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Results for “PALMITIC ACID”

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PubMed1993

The effect of digitonin and altered thyroid status on palmitic acid oxidation by isolated rat liver mitochondria.

The effect of altered thyroid status and food-deprivation on palmitic acid oxidation in isolated rat liver mitochondria was studied in the absence and presence of digitonin. Mitochondria prepared from triiodothyronine-treated (hyperthyroid) and food-deprived rats metabolized palmitic acid at the same rate as the untreated controls (euthyroid). Mitochondria prepared from thyroidectomized (hypothyroid) rats metabolized palmitic acid at a rate lower than was that seen with mitochondria from euthyroid controls in either the fed or fasted state. Fasting had no effect on palmitic acid oxidation by mitochondria prepared from euthyroid rats but diminished the rates seen in both hyper- and hypothyroid states. Digitonin (0.04 mg/mg mitochondrial protein) increased the sensitivity of the rate of fatty acid oxidation to inhibition by alpha-bromopalmitic acid. The addition of digitonin to the incubation mixture resulted in two-fold increases in the rate of palmitic acid oxidation in all states. This study shows that the limitations imposed by hypothyroidism on fatty acid oxidation in intact liver are preserved in isolated mitochondria.

Animals↗

PubMed2000

Kinetics of palmitic acid transport in insulin-dependent diabetic pregnancies: in vitro study.

BACKGROUND: The paucity of data relating to transport kinetics of free fatty acids (FFA) in pregnant diabetic women prompted the undertaking of the present study. METHODS: Transport kinetics of a model FFA, palmitic acid, have been investigated in Type I diabetic pregnancies, using in vitro perfusion of isolated placental lobules. National Cancer Tissue Culture medium diluted with Earle's buffered salt solution was used as the perfusate and control placental lobules were perfused for comparison. RESULTS: In five Type I diabetic women, the palmitic acid transport fraction (TF) averaged 5.6 +/- 0.42% of injected maternal bolus dose, representing 11.8 +/- 2.1% that of tritiated water used as reference. In control perfusions (n = 5), the palmitic acid TF represented 10.2 +/- 1.3% of tritiated water TF. Differential transport rates of palmitic acid for 10, 25, 50, 75 and 90% of efflux in fetal veins differed significantly from the corresponding values for tritiated water in both study and control series. However, palmitic acid transport rates for the various efflux fractions in the two series were not significantly different. For kinetic parameters, such as area under the curve, clearance, elimination constant, time for maximum response, absorption rate and elimination rate, the values for palmitic acid in the diabetic and control series also did not differ significantly. CONCLUSION: Transport kinetics of palmitic acid in Type I human diabetic pregnancies in in vitro conditions do not differ significantly from those observed in normal pregnancies.

Biological Transport↗

PubMed1993

Investigations into the growth of Mycobacterium leprae in a medium with palmitic acid under different gaseous environments.

Low oxygen tension has often been considered important for the growth of Mycobacterium leprae. Palmitic acid has been suggested as the oxidizable substrate for the in vitro cultivation of leprosy bacilli. The combined effects of palmitic acid and various known gas mixtures on the in vitro growth of M. leprae were investigated. When palmitic acid was included in the medium an optimal growth in both liquid and solid media was obtained between 16 to 20 weeks of incubation under gas mixtures containing 2.5 or 5% O2 and 5 or 10% CO2 as well as air. The use of different gas mixtures is tedious, time consuming and laborious. Since the cultures incubated under air gave the same cell yield as obtained when incubated under optimal gas mixtures, air alone can be used for the in vitro cultivation trials of M. leprae when palmitic acid is included in the culture medium.

Adenosine Triphosphate↗

PubMed1999

Dynamics of palmitic acid complexed with rat intestinal fatty acid binding protein.

