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PubMed1997

Palmitic acid anilide-induced respiratory burst in human polymorphonuclear leukocytes is inhibited by a protein kinase C inhibitor, Ro 31-8220.

Human polymorphonuclear leukocytes (PMNL) were exposed to palmitic acid anilide, an impurity in the case oils that caused the Spanish Toxic Oil Syndrome in 1981, and to the corresponding fatty acid, palmitic acid. The effects of these compounds were studied on the production of reactive oxygen metabolites (ROM) and changes in the levels of free intracellular calcium. Palmitic acid anilide induced the production of reactive oxygen metabolites in PMNL. Interestingly, the palmitic acid anilide-induced respiratory burst was completely blocked by a protein kinase C inhibitor, Ro 31-8220. Moreover, palmitic acid anilide additively amplified the production of ROM caused by a chemotactic peptide, formyl-Methionyl-Leucyl-Phenylalanine (FMLP). In contrast, palmitic acid anilide did not have any effect on the production of ROM induced by a tumor promoter, phorbol myristate acetate (PMA). Palmitic acid, in turn, did not markedly induce the production of ROM nor did it amplify the agonist-induced respiratory burst. Neither of the compounds, alone or in combination with FMLP, affected the levels of intracellular calcium in PMNL. These results indicate that the aniline moiety in palmitic acid modifies its effects on the activation of human PMNL, and the subsequent oxidative burst. The present results also suggest that palmitic acid anilide may activate PMNL through a protein kinase C-dependent mechanism.

Adult↗
PubMed1999

Reduced palmitate turnover in brain phospholipids of pentobarbital-anesthetized rats.

Our laboratory has reported that pentobarbital-induced anesthesia reduced the incorporation of intravenously injected radiolabeled palmitic acid into brain phospholipids. To determine if this decrease reflected a pentobarbital-induced decrease in palmitate turnover in phospholipids, we applied our method and model to study net flux and turnover of palmitate in brain phospholipids (1). Awake, light and deep pentobarbital (25-70 mg/kg, iv) anesthetized rats were infused with [9,10-3H]palmitate over a 5 min period. Brain electrical activity was monitored by electroencephalography. An isoelectric electroencephalogram characterized deep pentobarbital anesthesia. Net incorporation rates (J(FA,i)) and turnover rates (Fi) of palmitate were calculated. J(FA,i) for palmitate incorporated into phospholipids was dramatically reduced by pentobarbital treatment in a dose-dependent manner, by 70% and 90% respectively for lightly and deeply anesthetized animals, compared with awake controls. Turnover rates for palmitate in total phospholipid and individual phospholipid classes were decreased by nearly 70% and 90% for lightly and deeply anesthetized animals, respectively. Thus, pentobarbital decreases, in a dose-dependent manner, the turnover of palmitate in brain phospholipids. This suggests that palmitate turnover is closely coupled to brain functional activity.

Adjuvants, Anesthesia↗
PubMed1996

Comparison of the effects of diets enriched in lauric, palmitic, or oleic acids on serum lipids and lipoproteins in healthy women and men.

The degree to which different saturated fatty acids exert their cholesterol-raising effects is still unknown. Therefore, we studied the effect on serum lipids and lipoproteins of diets rich in lauric, palmitic, or oleic acids. Eighteen women and 14 men consumed in random order three experimental diets, each for 6 wk. The diets consisted of solid foods and contained 40% of energy as fat, of which 28% was supplied by the experimental fats. The fat high in lauric acid was a mixture of palm kernel oil (75%) and a high-oleic acid sunflower oil (25%); the fat high in palmitic acid consisted of dairy fat (55%), palmstearin (36%), and sunflower oil (9%); and the fat high in oleic acid consisted of dairy fat (37%) and sunflower oil (63%). The calculated nutrient composition was the same in each diet except for approximately equal to 8.5% of energy, which was provided by lauric, palmitic, or oleic acids. With the lauric acid diet the subjects' serum total cholesterol concentration increased by 0.22 mmol/L (P = 0.0121; 95% CI: 0.02, 0.41 mmol/L) as compared with the palmitic acid diet and by 0.48 mmol/L (P < 0.0001; 95% CI: 0.29, 0.67 mmol/L) compared with the oleic acid diet. Total cholesterol concentrations with the palmitic acid diet were 0.26 mmol/L (P = 0.0012; 95% CI: 0.07, 0.46 mmol/L) higher than with the oleic acid diet. High-density-lipoprotein (HDL)-cholesterol concentrations increased by 0.12 mmol/L (P = 0.006; 95% CI: 0.04, 0.20 mmol/L) with the lauric acid compared with the palmitic acid diet and by 0.14 mmol/L (P < 0.001; 95% CI: 0.07, 0.22 mmol/L) compared with the oleic acid diet. HDL-cholesterol concentrations with the palmitic acid and the oleic acid diet were the same. No effects were seen in serum triacylglycerol and lipoprotein(a) concentrations. We conclude that both lauric and palmitic acids are hypercholesterolemic compared with oleic acid. Lauric acid raises total cholesterol concentrations more than palmitic acid, which is partly due to a stronger rise in HDL cholesterol.

