PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “PALMITIC ACID”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 145 records · Page 8Linked to original sources
PubMed1967

Rates of tissue uptake of palmitic acid-1-14C complexed with albumin by two different procedures.

The effect was investigated of two different methods of preparing an albumin-palmitic acid complex on the tissue uptake of the palmitic acid, both in vivo and in vitro. Complex A was prepared by exposing monomolecular layers of palmitic acid-1-(14)C deposited on a solid surface to albumin dissolved in buffer. Complex B was prepared by the interaction of albumin with a micellar solution of palmitate-1-(14)C. The radioactivities and chemical compositions of the two complexes were almost identical. Rat epididymal fat pads took up, during a 1 hr incubation, about 2.5 times as much palmitic acid from complex A as from complex B; the extent of esterification of the incorporated label was equal for the two complexes. The fractional turnover rate of palmitic acid of complex A, administered intravenously to dogs, was about twice that of palmitic acid from complex B. The label of the two complexes recirculated in the esterified fatty acid fraction of plasma to an equal extent. It is proposed that differences in the orientation of the fatty acid molecules may affect their interaction with the binding sites of albumin and that the metabolic differences of the resulting complexes are related to differences in the ease of transfer of the fatty acid from the complex to receptor sites of tissues.

Adipose Tissue↗
PubMed1994

Synthesis and tissue biodistribution of [omega-11C]palmitic acid. A novel PET imaging agent for cardiac fatty acid metabolism.

In order to diagnose patients with medium-chain acyl-CoA dehydrogenase deficiency with a noninvasive diagnostic technique such as positron emission tomography, we have developed a synthesis of [omega-11C]palmitic acid. The radiochemical synthesis was achieved by coupling an alkylfuran Grignard reagent (7) with [11C]methyl iodide, followed by rapid oxidative cleavage of the furan ring to the carboxylate using ruthenium tetraoxide. Tissue biodistribution studies in rats comparing [omega-11C]palmitic acid and [1-11C]palmitic acid show that the %ID/g and %ID/organ in the heart tissue after administration of [omega-11C]palmitic acid is approximately 50% greater than after administration of [1-11C]palmitic acid, due to the diminished metabolism of the [omega-11C]palmitic acid. These studies show as well, low uptake in nontarget tissues (blood, lung, kidney, and muscle). PET images of a dog heart obtained after administration of [omega-11C]-and [1-11C]palmitic acid show virtually identical uptake and distribution in the myocardium. The differing cardiac washout of labeled palmitates measured by dynamic PET studies may allow diagnosis of disorders in cardiac fatty acid metabolism.

Acyl-CoA Dehydrogenase↗
PubMed2000

The origin of 1H NMR-visible triacylglycerol in human neutrophils. Highfatty acid environments result in preferential sequestration of palmitic acid into plasma membrane triacylglycerol.

Human neutrophils incubated for 1 h in vitro with 10% commercial pooled, human serum containing high levels of free fatty acids (1141 microM) displayed a distinct lipid signal, typical of triacylglycerol, in the 1H NMR spectrum. Concurrently their plasma membrane triacylglycerol mass increased 4.6-fold with a selective rise in the content of palmitic and linoleic acids. Although qualitatively similar, these effects were much greater than those observed after incubating neutrophils with 50 microg.mL-1 of lipopolysaccharide in the presence of 10% AB serum with normal free fatty acid content (345 microM, LPS/S). Incubation of neutrophils with an artificial mixture of free fatty acids at concentrations found in commercial serum, or with the fatty acid fraction isolated from commercial serum increased the 1H NMR-detectable triacylglycerol. The signal intensity of the 1H NMR-detectable triacylglycerol depended on the triacylglycerol composition, and correlated with increased membrane triacylglycerol mass. Cellular uptake of 3H-labelled palmitic or oleic acids increased in the presence of commercial serum but not with LPS/S, with little contribution in either case to the triacylglycerol pool that increased in mass. Pulse-chase experiments demonstrated that with LPS/S and commercial serum, radiolabelled palmitic acid was preferentially incorporated into triacylglycerol located in the plasma membrane. This process could occur at the plasma membrane, as cytoplasts efficiently convert exogenous fatty acids into triacylglycerol. We propose that LPS/S and serum containing high levels of free fatty acid, important in conditions of sepsis and inflammation, may facilitate the sequestration of palmitic acid into triacylglycerol by different pathways. This triacylglycerol originates from exogenous and endogenous free fatty acids, is 1H NMR-visible, and may have a role in regulating apoptosis.