Dynamics of palmitic acid (PA), isotopically enriched with 13C at the second, seventh, or terminal methyl position, were investigated by 13C NMR. Relaxation measurements were made on PA bound to recombinant rat intestinal fatty acid binding protein (I-FABP) at pH 5.5 and 23 degreesC, and, for comparison, on PA incorporated into 1-palmitoyl-2-hydroxy-sn-glycero-3-phosphocholine (MPPC) micelles, and dissolved in methanol. The 13C relaxation data, T1, and steady-state nuclear Overhauser effect (NOE) obtained at two different magnetic fields were interpreted using the model-free approach [Lipari, G., and Szabo, A. (1982) J. Am. Chem. Soc. 104, 4546-4559]. The overall rotational correlation time of the fatty acid.protein complex was 2.5 +/- 0.4 ns, which is substantially less than the value expected for the protein itself (>6 ns). Order parameters (S2), which are a measure of the amplitude of the internal motion of individual C-H vectors with respect to the PA molecule, while largest for C-2 and smallest for the methyl carbon, were relatively small (<0.4) in the protein complex. S2 values for given C-H vectors also were smaller for PA in the MPPC micelles and in methanol than in the protein complex. Correlation times reflective of the time scale of the internal motion of the C-H vectors were in all cases <60 ps. These results support the view that the fatty acid is not rigidly anchored within the I-FABP binding pocket, but rather has considerable freedom to move within the pocket.

Animals↗

PubMed1995

LDL receptor activity is down-regulated similarly by a cholesterol-containing diet high in palmitic acid or high in lauric and myristic acids in cynomolgus monkeys.

To determine the mechanisms whereby diets differing widely in fatty acid composition affect plasma LDL cholesterol and apolipoprotein B concentrations, LDL kinetics and receptor- and nonreceptor-mediated LDL catabolism were investigated in 27 cynomolgus monkeys fed diets containing 0.05 mg cholesterol/kJ and 40% fat energy as corn oil alone (unsaturated fat diet rich in oleic and linoleic acids), nonhydrogenated coconut oil alone (saturated fat diet, rich in lauric and myristic acids) or an oil blend (rich in palmitic acid). Consumption of the oil blend and saturated fat diets significantly elevated total cholesterol, LDL cholesterol and apolipoprotein B concentrations relative to the unsaturated fat diet and the saturated fat diet significantly increased plasma total cholesterol and LDL cholesterol compared with the oil blend diet. However, despite the greater increases in plasma total cholesterol, LDL cholesterol and apolipoprotein B in the saturated fat vs. the oil blend dietary group, the receptor-mediated LDL fractional catabolic rate was comparable in the oil blend and saturated fat diet groups. In addition, consumption of the oil blend or saturated fat diet increased the production rate of LDL apolipoprotein B and nonreceptor-mediated LDL apolipoprotein B transport (disposal) relative to the unsaturated fat diet. Our data, therefore, suggest that consumption of the oil blend or saturated fat diet elevated plasma total cholesterol and LDL cholesterol relative to the unsaturated fat diet, and the oil blend diet abundant in palmitic acid seems to have down-regulated the LDL receptor as much as a more saturated fat diet abundant in lauric and myristic acids.

Animals↗

PubMed1992

Palmitic acid enhances cholesterol gallstone incidence in Sasco hamsters fed cholesterol enriched diets.

In an established hamster model of cholesterol cholelithiasis, a semipurified lithogenic diet containing 4% butterfat and 0.3% cholesterol leads to the production of cholesterol gallstones in only 50-60% of animals after a 6-wk feeding period. The purpose of this study was to investigate whether gallstone incidence could be increased while feeding a nutritionally adequate diet of moderate cholesterol content. The semipurified lithogenic diet was modified as follows: (i) substitution of 1.2% palmitic acid for 4% butterfat, and (ii) varying the amount of dietary cholesterol from 0.0 to 0.3% with either butterfat or palmitic acid as the lipid component of the diet. Substitution of palmitic acid for butterfat produced a significantly higher incidence of cholesterol gallstones (94% vs. 53%). Palmitic acid also raised the incidence of gallstones when added to the 0.1% and 0.2% cholesterol diets as compared to butterfat: 0% vs. 44% and 50% vs. 81%, respectively. Gallstone incidence increased from 0% to nearly 100% when the cholesterol content of the palmitic acid diets was raised from 0.0% to 0.3%, indicating a dose response effect with respect to dietary cholesterol. Hamsters fed cholesterol-free diets did not form gallstones. Increased dietary cholesterol led to increased liver weight associated with a significant increase in liver cholesterol concentration. However, the palmitic acid groups had significantly lower liver cholesterol values than the corresponding butterfat groups. Serum and biliary cholesterol concentrations increased with increasing dietary cholesterol intake, but there were no differences between the butterfat and palmitic acid groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed2003

[Apoptosis-inducing effect of palmitic acids on rat pancreatic islet cells in primary culture: a preliminary study].