Adult↗
PubMed2005

Palmitate activates the NF-kappaB transcription factor and induces IL-6 and TNFalpha expression in 3T3-L1 adipocytes.

Fatty acids and their metabolites regulate gene expression and immunological pathways. Furthermore, obese individuals frequently have increased circulating fatty acid concentrations, and localized inflammation in adipose tissue may facilitate the systemic inflammation associated with the insulin resistance of obesity. Although palmitate induces inflammation (i.e., activates proinflammatory pathways) in myotubes, the effects of fatty acids on inflammatory processes in adipocytes have not been established. Therefore, we examined the potential for palmitate, laurate, and docosahexaenoic acid (DHA) to modulate inflammation in 3T3-L1 adipocytes. Palmitate, but not DHA or laurate, induced nuclear factor kappaB (NF-kappaB)-driven luciferase activity and interleukin-6 (IL-6) expression (P < 0.05). Inhibition of fatty acyl Co-A synthase (FACS) with triacsin C suppressed palmitate-induced NF-kappaB activation (P < 0.05), but caused an additive increase in palmitate-induced IL-6 expression (P < 0.05). Disrupting mitogen-activated protein kinase/Erk kinase (MEK) and protein kinase C (PKC) activity with U0126 and Bisindolylmaleimide (Bis), respectively, suppressed palmitate-induced IL-6 expression (P < 0.05), but had no effect on NF-kappaB reporter gene activity (P > 0.05). However, the phosphoinositide-3 kinase (PI3K) inhibitor, wortmannin, alone and additively with palmitate, activated the NF-kappaB reporter gene and induced IL-6 expression (P < 0.05). Palmitate also induced the mRNA expression of tumor necrosis factor alpha (TNFalpha) (P < 0.05), but the increase in mRNA abundance was not reflected in a greater protein concentration in the media (P > 0.05). These data indicate that palmitate induces inflammation in adipocytes, and that this is not a generalized effect of all SFA. Furthermore, PI3K may act constitutively to suppress inflammation. Consequently, inhibition of this enzyme may promote and exacerbate the inflammation in adipose tissue that is associated with obesity and insulin resistance.

3T3 Cells↗
PubMed2003

Palmitate movement across red and white muscle membranes of rainbow trout.

We examined the movement of [3H]palmitate across giant sarcolemmal vesicles prepared from red and white muscle of rainbow trout (Oncorhynchus mykiss). Red and white muscle fatty acid carriers have similar affinities for palmitate (apparent Km = 26 +/- 6 and 33 +/- 8 nM, respectively); however, red muscle has a higher maximal uptake compared with white muscle (Vmax = 476 +/- 41 vs. 229 +/- 23 pmol.mg protein-1.s-1, respectively). Phloretin (250 microM) inhibited palmitate influx in red and white muscle vesicles by approximately 40%, HgCl2 (2.5 mM) inhibited palmitate uptake by 20-30%, and the anion-exchange inhibitor DIDS (250 microM) inhibited palmitate influx in red and white muscle vesicles by approximately 15 and 30%, respectively. Western blot analysis of red and white muscle vesicles did not detect a mammalian-type fatty acid transporter (FAT); however, preincubation of vesicles with sulfo-N-succinimidyloleate, a specific inhibitor of FAT in rats, reduced palmitate uptake in red and white muscle vesicles by approximately 15 and 25%, respectively. A mammalian-type plasma membrane fatty acid-binding protein was identified in trout muscle using Western blotting, but the protein differed in size between red and white muscle. At low concentrations of free palmitate (2.5 nM), addition of high concentrations (111 microM total) of oleate (18:0) caused approximately 50% reduction in palmitate uptake by red and white muscle vesicles, but high concentrations (100 microM) of octanoate (8:0) caused no inhibition of uptake. Five days of aerobic swimming at approximately 2 body lengths/s and 9 days of chronic cortisol elevation in vivo, both of which stimulate lipid metabolism, had no effect on the rate of palmitate movement in red or white muscle vesicles.