Arachidonic Acid↗
PubMed1995

Lack of promoting effects of alpha-linolenic, linoleic or palmitic acid on urinary bladder carcinogenesis in rats.

Potential promoting effects of alpha-linolenic, linoleic and palmitic acids were investigated in a two-stage urinary bladder carcinogenesis model. In experiment 1, male F344 rats were given 0.05% N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN) in their drinking water for 4 weeks and then basal diet containing 10% alpha-linolenic, 10% linoleic or 10% palmitic acid along with 0.2% butylated hydroxyanisole (BHA) as an antioxidant for 24 weeks. The development of tumors in the urinary bladder was not increased by treatment with any of the fatty acids. In experiment 2, male F344 rats were given 10% alpha-linolenic, 10% linoleic or 10% palmitic acid along with 0.2% BHA in their diet for 8 weeks without prior BBN treatment. The administration of fatty acids was not associated with any increase in the 5-bromo-2'-deoxyuridine labeling index of the urinary bladder epithelium. Serum and/or urine fatty acid levels increased in the cases of alpha-linolenic and linoleic acid treatments, but not with palmitic acid. Under the present experimental conditions neither the two polyunsaturated nor the one saturated fatty acid exerted any promoting effect on urinary bladder carcinogenesis.

Animals↗
PubMed1996

Protective effect of lysozyme-galactomannan or lysozyme-palmitic acid conjugates against Edwardsiella tarda infection in carp, Cyprinus carpio L.

The protective effect of lysozyme-galactomannan or lysozyme-palmitic acid conjugates orally administered to carp, Cyprinus carpio L. was investigated using a virulent strain of Gram-negative Edwardsiella tarda isolated from an infected fish. Lysozyme-galactomannan conjugate was prepared through controlled Maillard reaction. Lysozyme-palmitic acid conjugate was prepared through base-catalyzed ester exchange using N-hydroxysuccinimide ester of palmitic acid. The conjugates provided substantial protection to carp infected with a Gram-negative bacteria fish pathogen E. tarda NG 8104. Lytic activities of lysozyme conjugates with galactomannan and palmitic acid were about 80 and 71% of native lysozyme using Micrococcus lysodeikticus as a substrate. Feeding with lysozyme conjugates, for 8 days, significantly enhanced fish protection against E. tarda infection. The survival rate was 30% for lysozyme-galactomannan conjugate treated fish and 20% for lysozyme-palmitic acid conjugate treated fish after 6 days cultivation while all control fish died within 3 days. On the other hand, a recovery rate of 40% after 6 days was observed in the fish group that were fed lysozyme-palmitic acid conjugate 3 and 2 h before and after E. tarda challenge, respectively, and for 6 consecutive days. The results of this work show the possibility of utilizing lysozyme conjugates with galactomannan or palmitic acid as a therapeutic for infection in fish.

Animals↗
PubMed1983

In vivo incorporation of [3H]palmitic acid into PO protein, the major intrinsic protein of rat sciatic nerve myelin.