OBJECTIVE: To investigate the in vitro apoptosis-inducing effect of palmitic acid on pancreatic islet cells in primary culture, thereby to understand the role of palmitic acid in the pathogenesis of type 2 diabetes mellitus. METHOD: SD rat pancreatic islet cells were isolated and cultured in monolayer in vitro followed by incubation with stepwise diluted palmitic acid (0, 0.125, 0.25 mmol/L and 0.5 mmol/L respectively), and the insulin concentrations in the culture medium were determined by radio immunological methods. Morphological observation with a fluorescence microscope was conducted after double staining of the cells with PI/Hoechst 33342. RESULTS: The glucose-stimulated insulin secretion was inhibited by palmitic acid at the concentration of 0.25 and 0.5 mmol/L, which also induced obvious cell apoptosis. CONCLUSION: Palmitic acid is capable of inducing islet cell apoptosis in a dose-dependent manner.

Animals↗

PubMed1984

Reconstitution of the lipid-depleted pyruvate oxidase system of Escherichia coli: the palmitic acid effect.

Previous work has shown that the coupling of the soluble Escherichia coli pyruvate oxidase to a lipid-depleted membrane terminal electron transport system requires the addition of ubiquinone and a neutral lipid fraction (C. Cunningham and L. P. Hager (1975) J. Biol. Chem. 250, 7139-7146). The active factor present in the neutral lipid fraction has now been isolated and characterized. NMR, uv, and mass spectroscopic analysis identifies palmitic acid as the active component. A comparison of palmitic acid with other fatty acids of varying chain lengths indicates that most fatty acids having chain lengths in the range C12 to C20 have comparable activity to palmitic acid. Exceptions are stearic and arachidic acid which have greatly reduced activity. Fatty acids of C6 to C10 chain length showed about one third the activity of palmitic acid. Fatty acids having chain lengths of 2 to 5 carbon atoms are essentially inactive. The carboxyl function of the fatty acid is required for activity. Derivatives of fatty acids in which the carboxyl group had been modified to an alcohol, aldehyde, or methyl ester function show greatly diminished activity. Both the cis and trans forms of unsaturated long-chain fatty acids are active. The stimulation of the electron transfer reaction by fatty acids occurs at the ubiquinone level of the electron transport chain. Ubiquinone-30 is rapidly reduced by pyruvate oxidase only in the presence of palmitic acid.

Chemical Phenomena↗

PubMed1984

An examination of the stereochemical course of acylation of 2-monoacylglycerols by rat intestinal villus cells using [2H3]palmitic acid.

The stereochemical course of acylation of 2-monoacylglycerols by rat intestinal mucosa was investigated using isolated villus cells with 2-lauroylglycerol and [2H3]palmitic acid as substrates. The newly synthesized X-1,2-diacylglycerols and triacylglycerols were recognized on the basis of the content, positional distribution and molecular association of the fatty acids by gas-liquid chromatography/mass spectrometry in combination with sterospecific analysis. It was found that the free X-1,2-[2H3]palmitoyllauroylglycerols contained 74% sn-1,2- and 26% sn-2,3-enantiomers, which were utilized for triacylglycerol formation in the same proportion. Some of the 2-monolauroylglycerol became hydrolyzed and the released lauric acid was utilized along with [2H3]palmitic acid for diacylglycerol and triacylglycerol formation via both the phosphatidic acid and the 2-monoacylglycerol pathway. The contribution of the phosphatidic acid pathway (12-16%) was determined by estimating the relative proportion of the newly synthesized triacylglycerols containing [2H3]palmitic acid in the sn-2 position. After correcting for the contribution of the phosphatidic acid pathway, the sn-1,2-/sn-2,3-enantiomer ratio in the X-1,2-[2H3]palmitoyllauroylglycerol was estimated to be 71/29. These results are consistent with those previously obtained with glycerol-labelled 2-monoacylglycerols and intact tissue or homogenates of rat intestinal mucosa. It is suggested that the 2-mono-acylglycerol transacylase, if a single enzyme, possesses a low stereospecificity, or that two enzymes exist of unequal concentration and/or activity.

