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At least 19 recordsLinked to original sources
PubMed1979

Amniotic fluid lecithin/sphingomyelin ratio, palmitic acid, palmitic acid/stearic acid ratio, total cortisol, creatinine, and percentage of lipid-positive cells in assessment of fetal maturity and fetal pulmonary maturity: a comparison.

Lecithin/sphingomyelin (L/S) ratio, creatinine, percentage of lipid-positive cells, palmitic acid, palmitic acid/stearic acid (P/S) ratio, and total cortisol were analyzed as tests for fetal maturity and fetal pulmonary maturity in 164 samples of amniotic fluid from 121 patients. Fifty samples were taken within 72 hours of delivery. The best tests for fetal maturity (37 weeks) with differential percentages were L/S ratio, palmitic acid, and P/S ratio. In the assessment of fetal pulmonary maturity, we studied an additional 174 samples in which only L/S ratio, creatinine, and lipid-positive cells were analyzed. All tests showed a high predictive value of an immature (positive) result was much less for all six parameters; the three best tests were total cortisol (33%), lipid-positive cells (26%) and L/S ratio (14%).

Amniotic Fluid↗
PubMed1988

Modification of CaCo-2 cell membrane fatty acid composition by eicosapentaenoic acid and palmitic acid: effect on cholesterol metabolism.

Membrane fatty acid composition of CaCo-2 cells was modified by incubating the cells for 8 days in medium containing 100 microM eicosapentaenoic acid or palmitic acid. The effect of membrane fatty acid changes on cholesterol metabolism was then studied. Cells incubated with eicosapentaenoic acid had significant changes in membrane fatty acid composition with an accumulation of 20:5 and 22:5 and a reduction in monoenoic fatty acids compared to cells grown in palmitic acid. Intracellular cholesteryl esters could not be detected in CaCo-2 cells grown in the presence of the n-3 polyunsaturated fatty acid. In contrast, cells incubated with the saturated fatty acid contained 2 micrograms/mg protein of cholesteryl esters. Cells grown in eicosapentaenoic acid, however, accumulated significantly more triglycerides compared to cells modified with palmitic acid. The rate of oleic acid incorporation into triglycerides was significantly increased in cells incubated with eicosapentaenoic acid. CaCo-2 cells modified by eicosapentaenoic acid had lower rates of HMG-CoA reductase and ACAT activities compared to cells modified with palmitic acid. The incorporation of the two fatty acids into cellular lipids also differed. Palmitic acid was predominantly incorporated into cellular triglycerides, whereas eicosapentaenoic acid was preferentially incorporated into phospholipids with 60% of it in the phosphatidylethanolamine fraction. The data indicate that membrane fatty acid composition is significantly altered by growing CaCo-2 cells in eicosapentaenoic acid. These modifications in membrane fatty acid saturation are accompanied by a decrease in the rates of cholesterol synthesis and cholesterol esterification.

Adenocarcinoma↗
PubMed1992

Comparison of effects of lauric acid and palmitic acid on plasma lipids and lipoproteins.

The effects of lauric acid (C12:0) on plasma lipids and lipoproteins were compared with the effects of palmitic acid (C16:0) and oleic acid (C18:1) in a metabolic-diet study of 14 men by using liquid-formula diets fed for 3 wk each in random order. Lauric acid was supplied in a synthetic high-lauric oil, palmitic acid was provided by palm oil and oleic acid in oleic-rich sunflower seed oil. The high-lauric oil resulted in higher concentrations of plasma total cholesterol (4.94 +/- 0.75 mmol/L [mean +/- SE]) and LDL cholesterol (3.70 +/- 0.57 mmol/L) when compared with high-oleic sunflower oil (4.44 +/- 0.54 and 3.31 +/- 0.44 mmol/L, respectively), but did not raise total and LDL cholesterol concentrations as much as did palm oil (5.17 +/- 0.65 and 3.93 +/- 0.51 mmol/L, respectively). No differences were noted in plasma triglycerides or HDL cholesterol. Lauric acid raises total and LDL cholesterol concentrations compared with oleic acid, but is not as potent for increasing cholesterol concentrations as is palmitic acid.

Adult↗
PubMed1986

Direct identification of palmitic acid as the lipid attached to p21ras.

p21v-H-ras, the transforming protein of Harvey murine sarcoma virus, contains a covalently attached lipid. Using thin-layer chromatography, we identified the acyl group as the 16-carbon saturated fatty acid palmitic acid. No myristic acid was detected in fatty acids released from in vivo-labeled p21v-H-ras. The p21v-K-ras protein encoded by Kirsten sarcoma virus was also palmitylated. The processing and acylation of p21v-K-ras however differed from that of p21v-H-ras. Three forms of [3H]palmitic acid-labeled p21ras proteins were detected in Kirsten sarcoma virus-transformed cells. This contrasted with Harvey sarcoma virus, in which two forms of p21v-H-ras contained palmitic acid. Analysis by partial proteolysis of p21v-H-ras labeled with [3H]palmitic acid suggested that all of the lipid found in intact p21v-H-ras was located in the C-terminal region. On sodium dodecyl sulfate-polyacrylamide gels, p21v-H-ras labeled with [3H]palmitic acid migrated slightly ahead of the majority of p21v-H-ras. Of the mature forms of p21v-H-ras, apparently only a subpopulation contains palmitic acid.

