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PubMed1995

Three-dimensional structure of bovine heart fatty-acid-binding protein with bound palmitic acid, determined by multidimensional NMR spectroscopy.

The three-dimensional structure of the holo form of recombinant cellular bovine heart fatty-acid-binding protein (H-FABPc), a polypeptide of 133 amino acid residues with a molecular mass of 15 kDa, has been determined by multidimensional homonuclear and heteronuclear NMR spectroscopy applied to uniformly 15N-labeled and unlabeled protein. A nearly complete set of 1H and 15N chemical shift assignments was obtained. A total of 2329 intramolecular distance constraints and 42 side-chain chi 1 dihedral-angle constraints were derived from cross-relaxation and J coupling information. 3D nuclear Overhauser enhancement and exchange spectroscopy combined with heteronuclear multiple-quantum coherence (NOESY-HMQC) experiments, performed on a sample of uniformly 13C-labeled palmitic acid bound to unlabeled cellular heart fatty-acid-binding protein revealed 10 intermolecular contacts that determine the orientation of the bound fatty acid. An ensemble of protein conformations was calculated with the distance-geometry algorithm for NMR applications (DIANA) using the redundant dihedral-angle constraint (REDAC) strategy. After docking the fatty acid into the protein, the protein-ligand arrangement was subject to distance-restrained energy minimization. The overall conformation of the protein is a beta-barrel consisting of 10 antiparallel beta-strands which form two nearly orthogonal beta-sheets of five strands each. Two short helices form a helix-turn-helix motif in the N-terminal region of the polypeptide chain. The palmitic acid is bound within the protein in a U-shaped conformation close to the two helices. The obtained solution structure of the protein is consistent with a number of fatty-acid-binding-protein crystal structures.

Amino Acid Sequence↗
PubMed1999

Effect of C2 ceramide on the inositol phospholipid metabolism (uptake of 32P, 3H-serine and 3H-palmitic acid) and apoptosis-related morphological changes in Tetrahymena.

Sphingomyelin metabolites have significant role in the regulation of many life processes of mammalian cells. In the present experiments the influence of phospholipid turnover and apoptosis related morphologic signs by one of this metabolite, C2 ceramide was studied, and compared to the control, untreated cells, in the unicellular Tetrahymena. The incorporation of phospholipid head group components (serine, phosphorus) show a clear time-dependence; while the incorporation of fatty acid component (palmitic acid) is very fast: no significant alterations were found between 5- and 60-min incubations. C2 ceramide treatment didn't alter 3H-palmitic acid incorporation into phospholipids, however 3H-serine incorporation was mainly inhibited. The amount of total incorporated 32P was also decreased, on the other hand the lover concentration C2 ceramide (10 microM) elevated the synthesis of inositol phospholipids. The higher concentration of C2 ceramide (50 microM) had inhibitory effect on the synthesis of each phospholipids examined. This means that in the presence of the C2 ceramide the synthesis, recovery and turnover of phospholipids, participating in signal transduction, are altered. However these observations were based the uptake of labeled phospholipid precursors, which gives information on the dynamics of the process, without using lipid mass measurements. C2 ceramide also caused the rounding off the cells, DNA degradation and nuclear condensation. These latter observations point to morphological signs of apoptosis. The results call attention to the role of sphingomyelin metabolites on signalization of unicellulars, to the cross-talk between the inositol phospholipids and sphingomyelin metabolites, and the role of these molecules in the apoptotic processes at a low evolutionary level.

Animals↗
PubMed1979

Synthesis and biologic distribution of mercapto derivatives of palmitic acid.

Mercapto derivatives of palmitic acid are capable of binding 99mTc. Based on the hypothesis that 99mTc-labeled palmitic acid derivatives would behave biologically like palmitic acid and thus could be used as myocardial imaging agents, three mercaptopalmitic acid derivatives have been prepared. The synthesis of 2-mercaptopalmitic acid, 2-mercapto-1,16-hexadecanedioic acid, and 16-mercaptopalmitic acid was accomplished by reaction of the corresponding bromo compound with thiourea. The 35S-labeled compounds and [16-14C]palmitic acid were evaluated in rats with a heat-inflicted myocardial infarction to study the effect of the introduction of the mercapto group. The organ distribution of 2-[35S]mercaptopalmitic acid was most similar to that of [16-14C]palmitic acid.

