PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “OLEIC 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 91 records · Page 5Linked to original sources

Linoleic acid, but not oleic acid, upregulates production of interleukin-8 by human vascular smooth muscle cells via arachidonic acid metabolites under conditions of oxidative stress.

OBJECTIVE: Preeclampsia is associated with oxidative stress, elevated plasma levels of linoleic acid (LA), and increased vascular smooth muscle expression of the inflammatory chemokine, interleukin-8 (IL-8). We hypothesized that increased levels of LA under conditions of oxidative stress would increased production of IL-8 by vascular smooth muscle cells because LA is the dietary precursor to arachidonic acid (AA) and its metabolites that mediate inflammation. We also hypothesized that oleic acid (OA), which is not metabolized to AA metabolites, would not increase IL-8 under conditions of oxidative stress. METHODS: To test this hypothesis, we cultured placental arterial smooth muscle (PASM) cells with an oxidizing solution enriched with LA (OxLA) or OA (OxOA). Media concentrations were analyzed for IL-8 and AA metabolites. Inhibitors were used to block the lipoxygenase and cyclooxygenase pathways. RESULTS: Exposure of cells to OxLA, but not to OxOA, significantly increased production of IL-8. OxLA also significantly increased production of AA metabolites. Nordihydroguaiaretic acid, an inhibitor of the lipoxygenase pathway, blocked IL-8 and leukotriene B4 (LTB4) production induced by OxLA, whereas indomethacin, an inhibitor of the cyclooxygenase pathway, blocked IL-8, prostaglandin E2 (PGE2), and thromboxane B2 (TXB2) production. Reverse transcriptase-polymerase chain reaction (RT-PCR) demonstrated gene expression in PASM cells for representative lipoxygenase (LTB4) and cyclooxygenase (thromboxane) metabolite receptors. CONCLUSION: PASM cells produced IL-8 in response to LA, but not OA, under conditions of oxidative stress. The IL-8 response was mediated by AA metabolites.

Arachidonic Acid↗

Fatty acid metabolism in Paramecium. Oleic acid metabolism and inhibition of polyunsaturated fatty acid synthesis by triparanol.

Paramecium requires oleic acid for growth and can grow in media containing no other fatty acids. In the present study, we have shown that this ciliate utilized oleate mainly as a carbon and energy source, even though this fatty acid was the only substrate available for synthesis of polyunsaturated fatty acids. Culture growth was inhibited by the addition of the drug triparanol. Triparanol decreased the formation of polyunsaturated fatty acids from oleate by preventing desaturation to form the dienoic acid, linoleate. Triparanol inhibition resulted in an altered phospholipid fatty acyl composition, an increased fragility and an altered behavioral response of the cells to a depolarizing stimulation solution. Therefore, although most of the dietary oleate was not used by the cells for polyunsaturated fatty acid synthesis, the desaturation of oleic acid was critical for normal culture growth, cell integrity and swimming behavior, all of which are expected to be dependent on normal membrane lipid composition.

Animals↗

Oleic acid uptake and binding by rat adipocytes define dual pathways for cellular fatty acid uptake.

Oleic acid (OA) uptake by rat adipocytes and the proportions of intracellular unesterified [3H]OA and its 3H-labeled esters were determined over 300 s. Uptake was linear for 20;-30 s, with rapid esterification indicating entry into normal metabolic pathways. Initial rates of OA uptake and its binding to plasma membranes were studied over a spectrum of oleic acid:bovine serum albumin (BSA) ratios, and expressed as functions of unbound OA concentrations calculated with both the 1971 OA:BSA association constants of Spector, Fletcher, and Ashbrook and more recent constants (e.g., the 1993 constants of Richieri, Anel, and Kleinfeld), which generate concentrations 10- to 100-fold lower. In either case, uptake was the sum of saturable and linear processes, with > or =90% occurring via the saturable pathway when the OA:BSA molar ratio was within the physiologic range (0.5;-3.0). Within this range, rate constants for saturable transmembrane influx (k(s)), calculated from both sets of constants, were similar (2.9 s(-1)) and were 10- to 30-fold faster than those for nonsaturable uptake (k(ns) = 0.26;-0.10 s(-1), t1/2 = 2.7;-6.6 s, based on the constants of Spector et al. and Richieri et al., respectively). The rate of oleic acid flip-flop into rat adipocytes (k(ff) = 0.16 +/- 0.02 s(-1), t1/2 = 4.3 +/- 0.5 s), computed from published data, was similar to k(ns). Thus, OA uptake occurs by both a saturable mechanism and passive flip-flop. This conclusion is independent of the OA:BSA association constants used to analyze the experimental measurements.

Adipocytes↗

Inhibitory effect of gymnemic acid on intestinal absorption of oleic acid in rats.

Gymnemic acid, a mixture of triterpene glycosides extracted from the leaves of Gymnema sylvestre, is known to inhibit the intestinal absorption of glucose in human and rats. This work examined the effect of gymnemic acid on oleic acid absorption by the method of intestinal perfusion in rats. The results showed the following. (i) Gymnemic acid potently inhibited the absorption of oleic acid in intestine. (ii) This inhibition was dose dependent and reversible. (iii) The extent of inhibition and the recovery progress were extremely similar to that of glucose absorption. (iv) Taurocholate did not affect the inhibitory effect of gymnemic acid on oleic acid absorption, but lowering its concentration facilitated the recovery from the inhibition. (v) The absorption of oleic acid was not affected by other glycosides such as phloridzin, stevioside, and glycyrrhizin. These new findings are important for understanding the roles of gymnemic acid in therapy of diabetes mellitus and obesity.

Animals↗

Fatty acid uptake and metabolism in CaCo-2 cells: eicosapentaenoic acid (20:5(n-3)) and oleic acid (18:1(n-9)) presented in association with micelles or albumin.