Animals↗
PubMed1992

Arachidonic and palmitic acid utilization in aged rat brain areas.

We have previously demonstrated that the arachidonic acid (20:4) incorporation into brain lipids differs according to the age of the animals used and the experimental conditions adopted. These differences led to a further investigation of arachidonic acid uptake in both aged and adult rat brains, its transformation into CoA derivatives, its incorporation into diacyl-glycerols and polar lipids, and finally its oxidation to CO2. These metabolic parameters were then compared with those obtained after using the saturated fatty acid palmitate (16:0). In both cases slices or mitochondria from different brain areas of 24-month-old and 4-month-old rats were examined. The results obtained indicate that the uptake of the fatty acids into cells is not modified by age. However, the successive metabolic transformations of the acids are altered to a considerable extent. In particular, in 24-month-old animals (compared with 4-month-old rats) there is a significant decrease of 20:4 in its incorporation into lipids as well as its oxidation to CO2, while arachidonoyl-CoA content increases by about 50%. This increased amount of CoA derivative, which has a potent detergent effect, may interfere with membrane structure and affect membrane physiological functions. Furthermore, because the free arachidonate pool is maintained in a dynamic equilibrium with its esterified forms, the final result may be a perturbation of this equilibrium.

Aging↗
PubMed1989

Effect of alpha-1-acid glycoprotein, albumin and palmitic acid on the brain and salivary gland extraction of warfarin in rats.

The effect of plasma protein binding of warfarin on its transfer into the brain and salivary gland was investigated using alpha-1-acid glycoprotein and human serum albumin (HSA) in combination or not with palmitic acid. The tissue extraction of [14C] warfarin relative to [3H]water was determined by intracarotid injection technique in male Wistar rats. The tissue extraction of warfarin varied inversely with the concentration of added serum protein, (HSA and alpha-1-acid glycoprotein), and addition of palmitic acid to HSA diminished the extraction. The fraction of drug uptaked by tissue (tissue available fraction) was always dramatically greater than the in vitro free drug fraction, and this was interpreted as an enhanced in vivo drug dissociation from the binding protein. The fraction of drug uptake by salivary gland was closer to the in vitro free fraction than the fraction of drug uptake by brain tissue. The addition of palmitic acid to HSA induced parallel changes in the in vitro free fraction of warfarin and in the brain tissue or salivary gland extraction of warfarin. These data indicate that a part of protein-bound warfarin (as determined in vitro) is available for tissue extraction via an enhanced in vivo dissociation of the drug-protein complex in the tissue microcirculation. The in vitro data were fitted to a saturable model of binding whereas the in vivo data could satisfactorily fit a model dealing with a nonsaturable model of binding, and this is probably the result of the several-fold increase in the in vivo dissociation constant.

Animals↗
PubMed1977

Modification of the binding of sulphamidochlorobenzoic acid to human albumin by palmitic acid contamination of albumin.

Palmitic acid a common contaminant of albumin preparations, competitively inhibits the binding of sulphamidochlorobenzoicacid (SCBA) to human albumin thus decreasing its observed affinity. The effect of palmitic acid depends on its concentration, i.e. the purity and concentration of the albumin preparation used. The correct value for SCBA affinity was obtained by correcting the experimental data according to the palmitic acid concentration by use of a multiligand analysis method.

Albumins↗
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↗
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↗
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↗
PubMed1987

Anomalous uncoupling of photophosphorylation by palmitic acid and by gramicidin D.

Palmitic acid and gramicidin D at low concentrations uncouple photophosphorylation in a mechanism that is inconsistent with classical uncoupling in the following properties: (1) delta pH, H+ uptake, or the transmembrane electric potential is not inhibited. (2) O2 evolution is stimulated under nonphosphorylating conditions but slightly inhibited in the presence of adenosine 5'-diphosphate + inorganic phosphate (Pi). (3) Light-triggered adenosine 5'-triphosphate (ATP)-Pi exchange is hardly affected, and ATPase activity is only slightly stimulated. (4) ATP-induced delta pH formation is selectively inhibited. This characteristic uncoupling is observed only when the native coupling sites of the electron transport system are used for energization such as for methylviologen-coupled phosphorylation. With pyocyanine, which creates an artificial coupling site, 1000-fold higher gramicidin D and higher palmitic acid concentrations are required for inhibition, and the inhibition is accompanied by a decrease in delta pH. Moreover, comparison between photosystem 1 and photosystem 2 electron transport and the effects of membrane unstacking suggest that low gramicidin D preferentially inhibits photosystem 2, while palmitic acid inhibits more effectively photosystem 1 coupling sites. The inhibitory capacity of fatty acids significantly drops when the chain length is reduced below 16 hydrocarbons or upon introduction of a single double bond in the hydrocarbon chain. It is suggested that palmitic acid and gramicidin D interfere with a direct H+ transfer between specific electron transport and the ATP synthase complexes, which provides an alternative coupling mechanism in parallel with bulk to bulk delta microH+. The sites of inhibition seem to be located in chloroplast ATP synthase, photosystem 2, and the cytochrome b6f complexes.

