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Results for “PALMITIC ACID”

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PubMed2002

The oxygen-substituted palmitic acid analogue, 13-oxypalmitic acid, inhibits Lck localization to lipid rafts and T cell signaling.

Palmitoylation of cysteines 3 and 5 is necessary for targeting Lck to lipid rafts and is needed for Lck function in T cell receptor (TCR) signaling. Point mutations of cysteines 3 and 5 result in a form of Lck that fails to associate with the plasma membrane, which limits the usefulness of this genetic approach to address the role of palmitoylation in the distribution of Lck within the plasma membrane. To circumvent this problem, we sought to identify a palmitic acid analogue that would enable plasma membrane association of Lck, but not facilitate its localization within lipid rafts. Here we examined the effects of the heteroatom-substituted analogue of palmitic acid, 13-oxypalmitic acid (13-OP), on Lck subcellular localization and function. 13-OP is similar in chain length to palmitic acid, but possesses reduced hydrophobicity. We found that treatment of cells with 13-OP inhibited incorporation of omega-[(125)I]iodopalmitate into Lck. 13-OP inhibited localization of Lck to lipid rafts without altering its membrane localization. Consistent with the dissociation of Lck from rafts, treatment with 13-OP abolished Lck association with the GPI-anchored protein, CD48, but not the transmembrane glycoprotein CD4. Jurkat T cells treated with 13-OP showed marked reduction in tyrosine phosphorylation and activation of mitogen-activated protein kinase upon TCR stimulation. In conclusion, the less hydrophobic analogue of palmitate, 13-OP, alters the normal acylation of Lck that provides Lck with the necessary hydrophobicity and tight packing order required for inclusion in lipid rafts.

Antigens, CD↗

PubMed2004

Phenotype of palmitic acid transport and of signalling in alveolar type II cells from E/H-FABP double-knockout mice: contribution of caveolin-1 and PPARgamma.

Based on the assumption that fatty-acid-binding proteins (FABPs) of the epidermal-type (E-FABP) and heart-type (H-FABP) in murine alveolar type II (TII) cells mediate the synthesis of dipalmitoyl phosphatidylcholine (DPPC), the main surfactant phospholipid, we analysed TII cells isolated from wild-type (wt) and E/H-FABP double-knockout (double-ko) mice. Application of labelled palmitic acid to these cells revealed a drop in uptake, beta-oxidation, and incorporation into neutral lipids and total phosphatidylcholine (PC) of TII cells from double-ko mice. Whereas incorporation of labelled palmitic acid into DPPC remained unchanged, degradation studies demonstrated a substantial shift in DPPC synthesis from de novo to reacylation. In addition, increased expression of mRNAs and proteins of caveolin-1 and PPARgamma, and an increase of the mRNA encoding fatty acid translocase (FAT) was observed in the double-ko phenotype. As caveolin-1 interacted with PPARgamma, we assumed that FAT, caveolin-1, and PPARgamma form a signalling chain for fatty acid or drug. Consequently, PPARgamma-selective pioglitazone was added to the diet of double-ko mice. We found that further activation of PPARgamma could 'heal' the E/H-FABP double-ko effect in these TII cells as transport and utilisation of labelled palmitic acid restored a wt phenocopy. This indicated that E-FABP and/or H-FABP are involved in the mediation of DPPC synthesis in wt TII cells.

Animals↗

PubMed2006

Growth arrest and decrease of alpha-SMA and type I collagen expression by palmitic acid in the rat hepatic stellate cell line PAV-1.

Liver fibrosis is characterized by an activation of hepatic stellate cells (HSC). During primary culture HSC evolve from a quiescent into an activated phenotype which is characterized by alpha-smooth muscle actin (alpha-SMA) up-regulation, increase in cell growth, and extracellular matrix secretion. HSC culture with trans-resveratrol can lead to deactivation of myofibroblast-like HSC. We used an HSC line, PAV-1, to check the role of retinol and palmitic acid in the deactivation process of HSC. Using mass and metabolic-based methods, Western blot and immunocytochemistry assays, we demonstrated that treatment with palmitic acid (75 muM) alone or in combination with retinol (2 muM) significantly decreased cell proliferation and alpha-SMA expression. We also established that the association of both compounds strongly decreased collagen type I expression. Our results suggest the potential use of palmitic acid alone or in combination with retinol to induce HSC deactivation.

