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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↗
PubMed1993

Purification and properties of a palmitoyl-protein thioesterase that cleaves palmitate from H-Ras.

H-Ras, the protein product of the cellular homologue of the Harvey ras oncogene, undergoes a complex series of post-translational modifications that include C-terminal isoprenylation, proteolysis, methylation, and palmitoylation. Palmitoylation has been shown to enhance the transformation efficiency of H-Ras about 10-fold in vivo. A recent study (Magee, A. I., Gutierrez, L., McKay, I. A., Marshall, C. J., and Hall, A. (1987) EMBO J. 6, 3353-3357) has provided strong evidence that the palmitate undergoes a dynamic acylation-deacylation cycle, but details concerning the enzymology of this process and its regulation are lacking. To begin to dissect this event, we have developed an assay for the enzymatic removal of palmitate from [3H]palmitate-labeled H-Ras. This substrate was produced in a baculovirus expression system and was used to purify to homogeneity a novel 37-kDa enzyme from bovine brain cytosol that removes the radiolabeled palmitate. The purified enzyme is sensitive to diethyl pyrocarbonate and insensitive to phenylmethylsulfonyl fluoride and N-ethylmaleimide. Interestingly, the thioesterase recognizes H-Ras as a substrate only when H-Ras is in its native conformation (bound to Mg2+ and guanine nucleotide). The palmitoylated alpha subunits of the heterotrimeric G proteins are also substrates for the enzyme.

Amino Acid Sequence↗
PubMed1994

[Interaction of palmitic acid with the ADP/ATP antiporter, reconstituted in liposomes].

Reconstituted adenine nucleotide transport has been studied in proteoliposomes with the ADP/ATP antiporter and bacteriorhodopsin as the membrane potential generator. The ADP(out)/ATP(in) exchange rate in the model system decreased after illumination of the proteoliposomes. This effect was reversed by both protonophore FCCP and palmitic acid. The data obtained are analysed in terms of the electrogeneity of the nucleotide transport by the antiporter. It is suggested that palmitic acid increases the conductivity of the proteoliposome membrane. The membrane conductivity of bacteriorhodopsin proteoliposomes (without the ADP/ATP antiporter) is unaffected by palmitic acid. Seemingly, the ADP/ATP antiporter mediated increase of the proteoliposomal membrane conductivity is induced by fatty acids. Stimulation of the adenine nucleotide transport by fatty acids was also observed in the reconstituted system, when the membrane potential was absent. Besides palmitic acid, other anionic uncouplers, DNP and FCCP, produce a similar, however, less pronounced effect. Gramicidin D is without effect. It is concluded that the observed stimulating effect is due to the anionic uncoupler interaction with the ADP/ATP antiporter rather than to the membrane proton conductivity increase.

Bacteriorhodopsins↗
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↗
PubMed1993

Water soluble complex of palmitic acid in media for cultivation of leprosy-derived psychrophilic mycobacteria from Mycobacterium leprae infected tissues.

Palmitic acid and palmitates were transformed into water soluble complexes with crystalline heptakis-2,6-di-0-methyl-beta-cyclodextrin. This formulation was incorporated into liquid and solid chemically well-defined media. The fatty acid served as C and energy source, ammonium thioglycolate as the sole source of N with the SH group as further source of energy. Minute amount of dimethyl-sulfoxide added was used for its known effect on cell membrane permeability. The media were inoculated with host grown Mycobacterium leprae cells isolated from human, armadillo and Nu mice foot pad lepromata. No growth occurred in the liquid medium at 22 or 32 degrees C, but cultures and subcultures of acid fast rods were grown at 10 degrees C. Bacilli in the cultures were solid, strongly acid fast rods, growing in clumps like globi. Growth on the semisolid media was visible as smooth round colonies, of white to ivory in colour, slowly expanding flatly at the periphery of the colony on the agar surface. Colonies developed within 2-3 weeks and reached maximum size at 50-80 days depending on the size of inoculum. Subcultures grow faster and more abundantly with adaptation to the media. No growth was seen without the water soluble complexes of palmitic acid or palmitates in the media. The free fatty acid or its salts had an equal growth supporting effect. Identical psychrophilic cultures were obtained from 7 out of 9 armadillo, 12 out of 12 Nu mice and 1 out of 2 human lepromata. None of the cultures grow on Loewenstein, Dubos or 7H9 media at 10 degrees C, 20 degrees C or 32 degrees C, respectively. The tested 4th to 7th subcultures of the strains were strongly positive for phenolic glycolipid-1. Heat killed suspensions of up to 7th subcultures gave negative late skin reaction in all of 16 LL cases. In 19 I, B and T cases the late skin reactions were all similar to that obtained with authentic human lepromin.