Separation of rat sciatic nerve myelin proteins by sodium dodecyl sulfate-slab gel electrophoresis 18 h after injection of [3H]palmitic acid into the nerve demonstrated acylation of the PO protein. When sciatic nerve myelin labeled with [3H]palmitic acid was extracted with acidified chloroform/methanol or chloroform/methanol, the radioactivity associated with PO was retained. These results provided evidence that the radioactivity derived from [3H]palmitic acid in PO protein was not due to labeled phospholipid bound to PO protein by strong physical interaction. Furthermore, the radioactivity associated with purified preparations of PO remained after dialysis and re-electrophoresis, providing additional evidence that [3H]palmitic acid was firmly bound to PO. Treatment of myelin proteins with hydroxylamine at pH 6.6 released most of the radioactivity, indicating that [3H]palmitic acid was covalently bound by ester linkage to PO. Cleavage of purified acylated PO with methanolic NaOH released 85% of the protein-bound radioactivity. Gas-liquid chromatography of the fatty acids released from PO showed labeling of methyl esters of palmitate, stearate, and oleate (56, 16, and 5%, respectively). In addition, a small unlabeled peak with retention time identical with methyl linoleate was also observed. Intraneural injection of a mixture of [3H]palmitic acid and [14C]fucose or [3H]palmitic acid and [35S]sulfate in vivo followed by disc gel electrophoresis and determination of incorporated radioactivity clearly showed that PO was glycosylated, sulfated, and acylated. The potential significance of fatty acids linked to PO is discussed.

Acylation↗
PubMed1984

Enhanced N-acylation of palmitic acid in sphingomyelin of antibody-stimulated L cells.

Metabolism of sphingomyelin was stimulated in a fibroblast-like transformed cell line, L-929, when the cells were incubated with antibodies of a specific rabbit antiserum. The cells responded with an increased incorporation of [3H] palmitic acid into sphingomyelin. The stimulated uptake of palmitic acid into sphingomyelin can not be explained by simple mass increases in cellular phospholipids but probably represents a selective N-acyl group turnover. Palmitic acid composed only 7.5 percent of the acyl substituents, as assessed by gas-liquid chromatographic analysis, but [3H] palmitic acid was incorporated at a two-fold higher level into the acyl position than into the long chain base precursor (sphingosine). Since it is known that palmitic acid is the predominant fatty acid forming sphingosine, this represents a considerable selection for N-acyl group turnover. Another saturated fatty acid, stearic acid, which was over twice as abundant constituently was incorporated at a much lower rate when the cells were stimulated. Thus palmitic acid was observed to be selectively turning over in a manner suggestive of acylation-reacylation cycles observed with other classes of phospholipids.

Acylation↗
PubMed1984

15(p-[123I]Iodophenyl)pentadecanoic acid as tracer of lipid metabolism: comparison with [1-14C]palmitic acid in murine tissues.

Uptake and turnover of 15-(p-[123I]iodophenyl)pentadecanoic acid (I-PPA), a radioiodinated free-fatty-acid analog, was examined in heart, lung, liver, kidneys, and spleen and compared with that of [1-14C]palmitic acid (PA). High cardiac uptake of both I-PPA (4.4% dose/g) and PA (2.8% dose/g) was followed by a two-component tracer clearance. Kinetics of I-PPA were linked to those of PA in tissues with primary oxidation of free fatty acids or their preferential storage. Tissue lipids of all organs investigated were labeled concordantly by both tracers. Fractional distributions of PA and I-PPA incorporation in tissue lipids were significantly correlated. Thus general pathways of FFA tissue metabolism are traced by this radioiodinated free-fatty-acid analog. High-quality metabolic imaging of the heart is possible by means of I-PPA with conventional scintigraphic equipment or cross-sectional imaging with single photon emission computerized tomography facilities.

Animals↗
PubMed1982

Exchange of palmitic acid from cytosolic proteins to microsomes, mitochondria and lipid vesicles.

The presence of two fractions with affinity for 1-14C palmitic acid was demonstrated in the 105,000 x g supernatant of rat liver homogenate by Sephadex G-75 gel filtration. The lowest molecular weight fraction was identified as fatty acid binding protein as judged by its relative elution volume in Sephadex G-75, its binding characteristics to sulfobromophthalein and palmitic acid binding inhibition by flavaspidic acid. Discontinuous sucrose gradient was used to study palmitic acid exchange from these cytosolic fractions to microsomes and mitochondria. Both fractions from rat liver were more effective than albumin in the exchange of palmitic acid to particulate material. Palmitic acid was exchanged from fatty acid binding protein to liposomes. This and perhaps other cytosolic protein/s participate in cellular fatty acid transport.