Animals↗
PubMed2002

Inhibition of fatty acid synthesis in bovine mammary homogenate by palmitic acid is not a detergent effect.

Supplemental fat fed to dairy cows affects the fat composition of milk by reducing the yield of mammary synthesized fatty acids. The effect has been attributed to a potential allosteric inhibition of acetyl coenzyme-A, a key enzyme in fatty acid synthesis. In vitro experiments have demonstrated an inhibition of fatty acid synthesis when long-chain fatty acids are added to incubations. However, in vitro inhibition can result from a nonspecific detergent effect arising from an inherent physical property of fatty acids. An allosteric role for palmitic acid has not been tested in bovine mammary tissue. The objective of this experiment was to test the hypothesis that palmitic acid is an allosteric inhibitor of fatty acid synthesis in mammary tissue. We tested for a detergent effect by including a synthetic detergent, sodium dodecyl sulfate, under identical incubation conditions. A subcellular supernatant fraction of mammary tissue was used for incubations in the present experiment. The incubation system produced free fatty acids in a linear fashion for time and protein content. Results indicated that fatty acid synthesis was affected by the addition of palmitic acid to the incubations but not by caprylic acid, a short-chain fatty acid. Sodium dodecyl sulfate did not affect fatty acid synthesis at the concentrations used. The results of the present experiment indicate that palmitic acid inhibited fatty acid synthesis, and the effect was not the result of a detergent effect.

Acetyl Coenzyme A↗
PubMed1990

Dietary palmitic acid (16:0) enhances high density lipoprotein cholesterol and low density lipoprotein receptor mRNA abundance in hamsters.

In order to examine the qualitative effect of different fats and specific fatty acids on plasma lipids and lipoprotein metabolism, six low fat, cholesterol-free diets were fed to young male hamsters (10/group) for a 4-week period. Fat blends were formulated with coconut oil, palm oil, soybean oil, high oleic acid safflower oil, butter, corn oil, and canola oil. Diets contained 13% energy as fat and dietary polyunsaturate/saturate ratios ranged from 0.12 to 1.04, one of which incorporated the American Heart Association-recommended concentrations of saturates, monoenes, and polyenes and another reflected the current American Fat Blend. In three diets the polyunsaturate/monounsaturate/saturate ratio was held constant while only the 12:0, 14:0, and 16:0 were varied. Plasma lipoproteins and apoproteins were assessed in conjunction with the abundance of specific hepatic and intestinal mRNA for the low density lipoproteins (LDL) receptor and various apolipoproteins associated with cholesterol metabolism. The plasma cholesterol response was lowest with the American Heart Association blend and equally elevated by the more saturated, low polyene diets (polyunsaturate/saturate, 0.12-0.38). Replacing 12:0 plus 14:0 from coconut oil with 16:0 as palm oil induced a significant increase in high density lipoprotein (HDL) cholesterol with a trend toward decreased LDL. These shifts in lipoprotein cholesterol were corroborated by measures of the LDL/HDL ratio, the plasma apolipoprotein B/apolipoprotein A1 ratio, and differences in the synthesis of apolipoproteins and the LDL receptor based on estimates of the mRNA for these proteins in the liver and gut, using specific cDNA probes for apolipoprotein A1, apolipoprotein B, apolipoprotein E, and the LDL receptor. Although it has been suggested that dietary polyenes lower total plasma cholesterol, including HDL, and that saturated fat increases both these pools of cholesterol, the current data represents the first evidence that a specific saturated fatty acid, i.e., palmitic acid, may enhance HDL production.

Animals↗
PubMed1994

Normalization of essential-fatty-acid-deficient keratinocytes requires palmitic acid.