Animals↗
PubMed1995

[The effect of p-chloromercuribenzoate on regulation of oxidative phosphorylation by ADP and ATP and stimulation of liver mitochondrial respiration by palmitate].

The effect of p-chloromercuribenzoate (pCMB) on oxidative phosphorylation and palmitate-stimulated respiration of liver mitochondria has been studied. pCMB (1 microM) does not affect oxidative phosphorylation but reduces the inhibiting effect of ATP on this process. Used at the same concentration, pCMB eliminates the inhibiting effect of ADP and ATP on mitochondrial respiration in the presence of 10 and 20 microM palmitate. pCMB has no effect on inhibition of oxidative phosphorylation by carboxyatractyloside or on palmitate-stimulated respiration of mitochondria. It is concluded that the SH-groups of mitochondria localized in the hydrophilic region outside the inner mitochondrial membrane participate in regulation of oxidative phosphorylation by ATP and in regulation of palmitate-stimulated respiration by ADP + ATP.

Adenosine Diphosphate↗
PubMed1979

Anomalous solution behavior of 2-palmitate esters of lincomycin and clindamycin.

The aqueous solubilities of lincomycin and clindamycin 2-palmitate esters are compared. Clindamycin 2-palmitate hydrochloride has an unusually high solubility at 25 degrees, which is due to micelle formation. Both compounds are surface active with relatively low critical micelle concentrations. However, since the Krafft point of lincomycin palmitate is approximately 43 degrees, it does not form micelles below that temperature and appears to be quite insoluble until heated above 43 degrees. The experimental monomeric solubilities of the two compounds agree with calculations based on group contributions to lipophilicity. Clindamycin 2-palmitate hydrochloride solutions are quite sensitive to ions, being salted out as unprotonated base in the form of oily droplets. Salting out correlates well with anionic strength, which is quite constant for the various salts studied. A viscosity maximum occurs with increasing salt addition, with the peaks of the different salts occurring at the same anionic strengths.

Clindamycin↗
PubMed1999

P450BM-3: absolute configuration of the primary metabolites of palmitic acid.

P450BM-3, a catalytically self-sufficient, soluble bacterial P450, contains on the same polypeptide a heme domain and a reductase domain. P450BM-3 catalyzes the oxidation of short- and long-chain, saturated and unsaturated fatty acids. The three-dimensional structure of the heme domain both in the absence and in the presence of fatty acid substrates has been determined; however, the fatty acid in the substrate-bound form is not adequately close to the heme iron to permit a prediction regarding the stereoselectivity of oxidation. In the case of long-chain fatty acids, the products can also serve as substrate and be metabolized several times. In the current study, we have determined the absolute configuration of the three primary products of palmitic acid hydroxylation (15-, 14-, and 13-OH palmitic acid). While the 15- and 14-hydroxy compounds are produced in a highly stereoselective manner (98% R, 2% S), the 13-hydroxy is a mixture of 72% R and 28% S. We have also examined the binding of these three hydroxy acids to P450BM-3 and shown that only two of them (14-OH and 13-OH palmitic acid) can bind to and be further metabolized by P450BM-3. The results indicate that in contrast to the flexibility of palmitoleic acid bound to the oxidized enzyme, palmitic acid is rigidly bound in the active site during catalytic turnover.

