainage was rapid, temperature sensitive, and chaotic, and the surface mobility of caseinate thin films also showed temperature sensitivity. The stepwise drainage is thought to be due to the layering of lecithin-caseinate submicelle complexes. Lecithin-stabilized thin films showed similar drainage behavior and temperature sensitivity. However, the films were approximately 66% thinner than caseinate films, and surface diffusion was very rapid. Removal of lipid from caseinate dramatically affects the thin film drainage properties and reduces temperature sensitivity. Reconstituted caseinate (i.e., extracted caseinate reconstituted with lipid), showed thin film properties similar to the commercial caseinate. Caseinate supplemented with lipid showed thin film drainage characteristics similar to caseinate, and surface mobility similar to lecithin. The presence of lecithin in caseinate thin films causes an increase in mobility, drainage, and stratification, along with a decrease in thin film thickness. This demonstrates that lecithin, possibly partially bound to the caseinate, is present at the interface disrupting protein-protein interactions. Copyright 1998 Academic Press.

Journal Article↗
PubMed1998

Effects of lecithinized SOD on sequential change in SOD activity after cerebral contusion in rats.

To analyze the effect of lecithinized superoxide dismutase (SOD) on superoxide accumulation after traumatic brain injury (TBI) in rats, we studied the SOD activity by NBT-reducing method and the expression of Cu,Zn-SOD mRNA by Northern blot analysis. As determined by the specific gravity method, the administration of lecithinized SOD decreased brain edema in the periphery of the lesion at 6 hr after contusion. SOD activity, without lecithinized SOD administration, increased at the peripheral portion at 30 min after contusion, but decreased to normal level at 6 hr after TBI. By administration of lecithinized SOD, the increase of SOD activity was preserved until 6 hr after TBI. The expression of Cu,Zn-SOD mRNA increased in the core lesion, peripheral portion, and contralateral hemisphere until 6 hr after TBI, then was suppressed in all three areas by lecithinized SOD. These results support the hypothesis that superoxide anions may play an important role in the development of brain edema after TBI, and that leciyhinized SOD appears to prevent brain edema through a protective effect against superoxide anions.

Animals↗
PubMed1995

Analysis of micellar and vesicular lecithin and cholesterol in model bile using 1H- and 31P-NMR.

The distribution of phospholipid and cholesterol between the vesicular and micellar phases in bile plays an important role in the formation of cholesterol gallstones. Conventional analytical procedures to determine the distribution are potentially unreliable because they disturb the distribution of these compounds between the two phases. In this work, we circumvent this problem by using NMR. 31P-NMR is used to quantify directly the micellar and the vesicular amount of lecithin. The previously described 1H-NMR method to determine directly the micellar lecithin (Groen et al., J Lipid Res 31: 1315-1321) has been optimized by the implementation of a spectral quantification method. The agreement between the 31P and 1H methods was excellent. In our hands, the method of Ellul et al. (FEBS Lett 300: 30-32) did not allow quantification of micellar cholesterol, although our fitting procedure offered the possibility of quantifying overlapping spectral peaks by the use of prior knowledge about all the parameters of the compounds visible in the spectrum. The micellar cholesterol concentration was so low compared to the overlapping lecithin peaks that no reliable quantification was possible. The same problem was encountered when using other characteristic cholesterol resonances for quantification. Our data suggest that cholesterol present in the vesicular phases is too immobile to give rise to high-resolution peaks and the amount of cholesterol present in the micellar phase is too low to allow quantitation by NMR. We conclude that 1H-NMR can be used to determine micellar lecithin, and 31P-NMR to determine micellar as well as vesicular lecithin in model bile.

Bile↗
PubMed1992

Lecithin cholesterol acyltransferase in human cerebrospinal fluid: reduced level in patients with multiple sclerosis and evidence of direct synthesis in the brain.

Several studies suggest that apolipoproteins and the low-density lipoprotein receptor are implicated in lipid transport in the brain. Given that cerebrospinal fluid has been reported to contain cholesteryl esterifying enzyme, and that lipid metabolism in the brain is abnormal in subjects with multiple sclerosis, we examined the cerebrospinal fluid from eight control subjects with a normal cerebrospinal fluid IgG index, and without active demyelinating disease, and from eight subjects (6 were diagnosed as having multiple sclerosis) with an increased IgG index and the presence of oligoclonal banding in the cerebrospinal fluid, for the presence of the enzyme lecithin cholesterol acyltransferase and apolipoprotein(a). None of the subjects demonstrated impairment of their blood-cerebrospinal fluid barrier, as estimated by the cerebrospinal fluid/serum quotient of albumin. Lecithin cholesterol acyltransferase was detected in the cerebrospinal fluid of all control subjects, being 0.12 +/- 0.06 microgram/ml (mean +/- SD) or about 2.2% of that in serum (5.4 +/- 1.4 micrograms/ml). The cerebrospinal fluid lecithin cholesterol acyltransferase index was 5.2 +/- 2.5, very similar to the cerebrospinal fluid index of apolipoprotein E, a protein known to be synthesized in the brain. Since lecithin cholesterol acyltransferase mRNA is also expressed in the brain, we can conclude that the protein is synthesized and secreted in the brain. The cerebrospinal fluid concentration of lecithin cholesterol acyltransferase in the subjects with active demyelinating disease or multiple sclerosis was only about one-half of that found in control subjects (0.06 +/- 0.02 microgram/ml).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1979

Plasma lecithin: cholesterol acyltransferase activity in liver disease.