Cultured adult human keratinocytes show accelerated growth rates in medium that is essential fatty acid deficient. The cells also show decreased amounts of the essential fatty acids 18:2, 20:3, and 20:4 and contain increased amounts of the monounsaturated fatty acids 16:1 and 18:1. These lower levels of polyunsaturated fatty acids were only partially restored by supplementing the medium with 18:2 and 20:4 fatty acid. The addition of the non-essential fatty acid 16:0 (5 microM), along with the essential fatty acids, resulted in the successful normalization of the major fatty acids in the deficient keratinocytes. Normalized cells showed a constant total fatty acid/mg of protein in the phospholipid fraction, as the total cell fatty acid content per cell increased with augmenting fatty acid supplementation. Supplementation of the medium with 16:0 and essential fatty acids decreased the growth and passage potential of the cells. Use of 18:1 in lieu of 18:2 fatty acid yielded essential-fatty-acid-deficient keratinocyte growth values. Likewise the least supplemented medium (5 microM 18:2 + 5 microM 16:0) also gave the accelerated cell growth rates. This study shows that manipulation of the essential fatty acid levels, if accompanied by 5 microM 16:0 in the growth medium, alters the growth properties of adult human primary keratinocytes.

Adult↗
PubMed1981

Investigation of [14C] linoleic acid conversion into [14C] arachidonic acid and placental transfer of linoleic and palmitic acids across the perfused human placenta.

In five separate experiments in which single placental lobes were perfused, [14C] antipyrine, [3H] dextran and a fatty acid mixture containing [14C] linoleic and [3H] palmitic acids were added to the maternal circuit. Samples of fetal and maternal perfusate, taken at intervals, were analysed for radioactivity and fatty acid content. The relative placental transport rates of antipyrine, linoleic and palmitic acids and the changes in maternal and fetal circuit content of linoleic, palmitic and arachidonic acids were measured. Mean transfer rates of 150, 0.023 and 0.034 mumol min-1 were obtained for [14C] antipyrine, [3H] palmitic and [14C] linoleic acids, respectively. The transfer of [3H] dextran was negligible. The transfer rates of linoleic and palmitic acids did not differ significantly from one another. The maternal circuit content of palmitic and arachidonic acids increased, whereas linoleic acid content decreased. The fetal content of all three acid increased but in the case of arachidonic and palmitic acids the increase was not as great as that seen in the maternal circuit. In no experiment was radioactivity detected in maternal or fetal perfusate arachidonic acid. It is concluded that linoleic and palmitic acids cross the placenta from the maternal to the fetal side. This transfer appears to be non-selective. The large amounts of arachidonic acid that are released into the perfusate probably originate from placental lipids other than free linoleic acid.

Antipyrine↗
PubMed1990

Interaction of fatty acid binding protein with microsomes: removal of palmitic acid and retinyl esters.

[14C] palmitic acid or [3H] retinyl esters incorporated in microsomal membranes were removed by a cytosolic fraction enriched in fatty acid binding protein. When mouse liver cytosol was fractionated by 70% ammonium sulphate, a precipitate and a soluble fraction were obtained. The soluble fraction containing the fatty acid binding protein was able to remove from microsomal membranes, [14C] palmitic acid or [3H] retinyl esters, whereas the precipitate fraction had no removal capacity. Retinoid analysis indicated that 70% ammonium sulphate soluble fraction was enriched in endogenous retinyl esters with regard to cytosol or 70% ammonium sulphate precipitate fraction.

Ammonium Sulfate↗
PubMed1997

Comparison of a carbohydrate-rich diet and diets rich in stearic or palmitic acid in NIDDM patients. Effects on lipids, glycemic control, and diurnal blood pressure.