Arachidonic Acid↗
PubMedDate not supplied

Renal palmitate transport: possible sites for interaction with a plasma membrane fatty acid-binding protein.

In previous studies from this laboratory, a mediated transport system for long chain fatty acids was observed in rat renal basolateral membrane vesicles. Transport was measured in the absence of albumin and indicated the presence of a Na+ independent anion exchange mechanism. The present experiments were done to characterize renal transport of fatty acids derived from fatty acid-albumin complexes. 3H-palmitate uptake by brush border (BBMV) and basolateral membrane vesicles (BLMV) isolated from rat renal cortex was determined using a rapid filtration technique. All incubation media contained 100 microM 3H-palmitate complexed to 100 microM bovine serum albumin. Up to 65% of initially bound fatty acid-albumin complexes were displaceable by washing with solution containing 0.1% albumin. Total palmitate uptake was measured as the remaining non-displaceable radioactivity. In BBMV in low ionic strength (300 mM mannitol) or ionic buffers (100 mM mannitol + 100 mM NaCl or KCl), total palmitate uptake at 15 sec did not differ from equilibrium (60 min) values of 10-11 nmoles/mg protein. Uptake was primarily due to binding. A similar pattern was seen with BLMV in 300 mM mannitol buffer. In BLMV in 100 mM NaCl or KCl buffers, equilibrium uptake was 10-fold lower than at 15 sec. This suggests binding followed by cation-dependent translocation. If a putative FABPPM is involved in transport only, its presence should be confined to BLMV.

Animals↗
PubMed1976

Palmitic acid-1-14C incorporation and turnover in lung phospholipids of rats treated with chlorphentermine, RMI 10.393 and Ro 4-4318.

The effects of 3 lipidosis-inducing drugs on the incorporation and turnover of palmitic acid-1-14C in lung phospholipids was studied. In rats treated with 1 dose of chlorphentermine or RMI 10.393, the incorporation of palmitate-1-14C into most lung phospholipid fractions was moderately decreased, but markedly lowered after 1 dose of Ro 4-4318. Eight doses of chlorphentermine and RMI 10.393 strongly inhibited the incorporation of palmitate-1-14C into lung phospholipids, whereas with 8 doses of Ro 4-4318 the incorporation was highly increased. Thirty hours after the last of 3 injections of the labeled palmitic acid the turnover of most lung phospholipids was considerably lower in chlorphentermine- and RMI 10.393-treated rats than in controls. Ro 4-4318, however, induced a highly increased turnover of most phospholipids. After 54 h, this effect had practically disappeared. Our studies showed that phospholipid storage after treatment with chlorphentermine and RMI 10.393 is mainly due to decreased degradation of phospholipids, whereas increased synthesis accounts for the effect of Ro 4-4318.

Amitriptyline↗
PubMed1991

Methyl palmitate prevents Kupffer cell activation and improves survival after orthotopic liver transplantation in the rat.

The purpose of this study was to determine whether prevention of Kupffer cell activation following orthotopic liver transplantation improves postoperative survival. First, particle phagocytosis by Kupffer cells was monitored continuously from the uptake of colloidal carbon by the perfused liver. Unstored livers took up carbon at rates of around 150 mg/g per hour, whereas storage for 24 h in Euro-Collins solution nearly doubled values to about 290 mg/g per hour. Treatment of rats with methyl palmitate, an inhibitor of phagocytosis by Kupffer cells, reduced carbon uptake to about one-third to one-half of control values in unstored and stored livers, respectively. Oxygen uptake, which was increased about 25% in stored and unstored livers by infusion of colloidal carbon, was only increased 5%-10% in both groups following treatment with methyl palmitate, suggesting that Kupffer cell activation was prevented by methyl palmitate. In livers transplanted after storage for 6 h in Euro-Collins solution (nonsurvival conditions), control rats survived only about 12 h, while treatment with methyl palmitate increased survival time significantly--more than threefold--to about 40 h. These data are consistent with the hypothesis that activation of Kupffer cells following cold ischemic storage and reperfusion is an early event involved in liver graft failure.