Animals↗
PubMed2002

Metabolic fate of long-chain unsaturated fatty acids and their effects on palmitic acid metabolism and gluconeogenesis in bovine hepatocytes.

The objectives were to determine the metabolic fate of different long-chain fatty acids, and their effects on palmitic acid metabolism and gluconeogenesis in bovine hepatocytes. Hepatocytes were isolated from four ruminating calves and exposed in suspension for 3 h to one of the following treatments: 1 mM palmitic acid (1C16), 2 mM palmitic acid (2C16), or 1 mM palmitic acid plus either 1 mM oleic (C18:1), linoleic (C18:2), linolenic (C18:3), eicosapentaenoic (C20:5), or docosahexaenoic acid (C22:6). Oxidation of [1-(14)C]palmitic acid or one of the [1-(14)C]-labeled treatment fatty acids to CO2 or incorporation into cellular triglycerides (TG), phospholipids, cholesterol, and cholesterol esters were measured. Rates of oxidation to CO2 were 3- to 4-fold higher for C22:6 than for other fatty acids, with the exception of C20:5, which had intermediate rates of oxidation to CO2. In general, treatments 2C16 and C18:1 yielded the highest rates of incorporation into most cellular lipids, whereas the polyunsaturated fatty acids were poor substrates for incorporation into cellular lipids. The most pronounced change was a large reduction of polyunsaturated fatty acid incorporation into cellular TG compared to 1C16, 2C16, and C18:1. The unsaturated fatty acids also influenced palmitic acid metabolism. The addition of C20:5 yielded the highest rates of palmitic acid oxidation to CO2 followed by addition of C18:1 and C22:6. Treatments containing polyunsaturated fatty acids decreased palmitic acid metabolism to TG and total cellular lipids compared with treatments 2C16 and C18:1. Rates of gluconeogenesis from propionate were significantly higher for the treatment containing C18:1. Long-chain fatty acids vary in their routes of metabolism and influence palmitic acid metabolism and gluconeogenesis in bovine hepatocytes.

Animals↗
PubMed2006

Validation of 18F-fluoro-4-thia-palmitate as a PET probe for myocardial fatty acid oxidation: effects of hypoxia and composition of exogenous fatty acids.

UNLABELLED: Fatty acid oxidation (FAO) is the predominant energy-producing pathway in the healthy heart. Abnormalities in FAO are associated with many ischemic and nonischemic disease states. The aim of the present study was to further validate 16-[(18)F]-fluoro-4-thia-palmitate ((18)F-FTP) as a metabolically trapped FAO probe in the isolated perfused rat heart model by examining both the effects of hypoxia and the effects of changes in exogenous fatty acid availability. METHODS: Hearts were excised from Sprague-Dawley rats and perfused in the Langendorff mode with Krebs-Henseleit solution under the following conditions: palmitate at 0.4 mmol/L with 95% oxygen, palmitate at 0.4 mmol/L with 35% oxygen, palmitate at 0.2 mmol/L plus oleate at 0.2 mmol/L with 95% oxygen, and palmitate at 0.2 mmol/L plus oleate at 0.2 mmol/L with 35% oxygen. Hearts were paced at 270 beats per minute, and the rate of left ventricular pressure change (LV dP/dt) was monitored. (18)F-FTP in the perfusion medium was administered for 20 min, and this step was followed by a 20-min washout period without tracer in the perfusion medium. (18)F kinetics in the whole heart were monitored externally, and the time-activity curves were analyzed to determine the fractional trapping rate for (18)F-FTP (FTR(FTP)). A "lumped constant" (LC) was defined as the ratio of FTR(FTP) to the fractional rate of oxidation of fatty acid in the perfusion medium. RESULTS: The kinetic data for (18)F-FTP demonstrated metabolic trapping of (18)F radioactivity that was insensitive to changes in the mixture of fatty acids in the perfusion medium but that was sensitive to the inhibition of mitochondrial FAO by hypoxia. LV dP/dt was reduced 47%-67% in hypoxic hearts relative to hearts with normal oxygenation (controls). FAO rates for palmitate and oleate were similar in group 3 (palmitate alone) and group 4 (palmitate and oleate). FAO was decreased 70%-76% with hypoxia, whereas FTR(FTP) was reduced 86%-88%, demonstrating hypersensitivity of a change in (18)F-FTP retention to FAO inhibition by oxygen deprivation. The (18)F-FTP LC was approximately 2 in myocardium with normal oxygenation and fell to 1.0-1.2 in hypoxic myocardium. CONCLUSION: The results confirm (18)F-FTP to be a metabolically trapped palmitate analog that is capable of indicating rates of myocardial oxidation of exogenous long-chain fatty acids. The heterogeneous nature of fatty acids in plasma does not alter the quantitative analysis of (18)F-FTP kinetics. However, the decreased LC value in hypoxic myocardium suggests the need to develop an understanding of the relationship of (18)F-FTP processing to natural fatty acids at key limiting transport and metabolism processes, analogous to previous studies examining the LC values for radiolabeled deoxyglucose tracers used to estimate the glucose metabolic rate.