Chloroplasts↗
PubMed1979

Bilayer rigidity of the erythrocyte membrane2H-NMR of a perdeuterated palmitic acid probe.

Perdeuterated palmitic acid was intercalated into the human erythrocyte membrane and its motion studied by dueterium nuclear magnetic resonance (2H-NMR). From analysis of temperature dependent changes in the 2H-NMR spectra and from an analysis of derived moments we conclude that the acyl chains of the erythrocyte lipids do not exhibit a detectable phase transition.

Deuterium↗
PubMed1975

Palmitic acid and lecithin measurements in amniotic fluid.

A method is described for the rapid and quantitative estimation of total amniotic fluid palmitic acid. Palmitic acid and lecithin were measured in 140 samples of amniotic fluid in normal and abnormal pregnancy, and the correlation coefficient between the two parameters was 0.93. It is concluded that amniotic fluid palmitic acid measurements are of value in the prenatal determination of fetal pulmonary maturity.

Amniocentesis↗
PubMed1990

Rapid clearance of surfactant-associated palmitic acid from the lungs of developing and adult animals.

Palmitic acid is a minor component of natural surfactant and has been used to modify lipid extracts of natural surfactants to optimize their in vitro surface properties. The metabolic fate of palmitic acid in surfactant is unknown. The clearance of surfactant-associated radiolabeled palmitic acid after intratracheal administration was investigated with trace doses of surfactant in the adult rabbit and with trace and treatment doses in the 28-d fetal rabbit and the 132-d fetal sheep. Palmitic acid was cleared rapidly from the airways, with less than 2% of the radiolabel recovered as free palmitic acid in the alveolar wash by 1 h in all models. Recovery as free palmitic acid in the total lung at 2 h was 2% in the adult rabbit and 3% both doses in the preterm rabbit. In the preterm sheep, the recovery as free palmitic acid in the total lung was approximately 2% of the trace dose and 1% of the treatment dose by 5 h. Between 5 and 15% of the instilled palmitic acid was used as substrate for phospholipid synthesis by the lung in the different models. About 30% of the palmitate derived label was recovered in lipid extracts of liver 30 min after tracheal instillation of labeled surfactant in adult rabbits, whereas only 5-10% of the palmitate derived label was found in liver lipids in the preterm animals. In contrast to palmitic acid, radiolabeled triglyceride was cleared much more slowly from the airspaces and lungs of preterm sheep. Inasmuch as large amounts of palmitic acid are cleared rapidly from airspaces and lung tissue, it will not have a prolonged effect on the surface properties of surfactant but it may serve as a precursor for lung lipid metabolism.

Animals↗
PubMed1989

Multiple classes of binding sites for palmitic acid on the fatty acid-binding protein molecule.

Binding characteristics of fatty acid-binding protein (FABP) toward palmitic acid were studied. On the analysis of the interaction between FABP and [3H]palmitic acid over a wide range of concentrations of the fatty acid, at least three saturation plateaux were observed. By Scatchard-plot analysis, it appeared that FABP possesses three classes of binding sites for palmitic acid with different affinities [Kd1 = 1 x 10(-6) M (N = 1), Kd2 = 4 x 10(-6) M (N = 2), Kd3 = 2 x 10(-5) M (N = 10)]. Results of both sedimentation analyses and chromatofocusing of FABPs labeled with various concentrations of [3H]palmitic acid suggested that the FABP used was homogeneous. These results indicate that several classes of binding sites for palmitic acid with different affinities are present on the FABP molecule.

Animals↗
PubMed1977

Determination of amniotic fluid palmitic acid concentration for the estimation of fetal lung maturity.

Palmitic acid concentrations in amniotic fluid (AF) were determined in 135 patients with normal and pathological pregnancies between the 27th and 42nd week of gestation. There was a sharp rise in the mean palmitic acid concentration after the 34th weeks of gestation from 2.7 mug/ml to 9.9 mug/ml at term. This increase is almost identical with the rise of AF-lecithin. It was found that between 70% and 100% of AF-palmitic acid originates from lecithin. 65 patients were delivered within 24 h after amniotic fluid sampling. 7 infants of these patients developed a respiratory distress syndrome (RDS). In all cases with RDS AF-palmitic acid concentration was far below 5 mug/ml. Assuming an AF-palmitic acid concentration greater than 5 mug/ml for characterising fetal lung maturity (=no RDS), there were no false negative results, but 16% false positive results. However, the determination of AF-palmitic acid concentration seems to be a most reliable method for the assessment of fetal lung maturity.

Amniotic Fluid↗