Acyltransferases↗

PubMed1997

Stable-isotope method for determining the gastrointestinal handling of [1-13C]palmitic acid.

The 13C enrichment in individual fatty acids extracted from human feces following the oral administration of [1-13C]palmitic acid has been determined using a novel approach based upon gas chromatography-isotope ratio mass spectrometry. The method was established and tested for precision and repeatability. Analytical precision was determined from 10 repeated injections of a sample containing 16:0 and 18:0 with levels of delta 13C abundance measured at -34.01 +/- 0.60 and -23.62 +/- 0.95 delta per mil (parts per thousand) (/1000), respectively (mean +/- SD). For the repeatability study, measurement of enrichment of the same mixture of unlabeled fatty acid methyl ester (FAME) standards (13:0, 14:0, 16:0, and 18:0) was found to have standard deviations (0.45, 0.56, 1.46 and 1.54/1000, respectively). When labeled [1-13C]palmitic acid was serially diluted with naturally enriched palmitic acid, a linear relationship was obtained to a dilution of 10% enriched compound (530/1000). FAME were prepared from two fecal samples from a normal healthy adult; the first, a baseline specimen, containing no added label and the second, followed a single oral dose of [1-13C]palmitic acid and was enriched. Enrichment in 13C was confined to the solvent-soluble fraction following lipid extraction, and was only identified with prior acidification. The enrichments were measured in triplicate, baseline sample -32.66 +/- 0.5/1000, enriched sample +268.61 +/- 8.0/1000. Enrichment was restricted to the labeled species consumed, 16:0. The methodology described here allows for the separation of compounds prior to the determination of enrichment and can be utilized to contribute to a more complete description of the gastrointestinal handling of labeled substrates than previously obtained.

Carbon Isotopes↗

PubMed1986

The effect of pH on the phase transition temperature of dipalmitoylphosphatidylcholine-palmitic acid liposomes.

The shift in the gel-liquid crystal phase transition temperature (tm) of dipalmitoylphosphatidylcholine liposomes induced by incorporation of 10 mol% palmitic acid, was measured by 90 degrees light scattering at different bulk pH values. It has been found that the tm shift decreases sigmoidally from 4.7 to -0.3 degrees C as the bulk pH is raised from 5 to 11. Since it is in this range that the carboxyl group of a membrane-bound fatty acid should ionize, our results can be interpreted to mean that there is relationship between the tm shift and the degree of dissociation of palmitic acid, the uncharged fatty acid increasing tm and its conjugate, anionic form, slightly decreasing the transition temperature of dipalmitoylphosphatidylcholine liposomes. The experimental results are fitted by a modified form of the Henderson-Hasselbach equilibrium expression which takes into account the effect of the anionic fatty acid on the surface potential and hence, on the surface pH of liposomes, according to Gouy-Chapman and Boltzmann equations, respectively. Best fit between theory and experiments is found when the intrinsic interfacial pK of palmitic acid is set equal to 7.7. This high pK value can be explained as due to the effect of the lower dielectric constant of the interfacial region, as compared to bulk water, on the acid-base dissociation of the carboxyl group. The results presented here show that upon incorporation of palmitic acid, the phase transition of dipalmitoylphosphatidylcholine bilayers becomes extremely sensitive to changes of pH in the vicinity of the physiological range. This property is not shown by the pure phospholipid bilayers in the same pH range.

1,2-Dipalmitoylphosphatidylcholine↗

PubMed1985

In vivo incorporation of palmitic acid and galactose in glycolipids of Trypanosoma cruzi epimastigotes.

Incubation of epimastigote forms of Trypanosoma cruzi with (3H)-palmitic acid and (3H)-galactose, respectively, results in the incorporation of both precursors into the lipopeptidophosphoglycan (LPPG) and in at least two glycosphingolipids. Palmitic acid was incorporated into sphinganine and sphingenine, identified after hydrolysis, respectively, of the major and the minor glycosphingolipid. The purified glycosphingolipids labeled with either precursor migrated with a Rf similar to that of a sample labeled by periodate oxidation and borotritide reduction in which sialic acids have been previously characterized. This, together with the fact that the palmitic acid labeled glycosphingolipids were partially hydrolysed with neuraminidase favors a ganglioside-like structure for these compounds.