OBJECTIVE: To compare the effects on lipid levels, glycemic control, and diurnal blood pressure of two diets rich in one of the two quantitatively most important saturated fatty acids, stearic and palmitic acid, with a carbohydrate-rich diet in NIDDM patients. RESEARCH DESIGN AND METHODS: A total of 15 NIDDM patients participated in a randomized crossover study with three 3-week diet interventions separated by 2-week washout periods. Patients started with a diet rich in stearic acid (44 E% [percent of total energy] fat [13 E% stearic acid], 40 E% carbohydrate, 15 E% protein), palmitic acid (45 E% fat [16 E% palmitic acid], 40 E% carbohydrate, 15 E% protein), or carbohydrate (29 E% fat, 51 E% carbohydrate, and 18 E% protein), then were shifted to the other two diets in a randomized block design. At the start and end of each intervention period, fasting blood samples were drawn for analysis of lipids and blood glucose. In addition, diurnal blood pressure was measured. RESULTS: At the end of the 3-week interventions, total cholesterol was significantly higher after the palmitic acid-rich diet than after the stearic acid-rich or carbohydrate-rich diets (5.3 +/- 1.3 vs. 5.0 +/- 1.2 and 4.9 +/- 1.2 mmol/l, respectively; P = 0.03). No significant differences in triglyceride, LDL, or HDL cholesterol levels were seen after the three intervention diets. No difference in effects between the diet periods were seen for fructosamine, HbA1c, fasting blood glucose, or diurnal blood pressure. CONCLUSIONS: For the first time, it has been demonstrated that a diet rich in palmitic acid was not as effective in lowering cholesterol levels as carbohydrate-rich and stearic acid-rich diets in NIDDM patients. No deleterious effects were seen on diurnal blood pressure, triglyceride levels, and glycemic control. Development of foods containing stearic acid rather than the more atherogenic saturated fatty acids may allow a wider choice of acceptable foods to NIDDM patients.

Adult↗
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↗
PubMed2003

Linoleic acid and antioxidants protect against DNA damage and apoptosis induced by palmitic acid.

Polyunsaturated fats are the main target for lipid peroxidation and subsequent formation of mutagenic metabolites, but diets high in saturated fats are more strongly associated with adverse health effects. We show that the common saturated fatty acid, palmitic acid, is a potent inducer of DNA damage in an insulin-secreting cell line, and in primary human fibroblasts. Damage is not associated with upregulation of inducible nitric oxide synthase, but is prevented by two different antioxidants, alpha-lipoic acid and 3,3'-methoxysalenMn(III) (EUK134), which also partly prevent palmitic acid-induced apoptosis and growth inhibition. Since mutagenic metabolites can be formed from peroxidation of polyunsaturated fatty acids, co-administration of palmitic and a polyunsaturated fatty acid might be particularly harmful. Palmitic acid-induced DNA damage is instead prevented by linoleic acid, which is acting here as a protective agent against oxidative stress, rather than as a source of mutagenic metabolites. These results illustrate the complexity of the relationship of dietary fat intake to genotoxicity.

Antioxidants↗
PubMed1993

Incorporation of stearic acid (18:0) and palmitic acid (16:0) in phospholipid molecular species studied in isolated rat liver cells.

The incorporation of [1-14C]16:0 and [1-14C]18:0 in the molecular species of PC and PE in isolated rat liver cells was studied. More [14C]18:0 than [14C]16:0 was esterified both in PC and PE. Also the chain elongated and desaturated products (16:1, 18:0 and 18:1) were incorporated. The main molecular phospholipid species formed from [14C]18:0 were 18:0-18:2, 18:0-20:4 and 18:0-22:6. 18:0-18:0 species was not detected, independent of the substrate concentration (0.1-0.9 mM). With [14C]16:0 at low substrate concentration (0.1 mM) the dominating species are 16:0-18:2, 16:0-20:4 and 16:0-22:6. These species were detected already after 10 min. The same main species are formed both in PC and PE, but the relative amounts differ. In PC the combination with 18:2 is most abundant for both saturated fatty acid substrates. In PE 18:0-20:4 dominates when 18:0 is the substrate, and 16:0-22:6 when 16:0 is. At higher substrate concentrations (0.4-0.9 mM) 16:0 is also esterified in 16:0-16:0. This molecular species is efficiently degraded in the cells within 2-3 h, in contrast to the other species formed. The results suggest that 16:0 and 18:0 are directly incorporated in the sn-1 position in physiologically important phospholipid molecular species. With an excess of 16:0, 16:0-16:0 is also formed in substantial amounts, but this uncommon species is thereafter removed.

Animals↗
PubMed2005

Anaerobic biodegradation of oleic and palmitic acids: evidence of mass transfer limitations caused by long chain fatty acid accumulation onto the anaerobic sludge.