Animals↗
PubMed1972

Stages of uptake and incorporation of micellar palmitic acid by hamster proximal intestinal mucosa.

The stages of uptake and incorporation of micellar palmitic acid by hamster proximal intestinal mucosa were investigated by incubation of everted sacs at 4 degrees C and 37 degrees C for 2, 5, 10, and 15 min in a micellar solution (10 micro moles of [1-(14)C]palmitic acid, 10 micro moles of monoolein, and 100 micro moles of sodium taurodeoxycholate) and subsequent serial rinsing of the sacs in ice-cold solutions as follows: one 20-sec rinse in unlabeled micellar solution, five 1-min rinses in Krebs-Ringer buffer (0.15 m, pH 6.3), and ten 2-min rinses in 2.5% albumin solution. The fatty acid-solubilizing capacity of all the rinsing solutions was always in excess of the amounts of radioactive palmitic acid released during each rinse. Radioactivity was determined in the tissue homogenates, rinsing solutions, and serosal fluids. The results indicate that a significant proportion of radioactive palmitic acid taken up by the sacs during the short incubation was released into the rinsing solutions. Rinsing in Krebs-Ringer buffer resulted in release of 15.5 +/- 2.4% of the labeled fatty acid, and this fraction was independent of the temperature of incubation. In contrast, the amounts of palmitic acid released in albumin were significantly greater and were markedly dependent on the temperature of incubation; a total of 48.6 +/- 7.0% and 26.3 +/- 5.1% was released from sacs incubated at 4 degrees C and 37 degrees C, respectively. While the proportion of radioactive palmitic acid in the free fatty acid fraction of the tissue after the rinsing sequence remained reasonably constant regardless of the temperature and duration of incubation, the radioactivity of the esterified palmitic acid in the tissue was much greater in the sacs incubated at 37 degrees C and tended to increase linearly up to 10 min of incubation. A highly significant inverse relationship was found between the fraction of radioactive palmitic acid released by rinsing in albumin and the fraction of the label in the tissue esterified fatty acids. The results suggest that the initial uptake of micellar fatty acid by intestinal mucosa may involve reversible binding to superficial sites with at least two strengths of binding: a weak, temperature-independent binding which could be easily dissociated by rinsing in Krebs-Ringer buffer, and a stronger, temperature-dependent binding which could be dissociated by rinsing in albumin, but not in Krebs-Ringer buffer. Analogous binding of micellar palmitic acid occurred in a brush border preparation of proximal intestine which was devoid of any fatty acid esterifying activity. This suggested that the reversible binding of fatty acid by the intestinal mucosa may be a property of its superficial components, namely the glycocalyx or microvillous membranes, and that it may be independent of the esterifying capacity of the tissue.

Animals↗
PubMed1994

Mechanisms of the stimulation of insulin release by saturated fatty acids. A study of palmitate effects in mouse beta-cells.