Animals↗

PubMed1975

Palmitic acid concentrations and lecithin/sphingomyelin ratios in amniotic fluid.

Palmitic acid concentrations and L/S ratios have been estimated in amniotic fluid specimens with and without centrifugation and cold acetone precipitation. Although the number of cases was small, both of these measurements in uncentrifuged fluid seemed to reflect only indirectly on lung maturation in normal pregnancy while with centrifuged fluid the L/S value predicted RDS in one infant more reliably than palmitic acid concentration.

Acetone↗

PubMed1995

Palmitic acid and linoleic acid metabolism in Caco-2 cells: different triglyceride synthesis and lipoprotein secretion.

Polarized monolayers of intestinal Caco-2 cells were used to study the effects of saturated palmitic acid (16:0) and polyunsaturated linoleic acid (18:2) on triglyceride synthesis and lipoprotein secretion. Monolayers were incubated for 24 h, at the apical or lumenal side, with palmitic acid (16:0) or linoleic acid (18:2) in physiological concentrations. Incubation with 1.0 mM 16:0 or 18:2 resulted in differences in the composition and amount of secreted lipoproteins. Radiolabeled lipids in the lipoproteins secreted during incubation with 18:2 were found in the chylomicron/VLDL (very low density lipoprotein) density whereas with 16:0 the secreted lipoproteins were in the intermediate density/low density lipoprotein (IDL/LDL) density range. More triglyceride was secreted into the (basolateral) medium during incubation with 1.0 mM 18:2 (41 +/- 12% of total triglyceride synthesized) than with 1.0 mM 16:0 (18 +/- 3% of total). The biochemical findings correlate with conspicuous morphological changes in the cells in the presence of 16:0, but not 18:2. Increasing concentrations of 16:0 (0.1-1.0 mM) caused gradual accumulation of intracellular membrane. Microvilli became strongly reduced in number. With 1.0 mM palmitic acid we found an increased incorporation of [1-14C]palmitic acid into phosphatidic acid (14.8% of total incorporation into phospholipid with 16:0 vs. < 0.5% with 18:2) and diacylglycerol (12.5% with 16:0 vs. < 0.5% with 18:2) and diacylglycerol (12.5% with 16:0 vs. 0.5% with 18:2) and the amount of intracellular phospholipid doubled. The morphological changes were completely reversed after 24 h with 1.0 mM 18:2. We conclude from our results that, compared to 18:2, 16:0 is not efficiently incorporated into triglycerides. 16:0 is incorporated into cellular phospholipids in a greater proportion than 18:2, causing accumulation of intracellular phospholipid and the precursors phosphatidic acid and diacylglycerol. Different processing of 18:2 and 16:0 by Caco-2 cells resulted in profound differences in triglyceride synthesis and lipoprotein composition and secretion.

Carbon Radioisotopes↗

PubMed1992

Differential diagnosis of hydroxydicarboxylic aciduria based on release of 3H2O from [9,10-3H]myristic and [9,10-3H]palmitic acids by intact cultured fibroblasts.

Intact cultured fibroblasts from patients with deficiency of long-chain 3-hydroxyacyl-CoA dehydrogenase release 3H2O from [9,10-3H]myristic acid and [9,10-3H]palmitic acid more slowly than normal. The ratio of activity (palmitate/myristate) is also low and the expression (rate with palmitate2/(rate with myristate) gives good differentiation between affected and unaffected cells. In some patients who have shown hydroxydicarboxylic aciduria when unwell there is reduced 3H2O production from [9,10-3H]myristic and [9,10-3H]palmitic acids by intact cultured fibroblasts but normal 3-hydroxyacyl-CoA dehydrogenase activities in disrupted cells. The palmitate/myristate ratio is higher than in long-chain 3-hydroxyacyl-CoA dehydrogenase deficiency. The basic defect in these patients is still unknown but it is suggested that caution be used over the administration of medium-chain triglyceride.

3-Hydroxyacyl CoA Dehydrogenases↗

PubMed1996

Structural position and amount of palmitic acid in infant formulas: effects on fat, fatty acid, and mineral balance.