Palmitic acid was the main long chain fatty acids (LCFA) that accumulated onto the anaerobic sludge when oleic acid was fed to an EGSB reactor. The conversion between oleic and palmitic acid was linked to the biological activity. When palmitic acid was fed to an EGSB reactor it represented also the main LCFA that accumulated onto the sludge. The way of palmitic acid accumulation was different in the oleic and in the palmitic acid fed reactors. When oleic acid was fed, the biomass-associated LCFA (83% as palmitic acid) were mainly adsorbed and entrapped in the sludge that became "encapsulated" by an LCFA layer. However, when palmitic acid was fed, the biomass-associated LCFA (the totality as palmitic acid) was mainly precipitated in white spots like precipitates in between the sludge, which remained "non-encapsulated." The two sludges were compared in terms of the specific methanogenic activity (SMA) in the presence of acetate, propionate, butyrate, and H(2)CO(2), before and after the mineralization of similar amounts of biomass-associated LCFA (4.6 and 5.2 g COD-LCFA/g of volatile suspended solids (VSS), for the oleic and palmitic acid fed sludge, respectively). The "non-encapsulated," sludge exhibited a considerable initial methanogenic activity on all the tested substrates, with the single exception of butyrate. However, with the "encapsulated" sludge only methane production from ethanol and H(2)/CO(2) was detected, after a lag phase of about 50 h. After mineralization of the biomass-associated LCFA, both sludges exhibited activities of similar order of magnitude in the presence of the same individual substrates and significantly higher than before. The results evidenced that LCFA accumulation onto the sludge can create a physical barrier and hinder the transfer of substrates and products, inducing a delay on the initial methane production. Whatever the mechanism, metabolic or physical, that is behind this inhibition, it is reversible, being eliminated after the depletion of the biomass-associated LCFA.

Acetates↗
PubMed2002

Short-term diets enriched in stearic or palmitic acids do not alter plasma lipids, platelet aggregation or platelet activation status.

OBJECTIVE: To determine whether healthy males who consumed increased amounts of dietary stearic acid compared with increased dietary palmitic acid through the consumption of commercially available foods, exhibited any changes in plasma lipids, platelet aggregation or platelet activation status. DESIGN: A randomised cross-over dietary intervention. SUBJECTS AND INTERVENTIONS: Nine free-living healthy males consumed two experimental diets (stearic acid enriched, diet S, and palmitic acid enriched, diet P) for 3 weeks in a randomised cross-over design separated by a 3 week washout phase. The diets consisted of approximately 30% of energy as fat (30% of which was derived from the treatment diets) providing approximately 13 g/day as stearic acid and 17 g/day as palmitic acid on diet S and approximately 7 g/day as stearic acid and 22 g/day as palmitic acid on diet P. The dietary ratio of stearic to palmitic acids was 0.76 on diet S compared with 0.31 on diet P. Blood samples were collected on days 0 and 21 of each dietary period. RESULTS: LDL cholesterol levels and platelet aggregation response to the agonist ADP were significantly decreased (P<0.025) in subjects on diet S compared with day 0. Apart from that, there were no significant changes in plasma lipids, platelet aggregation, mean platelet volume and platelet reactivity between diets. There were no significant changes in stearic or palmitic acid levels in plasma phospholipid or triacylglycerol. There was a significant difference in palmitic acid levels in platelet phospholipids between the two diets. CONCLUSIONS: Use of commonly available foods led to a 27% increase in stearic acid (diet S) and a 19% increase in palmitic acid (diet P), on diets S and P respectively, and no significant differences between the two diets in plasma lipoprotein concentrations, platelet aggregation or platelet activation status.

Adult↗
PubMed1974

Assessment of fetal lung maturity by estimation of amniotic fluid palmitic acid.

The measurement of palmitic acid in amniotic fluid has been shown to be a rapid means of assessing the lecithin concentration. The level of palmitic acid increases quickly when the fetal lung matures at about 35 weeks' gestation, and the level in amniotic fluid obtained 24 hours or less before delivery clearly distinguishes which infants are likely to develop respiratory distress syndrome and which are mature.

Amniotic Fluid↗