The mechanisms by which fatty acids increase insulin release are not known. In this study, mouse islets were used as a model and palmitate as a reference compound to study in vitro how saturated fatty acids influence pancreatic beta-cells. Palmitate (625 microM) was bound to albumin. It did not affect basal insulin release (3 mM glucose) but increased the release induced by 10-15 mM glucose. This effect was dependent on the concentration of free rather than total palmitate. It was reversible and abolished by epinephrine, diazoxide, nimodipine, or omission of extracellular Ca. Bromopalmitate and methyl palmoxirate, two inhibitors of fatty acid oxidation, were ineffective alone, and only bromopalmitate partially inhibited the effects of palmitate on insulin release. The increase in insulin release produced by palmitate could not be ascribed to a blockade of ATP-sensitive K(+)-channels because the fatty acid only barely decreased 86Rb efflux and did not depolarize beta-cells in 3 mM glucose. The small effect on 86Rb efflux might be attributed to a slight rise in the ATP/ADP ratio. No such rise occurred when palmitate was tested in 15 mM glucose, and the fatty acid consistently accelerated 86Rb efflux under these conditions. Measurements of beta-cell membrane potential (intracellular microelectrodes) and of free cytoplasmic calcium (Cai2+) in beta-cells (Fura 2 technique) showed that palmitate increases Ca2+ influx; it also caused a very small mobilization of intracellular Ca. The persistence of this stimulation of Ca2+ influx in the presence of diazoxide and high K+ suggests that palmitate might act on Ca2+ channels.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenine Nucleotides↗
PubMed2005

A prospective, randomized, double-blind, placebo-controlled trial of retinol palmitate (vitamin A) for symptomatic chronic radiation proctopathy.

PURPOSE: This study was designed to determine whether oral retinol palmitate (vitamin A) can reduce the symptoms of radiation proctopathy. METHODS: A randomized, double-blind trial comparing retinol palmitate (10,000 IU by mouth for 90 days) to placebo was conducted. Eligible patients were more than six months postpelvic radiotherapy and had significant symptoms as measured with the Radiation Proctopathy System Assessments Scale. Nineteen patients were randomized in total: ten to retinol palmitate and nine to placebo. The Radiation Proctopathy System Assessments Scale scores before and every 30 days for 90 days were measured. Five placebo nonresponders were crossed over to the retinol palmitate for another 90 days. Response was defined as a reduction in two or more symptoms by at least two Radiation Proctopathy System Assessments Scale points. RESULTS: Seven of ten retinol palmitate patients responded, whereas two of nine responded to placebo (P = 0.057). Mean pre-post-treatment change in Radiation Proctopathy System Assessments Scale (delta Radiation Proctopathy System Assessments Scale) in the retinol palmitate group was 11 +/- 5, whereas delta Radiation Proctopathy System Assessments Scale in the placebo group was 2.5 +/- 3.6 (P = 0.013, Mann-Whitney U test). Additionally, all five placebo nonresponders who were crossed over to treatment with retinal palmitate responded to treatment. CONCLUSIONS: In our trial, retinol palmitate significantly reduced rectal symptoms of radiation proctopathy, perhaps because of wound-healing effects. The current results can serve as the foundation for future trials examining retinol palmitate in the multi-institutional setting.

Aged↗
PubMed1998

Development of a method for quantitation of retinol and retinyl palmitate in human serum using high-performance liquid chromatography-atmospheric pressure chemical ionization-mass spectrometry.

A method for the quantitative analysis of the vitamin A compounds all-trans-retinol and all-trans-retinyl palmitate was developed using high-performance liquid chromatography-atmospheric pressure chemical ionization-mass spectrometry (APCI-LC-MS). Unlike previous quantitative mass spectrometric methods for vitamin A, HPLC separations were carried out using a C30 reversed-phase column instead of GC separation. Because no sample hydrolysis or derivatization was necessary, retinyl palmitate was preserved for analysis instead of being hydrolyzed to retinol. Human serum was analyzed following simple hexane extraction without saponification or any additional purification. A comparison of APCI and electrospray ionization showed that only APCI produced a linear response over all four orders of magnitude of retinol and three orders of magnitude of retinyl palmitate concentrations. Selected ion monitoring of the fragment ion of m/z 269 was used for APCI quantitation of both retinol and retinyl palmitate, since it was the base peak and the only abundant ion in the mass spectra of both compounds and the internal standard, retinyl acetate. The ion of m/z 269 corresponded to loss of water, loss of palmitic acid, or elimination of acetic acid from the protonated molecules of retinol, retinyl palmitate and retinyl acetate, respectively. The limit of detection of APCI-LC-MS for all-trans-retinol and all-trans-retinyl palmitate was determined to be approximately 34 fmol/microliter and 36 fmol/microliter (0.670 pmol all-trans-retinol and 0.720 pmol all-trans-retinyl palmitate injected in 20 microliters on-column), respectively. The limit of quantitation was approximately 500 fmol/microliter and 250 fmol/microliter (10 pmol and 5 pmol injected in 20 microliters on-column) for retinol and retinyl palmitate, respectively.