The structure of the triglycerides (TG) in human milk (HM) differs from those of vegetable oils used in infant formulas. In HM, palmitic acid is predominantly esterified to the center or beta-position of the TG, in vegetable oil, it is mainly at the external or alpha-positions. These differences in configuration affect intestinal fat absorption. Fat and mineral balances were investigated in three groups of 9 healthy term infants aged 5 weeks. Infants were randomly assigned to receive one of the three study formulas from birth: (a) formula beta, resembling the structure of HM fat most closely (24% palmitic acid, 66% esterified to beta-position), (b) formula intermediate (24% palmitic acid, 39% esterified to the beta-position), and (c) regular formula (20% palmitic acid; 13% esterified to the beta-position). Fat absorption was highest in infants fed the beta formula (97.6 +/- 0.9%), intermediate in those fed with the intermediate formula (93.0 +/- 1.8%), and lowest in infants receiving the regular formula (90.4 +/- 4.6%). Fecal calcium excretion was significantly lower in the beta group than in the other two groups (43.3 +/- 18.1 vs. 59.9 +/- 15.1 vs. 68.4 +/- 22.3 mg.kg-1.day-1 for beta, intermediate, and regular respectively). Dietary TG containing palmitic acid predominantly at the beta-position, as in HM, have significant beneficial effects on the intestinal absorption of fat and calcium in healthy term infants.

Calcium↗

PubMed1996

Comparison of pharmacokinetic parameters of a polypeptide, the Bowman-Birk protease inhibitor (BBI), and its palmitic acid conjugate.

PURPOSE: The alteration of the pharmacokinetic parameters of the polypeptide BBI through conjugation with palmitic acid was examined. METHODS: 125I-BBI or 125I-Pal-BBI was administered iv to 6 week old CF-1 mice at a dose of 3 mg/kg. The mice were sacrificed at 5, 10, 20, 60, 120, 240, 360, and 480 min and the total radioactivity was determined for blood and each organ. The blood was analyzed on a Sephadex G-50 size-exclusion column to determine the amount of intact polypeptide present in the blood. From the amount of intact polypeptide at each time point, the pharmacokinetic parameters were determined. RESULTS: By conjugating three palmitic acids to each BBI molecule, the area under the curve (AUC) and mean residence time (MRT) increase by a factor of 10.8 and 2.8, respectively. There was also a difference in the organ distribution between the two treatments; while 125I-BBI was rapidly cleared from the kidneys, 125I-Pal-BBI was predominantly to the liver. Subsequent studies suggested that the binding of the conjugate to non-albumin serum proteins was most likely the cause of the altered pharmacokinetics. CONCLUSIONS: The residence time in the blood and the lipophilicity of BBI were increased upon conjugation with palmitic acid through a reversible disulfide linkage. Pharmacokinetic studies showed an increase in the AUC and a decrease in kidney clearance in palmitic acid conjugates, indicating a potential increase of the therapeutic efficacy of the polypeptide drug.

Animals↗

PubMed1988

Cotranslational fatty acylation of mucus glycoprotein. Addition of palmitic acid to peptidyl-tRNA occurs prior to peptide chain completion and its release.

1. The fatty acylation of mucus glycoprotein nascent peptides was investigated using [3H]palmitic acid and [35S]methionine-labeled peptidyl-tRNA of rat gastric mucous cells. 2. The mucus glycoprotein peptidyl-tRNA fraction was found to contain covalently bound palmitic acid in its complexes. 3. RNase digestion of the mucus glycoprotein peptidyl-tRNA released [3H]palmitic acid labeled peptides which, on SDS-polyacrylamide gel, separated into a multitude of bands ranging in size from 2000 to 60,000 Da. 4. The analyses of low molecular weight peptides revealed that palmitic acid was present in methionine-labeled peptides containing 30-43 amino acids and those of 18-25 amino acids or larger devoid of methionine, but was not identified in methionine-labeled peptides containing 10-15 amino acids. 5. The results indicate that the N-terminal fatty acylation of mucus glycoprotein nascent peptides is a cotranslational process which is occurring in an immediate vicinity of the signal peptide fragment.

Acylation↗