Actins↗

PubMed2001

Effects of lung surfactant proteins, SP-B and SP-C, and palmitic acid on monolayer stability.

Langmuir isotherms and fluorescence and atomic force microscopy images of synthetic model lung surfactants were used to determine the influence of palmitic acid and synthetic peptides based on the surfactant-specific proteins SP-B and SP-C on the morphology and function of surfactant monolayers. Lung surfactant-specific protein SP-C and peptides based on SP-C eliminate the loss to the subphase of unsaturated lipids necessary for good adsorption and respreading by inducing a transition between monolayers and multilayers within the fluid phase domains of the monolayer. The morphology and thickness of the multilayer phase depends on the lipid composition of the monolayer and the concentration of SP-C or SP-C peptide. Lung surfactant protein SP-B and peptides based on SP-B induce a reversible folding transition at monolayer collapse that allows all components of surfactant to be retained at the interface during respreading. Supplementing Survanta, a clinically used replacement lung surfactant, with a peptide based on the first 25 amino acids of SP-B also induces a similar folding transition at monolayer collapse. Palmitic acid makes the monolayer rigid at low surface tension and fluid at high surface tension and modifies SP-C function. Identifying the function of lung surfactant proteins and lipids is essential to the rational design of replacement surfactants for treatment of respiratory distress syndrome.

Adsorption↗

PubMed1993

Disappearance of palmitic acid from plasma of fetal and newborn sheep.

These studies were undertaken to measure the kinetic constants that characterize the disappearance of a representative free fatty acid (FFA) from the plasma of fetal and newborn sheep. A bolus of albumin-complexed [14C]palmitic acid was infused intravenously, and during the next 8 min, 24 arterial samples were collected to characterize the disappearance curve. Palmitic acid disappearance from plasma was well described by a double-exponential model. When birth was simulated in utero, kinetic values were not changed by cooling. However, after intrauterine ventilation with O2, the volume of distribution of the FFA increased 29%, its plasma clearance rate decreased 26%, and its apparent half-life in the plasma lengthened from 0.8 to 1.2 min (all P < 0.01, n = 8). After umbilical cord occlusion, plasma clearance rate decreased a further 19% and half-life lengthened to 1.4 min. About 60% of the increase in FFA concentration during simulated birth is explained by increased release from adipose stores, and 40% is explained by decreased clearance. Further experiments tested the influence of FFA concentrations themselves. After infusion of unlabeled FFA, clearance of the tracer decreased 23% (P < 0.05, n = 5), a result consistent with a saturable membrane transporter of FFAs.

Animals↗

PubMed2007

Condensing effect of palmitic acid on DPPC in mixed Langmuir monolayers.

The interaction between deuterated dipalmitoylphosphatidylcholine (DPPC-d62) and palmitic acid (PA) in mixed Langmuir monolayers is studied using vibrational sum frequency generation (VSFG) spectroscopy. Palmitic acid is an additive in exogenous lung surfactant preparations such as Survanta and Surfaxin. The effect of PA on the chain conformation and orientation of DPPC in the liquid-expanded and condensed phases is explored. A condensing effect of PA on DPPC is observed with VSFG. At 12 mN/m, DPPC-d62 alone is in the liquid-expanded phase. Adding PA increases the conformational ordering of DPPC chains and causes DPPC to transition from the expanded phase into the condensed phase. At 42 mN/m, DPPC-d62 and PA form a mixed structure in the condensed phase. The presence of PA decreases the chain tilt angle of DPPC, increasing the orientational ordering of DPPC chains. At 42 mN/m, there is also evidence from the frequency red shift of the PO2- symmetric stretch that the carboxyl group of PA forms a hydrogen bond with the phosphate group of DPPC in the condensed phase. From this work the effect of PA on DPPC is 2-fold: (1) PA increases the chain ordering of DPPC and promotes the LE and TC phase separation and (2) due to the miscibility between DPPC and PA in the condensed phase, PA decreases the collapse pressure.