Chromatography, High Pressure Liquid↗
PubMed1992

Characterization of chylomicron remnant clearance by retinyl palmitate label in normal humans.

To characterize chylomicron remnant clearance by the liver, plasma elimination of retinyl palmitate-labeled chylomicron remnants was studied in 18 healthy subjects, ages 21-42 years. Autologous plasma containing retinyl palmitate-labeled chylomicrons and their remnants was injected intravenously, and retinyl palmitate disappearance was measured in serial plasma samples in all subjects and in lipoprotein fractions in 11 subjects. The injected doses (n = 18) ranged from 0.34 to 7.11 mumol retinyl palmitate in d less than or equal to 1.006 g/ml particles with an average molar ratio of 330/1 of retinyl palmitate/apoB-48 (n = 8). The label distributed in the intravascular space and exhibited apparent first order elimination, monoexponential in 6 and biexponential in 12 subjects. The first rapid component k1 (t1/2 18.8 +/- 11.4 min, n = 18) was shown to represent retinyl palmitate in particles of d less than or equal to 1.006 g/ml, i.e., chylomicron remnants, and the second slow component k2 (t1/2 123 +/- 62 min, n = 12) small amounts of retinyl palmitate (11 +/- 7%) injected in d greater than 1.006 g/ml particles (therefore excluded from analysis). Assuming a single-compartment model, initial rates of elimination (= dose x k1) of labeled chylomicron remnants obeyed (P = 0.06) Michaelis-Menten saturation kinetics: Km was 921 +/- 305 nmol retinyl palmitate label and Vmax 124 +/- 14 nmol/min corresponding to 0.88 nM apoB-48 for Km and 0.25 x 10(-3) nmol apoB-48.min-1.g-1 liver for Vmax. Their elimination was limited neither by the injected triglyceride dose nor theoretically by the liver blood flow. After the intake of 70 g of fat (cream) containing retinyl palmitate, the plasma retinyl palmitate concentration exceeded the estimated saturation concentration for 7 h. In conclusion, physiological chylomicron remnant catabolism by the liver appears to be saturable by ordinary lipid intake in healthy humans.

Adult↗
PubMedDate not supplied

Vitamin A palmitate photostability and stability over time.

Vitamin A palmitate photostability in relation to UVA and UVB was tested in hydroxy ethyl cellulose hydrogels at pH 4.0, 5.6, 7.0, and 8.0, alone and with the addition of sunscreens (3,4-methylbenzilidencamphor or butyl methoxy dibenzoylmethane) or an antioxidant (butylated hydroxy toluene). The photostability of vitamin A palmitate was also tested in encapsulated systems (Tagravit A1 microcapsules, Lipotec liposomes, phosphatidylcholine liposomes, and Lipotec nanocapsules) dispersed in gels at pH 5.6 and 7.0. The stability of retinyl palmitate over time in hydroxy ethyl cellulose hydrogels at pH 5.6 and 7.0 (stored one month at 25 degrees C or 40 degrees C), alone or with butylated hydroxy toluene, was also tested. The stability of retinyl palmitate over time in encapsulated systems, dispersed in gels at pH 5.6 and 7.0, was also studied. O/W emulsions were also prepared to compare the stability of vitamin A palmitate introduced in a lipophilic/hydrophilic medium (O/W emulsions) and a hydrophilic medium (hydrogels). HPLC analysis showed that encapsulated systems such as Lipotec nanocapsules, Tagravit A1 microcapsules, phosphatidylcholine liposomes, and Lipotec liposomes protect the vitamin A ester over time from hydrolysis and from oxidation to retinaldeide and retinoic acid, and that Lipotec nanocapsules and phosphatidylcholine liposomes also improve the vitamin's photostability. A change in pH (from 5.6 to 7.0) of the gels did not influence the vitamin ester's stability. pH levels of 4.0 and 8.0 determined a decrease in the stability of retinyl palmitate in the gels. A high concentration of sunscreens improved the photostability of retinyl palmitate in the gels at pH 5.6 and 7.0. Butylated hydroxy toluene protected retinyl palmitate from degradation induced by light at all the pH levels studied and by heat at pH 5.6 and 7.0, as can be seen from the study of the photostability of vitamin A palmitate under UVB and UVA and of stability over time. Rheological studies showed a slight decrease in the viscosity of the gels after UVB-UVA irradiation and a higher decrease in the viscosity of the gels and the emulsions after storage at 25 degrees C and 40 degrees C. This decrease can be attributed to a partial degradation of hydroxy ethyl cellulose and of emulsifier, as can be seen from the decrease in shear stress versus shear rate values under these conditions of storage, denoting a depolymerization of the rheological modifier.