Animals↗
PubMed2006

Palmitate induced lipoapoptosis of exocrine pancreas AR42J cells.

Chronic surplus of dietary consumption, typical to obesity, results in overflow of fat to non-adipose tissues. Intracellular accumulation of fat in non-adipose tissues is associated with cellular dysfunction and cell death and ultimately contributes to the pathogenesis of chronic diseases. The influence of fat overflow on the exocrine pancreas is not known. The purpose of this research was to study the lipotoxic and lipoapoptotic effect of prolonged (72 h) long chain saturated palmitic fatty acid (0.1 mM) on the survival of exocrine pancreas AR42J cells. We demonstrate that chronic exposure of AR42J cells to palmitic acid results in significant increase in triglycerides accumulation (up to 25% of cells area), compared to untreated cultures. Lipid accumulation prompted a typical apoptotic process, demonstrated by both DNA fragmentation and condensed chromatin appearance (DAPI staining). Quantitative real-time PCR studies demonstrated that prolonged palmitic acid supplementation induced down-regulation of the anti-apoptotic Bcl2 mRNA levels (22%) and up-regulation of the pro-apoptotic Bax mRNA levels (300%), leading to disruption of the pro/anti apoptotic balance (Bax/Bcl2=3). No major change was detected in iNOS mRNA expression. In conclusion, prolonged exposure to saturated palmitic acid induces lipoapoptosis in exocrine pancreatic AR42J cells, through disturbance of the Bax/Bcl-2 balance.

Animals↗
PubMed2006

Differential protective effects of palmitoleic acid and cAMP on caspase activation and cell viability in pancreatic beta-cells exposed to palmitate.

Saturated and mono-unsaturated fatty acids exert differential effects on pancreatic beta-cell viability during chronic exposure. Long chain saturated molecules (e.g. palmitate) are cytotoxic to beta-cells and this is associated with caspase activation and induction of apoptosis. By contrast, mono-unsaturated fatty acids (e.g. palmitoleate) are not toxic and can protect against the detrimental effects of palmitate. In the present study, we show that the protective actions of palmitoleate in BRIN-BD11 beta-cells result in attenuated caspase activation following exposure to palmitate and that a similar response occurs in cells having elevated levels of cAMP. However, unlike palmitoleate, elevation of cAMP was unable to prevent the cytotoxic actions of palmitate since it caused a diversion of the pathway of cell death from apoptosis to necrosis. Palmitoleate did not alter cAMP levels in BRIN-BD11 cells and the results suggest that a change in cAMP is not involved in mediating the protective effects of this fatty acid. Moreover, they reveal that attenuated caspase activation does not always correlate with altered cell viability in cultured beta-cells and suggest that mono-unsaturated fatty acids control cell viability by regulating a different step in the apoptotic pathway from that influenced by cAMP.

1-Methyl-3-isobutylxanthine↗
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↗
PubMed1995

Hyperpolarization of the liver cell membrane by palmitate as affected by glucose and lactate: implications for control of feeding.