Journal Article↗

PubMed1995

Effect of sodium dodecyl sulfate and palmitic acid on the equilibrium unfolding of bovine beta-lactoglobulin.

The unfolding of bovine beta-lactoglobulin, a small globular protein that unfolds reversibly at low pH in the presence of urea or guanidine hydrochloride, has been studied at pH 6.72 in phosphate buffer at 21 degrees C. The midpoint urea concentration for the loss of CD intensity at 220 nm, loss of CD intensity at 293 nm, quenching of intrinsic fluorescence, shift in the wavelength of the maximum of the intrinsic fluorescent emission, and loss of fluorescence intensity from 1-anilino-8-naphthalenesulfonate (ANS) (and probably the hydrophobic binding site) was close to 4.4 M. Addition of sodium dodecyl sulfate (SDS) at concentrations less than 100 microM to the beta-lactoglobulin solutions increased the midpoint urea concentration for the CD and intrinsic fluorescence parameters to about 5.8 M. Palmitic acid had a similar effect to that shown by SDS in altering the CD intensity at 293 nm, and both SDS and palmitic acid attained a maximum effect in altering the CD at 293 nm at a 1:1 molar ratio to beta-lactoglobulin. It seems likely that the beta-sheet structure of beta-lactoglobulin breaks down simultaneously with the loss of the hydrophobic binding site and exposure of tryptophan-19 to the external environment, supporting the view that the major hydrophobic binding site of beta-lactoglobulin is closely involved with the beta-sheet core of the protein.(ABSTRACT TRUNCATED AT 250 WORDS)

Anilino Naphthalenesulfonates↗

PubMed2005

Urea biosensors based on PVC membrane containing palmitic acid.

A new urea biosensor was prepared by immobilizing urease with four different procedures on poly(vinylchloride) (PVC) ammonium membrane electrode containing palmitic acid by using nonactine as an ammonium-ionophore. The analytical characteristics were investigated and were compared those of the biosensor prepared by using carboxylated PVC. The effect of pH, buffer concentration, temperature, urease concentration, stirring rate and enzyme immobilization procedures on the response to urea of the enzyme electrode were investigated. The linear working range and sensitivity of the biosensor were also determined. The urea biosensor prepared by using the PVC membranes containing palmitic acid showed more effective performance than those of the carboxylated PVC based biosensors. Additionally, urea assay in serum was successfully carried out by using the standard addition method.

Biosensing Techniques↗

PubMedDate not supplied

The effect of histone deacetylase inhibitor trichostatin A (TSA) on the incorporation of 32P (Pi) and 3H-palmitic acid into the phospholipids of Tetrahymena.

Histone deacetylases (HDACs) are able to control also the acetylation of tubulin. In the present experiments the effect of trichostatin A (TSA), a HDAC inhibitor was studied on the incorporation of 3H-palmitic acid and 32P to the phospholipids (PI, PIP, PS, PC, PA, PE) of Tetrahymena pyriformis, considering earlier observations on the microtubular system's influence on signalling in this unicellular eukaryote. Treatment with 1, 5, or 10 microM TSA was studied. The incorporation of hydrophobic tail component, palmitic acid was inhibited in a concentration dependent manner into all the phospholipids, except for PA, where the incorporation was increased. 32P incorporation was also inhibited. The possible relation between the microtubular system and signalling is discussed.

Animals↗

PubMed2005

Increasing dietary palmitic acid decreases fat oxidation and daily energy expenditure.