Animals↗
PubMed1984

Plasma clearance of chylomicrons labeled with retinyl palmitate in healthy human subjects.

To estimate hepatic uptake of chylomicron remnants in humans, chylomicrons and intestinal very low density lipoproteins (VLDL) were endogenously labeled with retinyl esters, harvested by plasmapheresis, and pulse-injected into the donor 44 hr after plasmapheresis. Plasma decay of retinyl palmitate was measured in eight healthy volunteers. Retinyl palmitate plasma disappearance obeyed an apparent first order function in seven studies and, in one study, a biexponential function with the second, slow exponential accounting for only 13% of the retinyl palmitate plasma decay. The mean fractional removal of rate was 0.037 +/- 0.037 min-1 (mean +/- SD) in a one-compartment model. The apparent volume of distribution, Vd, was 109 +/- 25% of the estimated plasma volume. Plasma clearance of retinyl palmitate was 130 +/- 97 ml/min calculated as Vd x Ke. Mean T 1/2 was 29 +/- 16 min. Both in vitro and in vivo the retinyl palmitate remained largely within chylomicrons and intestinal VLDL. Only 4.3% was transferred from chylomicrons to other lipoprotein classes during in vitro incubation for 5 hr. After plasma was stored for 42 hr, 5% was transferred to higher density lipoproteins. During 12 hr after a test meal containing retinyl palmitate, only 6.4 +/- 1.5% of the retinyl palmitate absorbed was found in the LDL fraction and 3.1 +/- 3.8% in the d 1.063 g/ml lipoproteins. We conclude that retinyl palmitate is a useful marker for chylomicrons and their remnants in humans and that the plasma clearance of retinyl palmitate-labeled chylomicrons is probably an estimate of chylomicron remnant plasma clearance in man.

Adult↗
PubMed1983

Isomerization of retinyl palmitate using conventional lipid extraction solvents.

The use of a chloroform-ethanol-water solvent system for the direct extraction of retinyl palmitate isomers from fortified food products was previously shown to be unsuitable because significant isomerization of all-trans-retinyl palmitate occurred during the extraction. This study investigated the extent of isomerization of retinyl palmitate in various extraction solvents when subjected to gold fluorescent laboratory light. Purified solutions of all-trans-retinyl palmitate in hexane were diluted with methyl t-butyl ether, hexane, methylene chloride, and stabilized chloroform and subjected to gold fluorescent laboratory light for 2, 4, and 6.5 h. Similar solutions were subjected to light or kept in the dark for 3.5 h. All-trans-, 9-cis-, and 13-cis-retinyl palmitate esters in the solutions were determined by using normal phase high performance liquid chromatography with fluorometric detection. Results demonstrated a noticeable increase in the 9-cis-retinyl palmitate concentration and a corresponding decrease in all-trans-retinyl palmitate concentration with time, in chloroform and methylene chloride compared with hexane. Chlorinated solvents in the absence of light did not promote isomerization of retinyl palmitate. Use of chlorinated solvents for the extraction of vitamin A esters should be avoided because they promote isomerization of retinyl palmitate when subjected to light, including gold fluorescent laboratory light.

Diterpenes↗
PubMed1982

Unsaturated fatty acid requirement in Escherichia coli: mechanism of palmitate-induced inhibition of growth of strain WN1.