The plasma lecithin: cholesterol acyltransferase was determined in patients with various liver diseases and the relationship between this enzyme activity and the other liver function tests were studied including long term observations. Lecithin: cholesterol acyltransferase activity in fulminant hepatitis and liver cirrhosis showed a significant decrease in comparison with normal volunteers. Although the enzyme activity of hepatoma showed significant decrease, they were ascribed to the influence of concomitant liver cirrhosis. The enzyme activity showed insignificant changes in the acute and chronic hepatitis and alcoholic liver disease. Lecithin: cholesterol acyltransferase activity was correlated with the concentration of cholesterolester rather than with the ratio of esters to cholesterol. In addition, it was well correlated with pseudocholine esterase and serum albumin. The lecithin: cholesterol acyltransferase activity in the cases during follow-up period varied in good parallel with cholesterol-esters concentration and pseudocholine esterase in the cases with acute hepatitis; with serum albumin in the cases with liver cirrhosis. Furthermore, it varied inversely with SGPT in the cases with acute hepatitis. In a case with hepatoma, lecithin: cholesterol acyltransferase activity decreased more sharply than the cholesterolesters concentration and serum albumin immediately before death.

Adult↗
PubMed1977

Reappraisal of cholesterol solubilization in bile salt-lecithin solution and the stability of bile.

On the basis obtained in a preceding study, cholesterol solubilization in aqueous bile salt-lecithin solution was investigated. The alteration of mixing sequence was found to yield differences not only in the rate but also in the magnitude of cholesterol solubilization. Both the rate and the magnitude were remarkably bigger in the system solubilizing cholesterol and lecithin mixture by bile salt than that solubilizing cholesterol crystal by bile salt with solubilized lecithin. A linear relation between the quantity of solubilized cholesterol and the concentration of bile salt except for lower concentration range was obtained for every bile salt-lecithin system. Values of k, the slope of the partial straight line, determined for cholate, chenodeoxycholate, deoxycholate and equimolar cholate-deoxycholate systems were 5.85 X 10(-2), 7.60 X 10(-2), 9.50 X 10(-2) and 7.17 X 10(-2), respectively. Cholesterol solubilizing power of bile salt was thus enhanced by the addition of lecithin. Since the solubilizing power could be given by the ratio of the solubilizate to the solubilizer, it was expressed graphically by the ratio of cholesterol to bile salt as ordinate and the concentration of bile salt as abscissa. The saturability of cholesterol solubilization in bile was purposefully exhibited in this graph by plotting assayed data of biliary lipid components.

Bile↗
PubMed1977

Enhancement of biliary phospholipid radioactivity by intestinal administration of labeled precursors of hepatic lecithin synthesis.

An animal model is used to study the effects of different radioactive precursors of lecithin, administered intestinally, upon biliary lecithin synthesis. Choline caused greater biliary lecithin radioactivity than choline-labeled lecithin or palmitic acid. The clinical application of this finding is discussed with relation to patients with gallstones or potentially lithogenic bile. Oral administration of choline may increase biliary lecithin concentration and, thus, cholesterol-holding capacity in this patient group, thereby changing the character of the bile to a non-lithogenic state.

Animals↗
PubMed1975

Lipid absorption in bile fistula rats. Lack of a requirement for biliary lecithin.

The role of biliary or dietary phosphatidylcholine (lecithin) in the process of lipid absorption was studied in bile fistual rats. Jejunal lipid-reesterifying enzyme activities were determined in experimental rats given diet, bile salts and phosphatidylethanolamine and results compared to controls given diet alone. Lipid absorption was also studied in vivo with radioactive techniques. Two groups of bile tistula rats were used. Both received diet and bile salts. In addition, one group was given phosphatidylethanolamine and the other received lecithin. Enzyme activities were moderately but significantly reduced in bile tistula rats receiving phosphatidylethanolamine. This was associated with an abnormal phospholipid composition of the microsomal membrane. Despite the changes in mucosal enzyme activity, however, no abnormality of lipid absorption was noted in bile fistula rats that received phosphatidylethanalamine. Results in this group were similar to controls and to the other bile fistula group given lecithin. In all groups, significant amounts of lecithin were recovered from the lumen of the small bowel. It is concluded that if lecithin is required for lipid absorption, it does not have to be supplied to the small bowel via the diet or in bile.