BACKGROUND: Oleic acid (OA) is oxidized more rapidly than is palmitic acid (PA). OBJECTIVE: We hypothesized that changing the dietary intakes of PA and OA would affect fatty acid oxidation and energy expenditure. DESIGN: A double-masked trial was conducted in 43 healthy young adults, who, after a 28-d, baseline, solid-food diet (41% of energy as fat, 8.4% as PA, and 13.1% as OA), were randomly assigned to one of two 28-d formula diets: high PA (40% of energy as fat, 16.8% as PA, and 16.4% as OA; n = 21) or high OA (40% of energy as fat, 1.7% as PA, and 31.4% as OA; n = 22). Differences in the change from baseline were evaluated by analysis of covariance. RESULTS: In the fed state, the respiratory quotient was lower (P = 0.01) with the high OA (0.86 +/- 0.01) than with the high-PA (0.89 +/- 0.01) diet, and the rate of fat oxidation was higher (P = 0.03) with the high-OA (0.0008 +/- 0.0001) than with the high-PA (0.0005 +/- 0.0001 mg . kg fat-free mass(-1) . min(-1)) diet. Resting energy expenditure in the fed and fasting states was not significantly different between groups. Change in daily energy expenditure in the high-OA group (9 +/- 60 kcal/d) was significantly different from that in the high-PA group (-214 +/- 69 kcal/d; P = 0.02 or 0.04 when expressed per fat-free mass). CONCLUSIONS: Increases in dietary PA decrease fat oxidation and daily energy expenditure, whereas decreases in PA and increases in OA had the opposite effect. Increases in dietary PA may increase the risk of obesity and insulin resistance.

Adult↗

PubMed1982

Diagnosis and differentiation of fat malabsorption in children using 13C-labeled lipids: trioctanoin, triolein, and palmitic acid breath tests.

Three substrates labeled with nonradioactive 13C have been employed to establish a trilogy of noninvasive breath tests to detect fat malabsorption in children and then to differentiate the etiology of the steatorrhea. Administration of 17 mg/kg of (13C)triolein Lipomul (The Upjohn Co., Kalamazoo, Mich.) resulted in a peak excretion rate of 13CO2 greater than 2.7% dose/h in 10 normal subjects (mean value 4.96 +/- 2.2% dose/h) whereas all 17 subjects with fat malabsorption were below this value (mean value, 0.75% +/- 0.63% dose/h); p less than 0.001). For the detection of fat malabsorption, the discriminative value of (13C)triolein was superior, 100% sensitive, and 89% specific, while the use of (13C)palmitic acid (17 mg/kg) or (13C)trioctanoin (7.5 mg/kg) alone yielded both false-positive and false-negative results. In 6 out of 6 cases, pancreatic insufficiency could be differentiated from mucosal disease (7 patients) or bile salt deficiency (4 patients) by the presence of abnormal triolein or trioctanoin breath tests, or both but normal palmitic acid breath tests. However, further differentiation of mucosal disorders from bile salt disorders could not be achieved using either a single- or a multiple-substrate breath test. The use of the single triolein breath test in children offers an attractive, sensitive alternative to conventional fecal fat measurements to establish the presence of steatorrhea, and when using 12C-lipid with multiple substrates, the tests are capable of providing additional insight into the mechanism of fat malabsorption.

Adolescent↗

PubMed1988

A carboxyl-terminal cysteine residue is required for palmitic acid binding and biological activity of the ras-related yeast YPT1 protein.

The Saccharomyces cerevisiae YPT1 gene codes for a ras-like, guanine nucleotide-binding protein which is essential for cell viability. The functional significance of two consecutive cysteines at the very carboxyl-terminal end of this protein and in ypt homologues of other eukaryotic species was examined. YPT1 gene mutations were generated that either led to substitutions by serine or the deletion of one or both C-terminal cysteines. The consequences of the mutations were checked in cells after replacing the wild type with the mutant genes. It was found that as long as one of the cysteines was retained, the protein was fully functional. The YPT1 protein could be labelled with [3H]palmitic acid that appeared to be bound in an ester linkage. The wild-type protein was evenly distributed between soluble and membrane-associated proteins, the palmitoylated form was predominantly in the crude membrane fraction. The mutant protein lacking the C-terminal cysteines was not palmitoylated and was exclusively found in the soluble fraction. The extension by three residues, -Val-Leu-Ser, generating a ras-typical C-terminal end, did not interfere with the mutant YPT1 protein's function although it resulted in a reduced labelling with palmitic acid.

Amino Acid Sequence↗

PubMed1999

[Palm oil derivatives with different concentration of palmitic acid and antioxidants. Effects upon plasmatic lipids and platelet aggregation].