The minimum requirement for unsaturated fatty acids was investigated in E. coli using a mutant impaired in the synthesis of vaccenic acid. Exogenously supplied palmitic acid was incorporated by this mutant which led to a reduction in the proportion of cellular unsaturated fatty acids. Growth was impaired as the level of saturated fatty acids approached 76% at 37 degree C and 60% at 30 degree C. The basis of this growth inhibition was investigated. Most transport systems and enzymes examined remained active in palmitate-grown cells although the specific activities of glutamate uptake and succinic dehydrogenase were depressed 50%. Fluorescent probes of membrane organization indicated that fluidity decreased with palmitate incorporation. Temperature scans with parinaric acid indicated that rigid lipid domains exist in palmitate-grown cells at their respective growth temperature. Freeze-fracture electron microscopy confirmed the presence of phase separations (particle-free areas) in palmitate-grown cells held at their growth temperature prior to quenching. The extent of this separation into particle-free and particle-enriched domains was equivalent to that induced by a shift to 0 degree C in control cells. The incorporation of palmitate increased nucleotide leakage over threefold. The cytoplasmic enzyme beta-galactosidase was released into the surrounding medium as the concentration of unsaturated fatty acid approached the minimum for a particular growth temperature. Lysis was observed as a decrease in turbidity when cells which had been grown with palmitate were shifted a lower growth temperature. From these results we propose that leakage and partial lysis are the major factors contributing to the apparent decrease in growth rate caused by the excessive incorporation of palmitate. Further, we propose that membrane integrity may determine the minimum requirement for unsaturated fatty acids in E. coli rather than a specific effect on membrane transport and/or membrane-bound enzymes.

Biological Transport, Active↗
PubMed1991

Effect of palmitic acid and fatty acid binding protein on ventricular fibrillation threshold in the perfused rat heart.

The effects of increased free fatty acid (FFA) levels on ventricular arrhythmias remain controversial. Using ventricular fibrillation threshold (VFT), we examined the relationship between FFA levels and ventricular arrhythmias. Isolated rat hearts were perfused with palmitate bound to either albumin or fatty acid binding protein (FABP) by Langendorf's method. The VFT was determined by electrical stimulation. Perfusion with 0.12 mM albumin alone, 0.12 mM palmitate bound to 0.12 mM albumin, and 0.36 mM palmitate bound to 0.12 mM albumin did not lower the VFT significantly. However, 0.60 mM palmitate bound to 0.12 mM albumin lowered VFT from 2.19 +/- 0.20 mA to 1.56 +/- 0.13 mA. The perfusion of 0.36 mM palmitate bound to 0.12 mM FABP lowered the VFT from 2.05 +/- to 0.19 mA to 1.47 +/- 0.23 mA, but 0.12 mM FABP alone did not affect the VFT. Perfusion with 0.36 mM palmitate bound to 0.12 mM FABP caused the VFT to fall more than perfusion with 0.36 mM palmitate bound to 0.12 mM albumin. Then the effects of verapamil perfusion or a low concentration of perfusate Ca2+ on VFT were examined. VFT was determined by electrical stimulation. Palmitate (0.6 mM) bound to 0.12 mM albumin lowered VFT. Verapamil 10(-7) M perfusion and a low concentration of Ca2+ (Ca2+ 1.67 mM) suppressed the FFA-induced fall of VFT. These results suggested that the arrhythmogenic action of FFA was related to Ca2+ overload in myocardial cells.

Albumins↗
PubMed1983

Incomplete palmitate oxidation in cell-free systems of rat and human muscles.

The palmitate oxidation capacity was determined in whole homogenates, postnuclear fractions and mitochondrial fractions of various rat and human muscles and in rat liver, kidney, brain and lung. The oxidation rate (production of 14CO2 and 14C-labeled acid-soluble intermediates) was [1-14C]palmitate greater than [U-14C]palmitate greater than [16-14C]palmitate in all cell-free systems. Oxidation rates were highest in rat heart and liver, intermediate in kidney, diaphragm and m. quadriceps, and low in brain and lung. The capacity of human heart was much lower than that of rat heart and about twice that of human skeletal muscles. Omission of L-carnitine and addition of malonyl-CoA, KCN or antimycin A decreased the oxidation rates in whole homogenates and mitochondrial fractions. Antimycin or KCN increased and malonyl-CoA decreased the ratio of the oxidation rates with [1-14C]- and [16-14C]palmitate. The carnitine concentration had no significant effect on the ratio. 14C-labeled dodecanoic and tetradecanoic acids were identified in homogenates and mitochondrial fractions of m. quadriceps and liver of rat as acid-insoluble intermediates of [16-14C]palmitate oxidation in the presence and absence of antimycin A. Their amounts recovered can account for the differences in oxidation rates found with [1-14C]- and [16-14C]palmitate. The incomplete palmitate oxidation in cell-free systems appears to be mainly caused by an inadequate mitochondrial degradation of peroxisomal oxidation products.

Animals↗