Acyltransferases↗
PubMed1982

In vitro modulation of the distribution of normal human plasma high density lipoprotein subfractions through the lecithin: cholesterol acyltransferase reaction.

The effect of the lecithin: cholesterol acyltransferase reaction on the chemical composition, morphology and distribution of normal human plasma high density lipoprotein (HDL) subclasses was studied in vitro. Incubation of plasma in the presence of polyenephosphatidylcholine (PPC) resulted in a 45 +/- 11% (n = 6) decrease in unesterified cholesterol after 20 h. This effect was abolished by prior heating of the plasma at 56 degrees C or by the addition of diisopropyl fluorophosphate (DIFP). Plasma triacylglycerol levels were constant. Analysis of the plasma lipoproteins by zonal ultracentrifugation and isopycnic equilibrium banding revealed a bimodal distribution of the HDL of native plasma and both heat-inactivated or DIFP-treated samples with peak maxima at d = 1.084 g/ml and d = 1.110 g/ml. Following the lecithin:cholesterol acyltransferase reaction essentially all of the HDL material had flotation characteristics typical of HDL2. The peak maximum was d = 1.086 g/ml. There were no apparent changes in the distribution of the lipoproteins of d less than 1.063 g/ml. The newly formed HDL were poor in PC and unesterified cholesterol but rich in cholesteryl ester, sphingomyelin and lyso-PC. The HDL apolipoprotein pattern was unaltered. HDL morphology was not affected by the lecithin:cholesterol acyltransferase reaction. Similar results were obtained in the absence of PPC. However, under these conditions the total phospholipid content of the HDL was reduced and lyso-PC was not demonstrable as a product of the lecithin:cholesterol acyltransferase reaction after 20 h. The results are interpreted to indicate that lecithin:cholesterol acyltransferase is involved in the transformation of HDL3 into HDL2.

Female↗
PubMed1986

Isolation and characterization of lecithin-cholesterol acyltransferase from hog plasma.

Lecithin-cholesterol acyltransferase (EC 2.3.1.43) was purified from hog plasma by a highly efficient procedure. The final enzyme preparation was purified 30,000-fold over the starting material and was homogeneous as indicated by polyacrylamide gel electrophoreses in the presence of both SDS and urea. 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%. The amino acid composition analysis showed that hog lecithin-cholesterol acyltransferase contains four half cystines per mol; two cysteines were titrated at neutral pH with 5,5'-dithiobis(2-nitrobenzoic acid). Nearly all the phenolic groups were unavailable to the solvent at neutral pH, while they become exposed at around pH 11. Hog lecithin-cholesterol acyltransferase was found to be associated with HDL in the plasma and it prefers HDL as a substrate. The physicochemical properties of hog lecithin-cholesterol acyltransferase were generally similar to those of the human and the rat enzyme.

Amino Acids↗
PubMed1987

In vitro formation of HDL-2 from HDL-3 and triacylglycerol-rich lipoproteins by the action of lecithin:cholesterol acyltransferase and cholesterol ester transfer protein.

In order to study the factors responsible for the formation of high-density lipoprotein subfraction-2 (HDL-2), very-low-density lipoproteins (VLDL) and HDL-3 were mixed and incubated with purified bovine milk lipoprotein lipase, human serum lecithin:cholesterol acyltransferase, cholesteryl ester transfer protein and mixtures thereof. The results can be summarized as follows: Incubation of HDL-3 and VLDL for 24 h at 37 degrees C without enzymes did not cause any significant change in the protein:lipid ratio or in the flotation constant of the HDL. Cholesteryl ester transfer protein treatment caused only an exchange of part of the HDL cholesteryl esters with VLDL triacylglycerols. Lipoprotein lipase caused a slight shift of HDL-hydrated density to lower values; HDL-2b, however, was not formed. Incubation of HDL-3 and VLDL with lecithin:cholesterol acyltransferase or mixtures of lecithin:cholesterol acyltransferase and lipoprotein lipase reduced the HDL-protein:lipid ratio and increased the HDL-flotation rate. The newly formed HDL resembled that of native HDL-2a. The incubation of HDL-3 and VLDL with lecithin:cholesterol acyltransferase and cholesteryl ester transfer protein caused a shift of the HDL-3 into an HDL-2b-like fraction. Particles resembling HDL-2b in the analytical ultracentrifuge were also formed if VLDL + HDL-3 were incubated with lipoprotein lipase or lipoprotein lipase + cholesteryl ester transfer protein in a medium containing low amounts of albumin, insufficient for binding all liberated fatty acids during hydrolysis. The incubation of mixtures of HDL-3 and chylomicrons enriched with apoAI in the presence of lecithin:cholesterol acyltransferase and cholesteryl ester transfer protein caused the formation of HDL-2-like particles which resembled those of native HDL-2 also with respect to the apoAI/AII ratio.

Carrier Proteins↗