Animals↗
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↗
PubMed1988

Structure and phase behavior of hydrated mixtures of L-dipalmitoylphosphatidylcholine and palmitic acid. Correlations between structural rearrangements, specific volume changes and endothermic events.

Several new features of the phase diagram of L-dipalmitoylphosphatidylcholine (DPPC)/palmitic acid mixtures in excess water were established by means of static and time-resolved X-ray diffraction, densitometry and differential scanning calorimetry (DSC). At low temperatures, palmitic acid has a biphasic effect on the lamellar subgel phases: at concentrations below 5-6 mol%, it prevents formation of the DPPC subgel phase (Lc), while at higher contents (between about 40 and 90 mol%) another subgel phase (Lccom) is formed as a result of lipid co-crystallization at 1 DPPC: 2 palmitic acid stoichiometry. A crystalline palmitic acid phase separates from Lccom above 70-80 mol% of fatty acid. The Lccomphase transforms into a lamellar gel phase (L beta) in an endothermic transition centered at 38 degrees C. At high temperatures, the mixtures form hexagonal liquid-crystalline phase (HII) in the region of 60-70 mol% and an isotropic phase (I) at 90-100 mol% of palmitic acid. No coexistence of HII phase with the fluid lamellar phase of DPPC was observed at intermediate compositions (20 and 50 mol% of palmitic acid) but rather formation of a complex phase with non-periodic geometry characterized by molten chains and a broad, continuous small-angle scattering band. No evidence for fluid phase coexistence was found also at compositions between HII and I phases. The L beta--HII transition at 60-70 mol% of palmitic acids is readily reversible and two-state in both heating and cooling modes. It is characterized by the coexistence of initial and final phases with no detectable intermediates by time-resolved and static X-ray diffraction. The crystalline-isotropic transition in palmitic acid is two-state only in heating direction. On cooling, it is characterized by strong undercooling and gradually relaxing lamellar crystalline structures. The slowly reversible Lccom--L beta transition proceeds continuously through intermediate states. Although clearly discernible by both DSC and X-ray diffraction, it is not accompanied by specific volume changes.

1,2-Dipalmitoylphosphatidylcholine↗
PubMed1984

In vitro acylation of rat gastric mucus glycoprotein with [3H]palmitic acid.

The incorporation of fatty acids into gastric mucus glycoproteins was studied by incubating rat gastric mucosal cell suspensions with [9,10-3H]palmitic acid and [3H]proline. The mucus glycoprotein polymer, secreted into the growth medium (extracellular) and that contained within the cells (intracellular), was purified from the other components of the secretion, thoroughly delipidated, and then analyzed for the radiolabeled tracers. Both pools of mucus glycoprotein, incubated in the presence of [3H]palmitic acid, contained radioactive label which could not be removed by gel filtration, CsCl density gradient centrifugation, sodium dodecyl sulfate-gel electrophoresis, or lipid extraction. Treatment of the purified mucus glycoprotein with 1 M hydroxylamine or 0.3 M methanolic KOH released the radioactivity, thus indicating that [3H]palmitic acid was covalently bound by ester linkage to the glycoprotein. The released radioactivity was associated mainly (87%) with palmitic acid. The incorporation ratio of [3H]proline to [3H]palmitic acid was 0.12:1.0 in the extracellular glycoprotein and 1.38:1.0 in the intracellular glycoprotein, which suggested that acylation of mucus glycoprotein occurs in the intracellular compartment after completion of its polypeptide core. The fact that incorporation of [3H]palmitic acid was greater in the glycoprotein subunits than in the glycoprotein polymer indicates that acylation takes place near the end of subunit processing but before their assembly into the high molecular weight mucus glycoprotein polymer.

Acylation↗