It was evaluated the effect of diet rich with cholesterol (0.1%) and different concentration of palmitic acid (16:0) and antioxidants (vitamin C, alpha tocopherol and retinol) upon plasmatic lipids and platelet aggregability in rabbits. The animals were distributed in three groups: I. Standard chow meal (Rp Conejarina) + cholesterol (chol) 0.1%; II. Standard chow meal + chol 0.1% + semipurified palm oil 10% (16:0 = 39.8%, oleic acid 48.7%, linoleic acid 11.4%, retinol 7.3 ug/dL, alpha tocopherol 157.6 ug/dL; III. Standard chow meal + chol 0.1% + crude palm oil 10% (16:0 = 45.3%, oleic acid 46.3%, linoleic acid 7.9%, retinol 96.4 ug/dL, alpha tocopherol 322.8 ug/dL). Monthly determination of plasmatic lipids were done (Enzymatic methods) and at ten months platelet aggregability with ADP, plasmatic vitamin C, retinol and, alpha tocopherol determination were done. Total plasmatic cholesterol (TC) and LDLc increased significantly in the three groups of animals. Significant differences between groups were not found. Platelet aggregability was lower in the animals fed with palmitic acid rich diet (groups II and III) (P = 0.002 and 0.001). Retinol, alpha tocopherol plasmatic concentrations revealed no significant differences. Vitamin C in the groups I was lower than groups II and III (P < 0.05 < 0.02). In this study hypercholesterolemic rabbits fed with rich diets (crude and semipurified) had lower platelet aggregability without changes in plasmatic lipids concentrations.

Animals↗

PubMedDate not supplied

[Incorporation of 1-C14 palmitic acid into liver lipids of rats in different hormanal states].

Adrenalectomy and/or cortisol-induced variations in the in vivo and in vitro incorporation of 14C-palmitic acid 1 into the different fractions of rat liver lipids were studied. The different fatty acids incorporations follow analogous patterns in every hormonal state in vitro. Incorporation rate is faster in normal animals, but adrenalectomy or the administration of cortisol produces a marded delay. Cortisol does not modify the anomalism observed in the adrenoprival state. In vivo, the incorporation of palmitic acid into the different liver lipids--for the same hormonal state--does not follow the same pattern.

Adrenalectomy↗

PubMed2003

Exchanging partially hydrogenated fat for palmitic acid in the diet increases LDL-cholesterol and endogenous cholesterol synthesis in normocholesterolemic women.

Partial hydrogenation of oil results in fats containing unusual isomeric fatty acids characterized by cis and trans configurations. Hydrogenated fats containing trans fatty acids increase plasma total cholesterol (TC) and LDL-cholesterol while depressing HDL-cholesterol levels. Identifying the content of trans fatty acids by food labeling is overshadowed by a reluctance of health authorities to label saturates and trans fatty acids separately. Thus, it is pertinent to compare the effects of trans to saturated fatty acids using stable isotope methodology to establish if the mechanism of increase in TC and LDL-cholesterol is due to the increase in the rate of endogenous synthesis of cholesterol. Ten healthy normocholesterolemic female subjects consumed each of two diets containing approximately 30% of energy as fat for a fourweek period. One diet was high in palmitic acid (10.6% of energy) from palm olein and the other diet exchanged 5.6% of energy as partially hydrogenated fat for palmitic acid. This fat blend resulted in monounsaturated fatty acids decreasing by 4.9 % and polyunsaturated fats increasing by 2.7%. The hydrogenated fat diet treatment provided 3.1% of energy as elaidic acid. For each dietary treatment, the fractional synthesis rates for cholesterol were measured using deuterium-labeling procedures and blood samples were obtained for blood lipid and lipoprotein measurements. Subjects exhibited a higher total cholesterol and LDL-cholesterol level when consuming the diet containing trans fatty acids while also depressing the HDL-cholesterol level. Consuming the partially hydrogenated fat diet treatment increased the fractional synthesis rate of free cholesterol. Consumption of hydrogenated fats containing trans fatty acids in comparison to a mixtur e of palmitic and oleic acids increase plasma cholesterol levels apparently by increasing endogenous synthesis of cholesterol.

Adult↗

PubMed2000

Quantitative determination of dipalmitoylphosphatidylcholine and palmitic acid in porcine lung surfactants used in the treatment of respiratory distress syndrome.