Since the membrane potential of liver cells being in contact with vagal afferents has been proposed to represent a major signal in metabolic control of food intake, we investigated the effect of palmitate, glucose and lactate on the membrane potential of hepatocytes with microelectrodes using superfused mouse liver slices. The mice used for the experiments were fed a fat-enriched diet (18% fat). Palmitate (0.5 mM) hyperpolarized the membrane of hepatocytes by 3-4 mV, and this hyperpolarization was not affected by 5-10 mM glucose and 0.5-1 mM lactate. Glucose alone did not influence the potential, even when mice fed a high carbohydrate diet were employed. At lactate concentrations > or = 2 mM the palmitate induced hyperpolarization was eliminated and 5 mM lactate or pyruvate alone hyperpolarized the liver cell membrane. Similar to the palmitate induced hyperpolarization, the lactate induced hyperpolarization was prevented by the K-channel blocker TEA, suggesting that activation of K channels is involved in the hyperpolarization. The results show that physiological concentrations of glucose and lactate do not affect the hyperpolarization of the liver cell membrane due to fatty acid oxidation. The implications of these findings with regard to control of food intake by fatty acid oxidation and lactate metabolism are discussed. The observations are consistent with a signal function of the hepatic membrane potential in physiological control of food intake by fatty acid oxidation. Hepatic lactate metabolism at supraphysiological lactate concentrations may also produce a satiety signal coded by the hepatic membrane potential.

Animals↗
PubMed1989

Direct evidence for the oxidation of palmitic acid by host-grown Mycobacterium leprae.

Oxidation of palmitic acid by whole-cell suspensions of Mycobacterium leprae free from host tissues was investigated using manometric techniques. After a lag period of about 6-8 h, M. leprae suspensions catalysed an active oxidation of palmitic acid, and the oxidative process (oxygen uptake) was quite sensitive to rotenone, atabrine, amytal, antimycin A and cyanide. The spectrophotometric observations indicated that the M. leprae cytochrome system, under anaerobic conditions, was reduced in the presence of palmitic acid which was completely oxidized by oxygen. These data provide direct evidence that M. leprae cells are capable of oxidizing palmitic acid, and that oxidation is mediated by the electron transport system using oxygen as the terminal electron acceptor.

Animals↗
PubMed2005

Expression analysis of a human hepatic cell line in response to palmitate.

Saturated fat plays a role in common debilitating diseases such as obesity, type 2 diabetes, and coronary heart disease. It is also clear that certain fatty acids act as regulators of metabolism via both direct and indirect signalling of target tissues. As the molecular mechanisms of saturated fatty acid signalling in the liver are poorly defined, hepatic gene expression analysis was undertaken in a human hepatocyte cell line after incubation with palmitate. Profiling of mRNA expression using cDNA microarray analysis revealed that 162 of approximately 18,000 genes tested were differentially expressed after incubation with palmitate for 48 h. Altered transcription profiles were observed in a wide variety of genes, including genes involved in lipid and cholesterol transport, cholesterol catabolism, cell growth and proliferation, cell signalling, beta-oxidation, and oxidative stress response. While palmitate signalling has been examined in pancreatic beta-cells, this is the first report showing that palmitate regulates expression of numerous genes via direct molecular signalling mechanisms in liver cells.

Cell Line↗
PubMed2006

Palmitic acid-induced activation of human T-lymphocytes and aortic endothelial cells with production of insulin receptors, reactive oxygen species, cytokines, and lipid peroxidation.

Diabetic conditions are associated with hyperglycemia and hyperlipidemia, but the role of saturated fatty acids (SFA) vs. unsaturated fatty acids (UFA) in activation of T-lymphocytes and human aortic endothelial cells (HAEC) is not known. We investigated in vitro effects of various concentrations of SFA (palmitate) and UFA (oleic, linoleic, linolenic, and arachidonic) acids in activation of these cells. These cells in presence of palmitate, but not UFA, exhibited time, and concentration-dependent emergence of insulin receptors, GLUT 4 expression, generation of ROS, cytokines, lipid peroxidation, and IRS-1. We conclude that both T-lymphocytes and HAEC share common characteristics in exhibiting activation of these cells to palmitate, but not to UFA, by developing insulin receptors and becoming insulin responsive tissues, a hitherto unknown response to palmitate. We hypothesize that these events may serve as protective defense mechanisms against acute effects of glucotoxicity and lipotoxicity in these cells.

Aorta↗