A high-performance liquid chromatography (HPLC) method was developed that can separate and quantify dipalmitoylphosphatidylcholine and its degradation product, palmitic acid from various phospholipids contained in a porcine lung surfactant used in the treatment of respiratory distress syndrome, which was recently approved for use by the FDA. The method used a C8 reversed-phase HPLC column with a (50:45:10) acetonitrile/methanol/acetic acid mobile phase, and refractive index detection. The active component of the lung surfactant, dipalmitoylphosphatidylcholine (DPPC) and palmitic acid (PA), could be quantified following a liquid-liquid extraction procedure along with an internal standard, dimyristoylphosphatidylcholine (DMPC). The assay was validated for linearity, accuracy, precision, reproducibility and ruggedness. Column stability was measured by performing the assay over time and monitoring the system suitability parameters. The extraction procedure has a 90% recovery and the assay is linear over a range of 5 microg/ml to 300 microg/ml. The assay is used to release commercial product and monitor stability of existing lots of material.

1,2-Dipalmitoylphosphatidylcholine↗

PubMed1994

Effect of a bovine lung surfactant protein isolate (SP-B/C) on egg phosphatidylglycerol acyl chain order in a lipid mixture with dipalmitoylphosphatidylcholine and palmitic acid.

Dynamic surface tension measurements of films of a d62 1,2-dipalmitoyl-sn-glycero-3-phosphatidylcholine:L-alpha-phosphatidyl-DL - glycerol:d31 palmitic acid (d62-DPPC:EggPG:d31-PA) lipid matrix in the presence of a bovine pulmonary surfactant protein isolate (SP-B/C) demonstrate the improved surface activity over that of the lipids alone. Thus, significant interaction of the proteins with the lipid matrix is demonstrated. The effect of SP-B/C on the acyl chain order of the negatively charged EggPG within a d62-DPPC:EggPG:d31-PA lipid matrix in D2O saline was investigated in thermal perturbation Fourier transform IR spectroscopic studies. The EggPG thermotropic phase behavior was determined independently of the other lipid components with perdeuterated lipids and D2O. The data demonstrate the high degree of EggPG acyl chain disorder in the absence of the protein isolate. A broad transition occurs between 30 and 40 degrees C. The addition of the protein isolate did not alter the acyl chain order at 0.281 and 1.46 mg/mL of protein. However, alterations in the lipid carbonyl vibrational mode were observed.

1,2-Dipalmitoylphosphatidylcholine↗

PubMed2000

Intravenously injected [1-14C]arachidonic acid targets phospholipids, and [1-14C]palmitic acid targets neutral lipids in hearts of awake rats.

The differential uptake and targeting of intravenously infused [1-14C]palmitic ([1-14C]16:0) and [1-14C]arachidonic ([1-14C]20:4n-6) acids into heart lipid pools were determined in awake adult male rats. The fatty acid tracers were infused (170 microCi/kg) through the femoral vein at a constant rate of 0.4 mL/min over 5 min. At 10 min postinfusion, the rats were killed using pentobarbital. The hearts were rapidly removed, washed free of exogenous blood, and frozen in dry ice. Arterial blood was withdrawn over the course of the experiment to determine plasma radiotracer levels. Lipids were extracted from heart tissue using a two-phase system, and total radioactivity was measured in the nonvolatile aqueous and organic fractions. Both fatty acid tracers had similar plasma curves, but were differentially distributed into heart lipid compartments. The extent of [1-14C]20:4n-6 esterification into heart phospholipids, primarily choline glycerophospholipids, was elevated 3.5-fold compared to [1-14C]16:0. The unilateral incorporation coefficient, k*, which represents tissue radioactivity divided by the integrated plasma radioactivity for heart phospholipid, was sevenfold greater for [1-14C]20:4n-6 than for [1-14C]16:0. In contrast, [1-14C]16:0 was esterified mainly into heart neutral lipids, primarily triacylglycerols (TG), and was also found in the nonvolatile aqueous compartment. Thus, in rat heart, [1-14C]20:4n-6 was primarily targeted for esterification into phospholipids, while [1-14C]16:0 was targeted for esterification into TG or metabolized into nonvolatile aqueous components.

Animals↗