In vivo, long-chain fatty acids are incorporated into bile salt micelles, which solubilize the hydrophobic fatty acids before they are transported across the unstirred water layer to the intestinal brush border membrane. In the present study we have used CaCo-2 cells, cultured on filter membranes as a model of human enterocytes, and compared presentation of fatty acids bound to albumin with a micellar form. Absorption of eicosapentaenoic acid and oleic acid from micellar solutions was 4-times faster than from fatty acid-albumin complexes after 5 h incubation, and resulted in a corresponding increase in triacylglycerol synthesis and secretion. Mass determination of newly synthesized, cell-associated triacylglycerol after 5 h incubation, indicated a 5-fold increase in cells exposed to a micellar solution versus albumin-complexed fatty acids. A 2-fold larger fraction of the absorbed fatty acids was incorporated into triacylglycerol than into phospholipids when the fatty acids were presented as micelles. Analysis by resistive pulse technique showed that secreted lipoproteins of density less than 1.006 g/ml were in the same size-range as chylomicrons derived from human plasma. In spite of an increased amount of secreted triacylglycerol from cells supplemented with micellar fatty acids, there was no increase in the mean size of these particles. Synthesis and secretion of triacylglycerol in cells exposed to eicosapentaenoic acid and oleic acid were similar regardless of whether the fatty acids were presented to the cells associated with albumin or micelles, although the total amount of triacylglycerol synthesized and secreted was highest with micelles. When incubating CaCo-2 monolayers with eicosapentaenoic acid or oleic acid bound to albumin, a similar amount of radioactivity was released as CO2 and acid soluble products into the medium with less than 3% of the lipids being oxidized after 5 h of incubation. The oxidation rate of fatty acids in cells incubated with micelles was increased 40 to 100%. In conclusion, micellar fatty acids are absorbed, metabolized and influence secretion of lipoprotein particles to a higher extent than albumin-bound fatty acids in CaCo-2 cells, and there is no major difference between eicosapentaenoic acid and oleic acid.

Albumins↗

Phase transfer of oleic acid capped Ni(core)Ag(shell) nanoparticles assisted by the flexibility of oleic acid on the surface of silver.

The phase transfer protocols in vogue for the oleic acid capped silver nanoparticles, viz., salt-induced precipitation and redispersion or phosphoric acid-induced method, are examined and compared thoroughly. A comprehensive evaluation with respect to the mechanistic aspects involved is made and the merits and demerits of the different procedures are delineated. It is found that the salt-induced precipitation and redispersion is more versatile in that the precipitate can actually be redispersed in both aqueous and organic media. However, in terms of mechanism both the routes seem to be very similar wherein the orientational change of oleic acid on the silver surface in the two different environments-organic and aqueous-plays a crucial role in the adaptability of the system to the different environments. Subsequently, this change of orientation of oleic acid on silver surface in aqueous and organic media has been utilized to phase transfer Ni-based nanoparticulate systems. The nascent oleic acid-capped Ni nanoparticles, which were synthesized by a foam-based protocol, were dispersible in water but not in nonpolar organic media such as cyclohexane or toluene. Then, just by coating a thin shell of silver on them we could achieve complete phase transfer of the Ni(core)Ag(shell) from aqueous to organic media following similar procedures used for oleic acid-capped silver nanoparticles. Here, the phase transfer seems to be facilitated by the orientational flexibility of oleic acid on the silver surface as opposed to other metal surfaces as evidenced from the infrared and thermogravimetric analyses of oleic acid-capped Ni and Ni(core)Ag(shell) nanoparticles. This orientation-assisted phase transfer method could be generalized and can be adapted to other systems where, if the nascent nanoparticles cannot be phase transferred as is, they can be coated by a silver shell and oleic acid making them suitable for dispersion in both aqueous and organic media.

Journal Article↗

Effect of dietary fatty acids on jejunal and ileal oleic acid uptake by rat brush border membrane vesicles.

To test the effect of dietary fatty acids on fatty acid uptake, the influx kinetics of a representative long-chain fatty acid, 3H-oleic acid, in both the jejunum and ileum of rats has been studied using brush border membrane vesicles (BBMV). Animals were fed with semipurified diets containing 5 g fat/100 g diet, as corn oil (control group), safflower oil (unsaturated group) and coconut oil hydrogenated (saturated group). With increasing unbound oleate concentration in the medium, the three dietary groups showed saturable kinetics in both jejunal and ileal BBMV (controls: Vmax = 0.15 +/- 0.01 nmol x mg protein-1 x 5 min-1 and Km = 136 +/- 29.1 nmol for jejunum, and Vmax = 0.23 +/- 0.03 nmol x mg protein-1 x 5 min-1 and Km = 196 +/- 50.3 nmol for ileum; unsaturated: Vmax = 0.28 +/- 0.05 nmol x mg protein-1 x 5 min-1 and Km = 242.7 +/- 91.8 nmol for jejunum, and Vmax = 1.29 +/- 0.06 nmol x mg protein-1 x 5 min-1 and Km = 509.8 +/- 97.5 nmol for ileum; saturated: Vmax = 0.03 +/- 0.01 nmol x mg protein-1 x 5 min-1 and Km = 124.5 +/- 72.6 nmol for jejunum, and Vmax = 0.04 +/- 0.01 nmol x mg protein -1.5 min-1 and Km = 205.6 +/- 85.3 nmol for ileum). These results support the theory that feeding an isocaloric diet containing only unsaturated fatty acids enhanced oleic acid uptake, and feeding an isocaloric diet containing only saturated fatty acids decreased oleic acid uptake. The results obtained in the present work also show the adaptative ability of jejunum and ileum to the type of dietary fat.

Animals↗

Effects of dehydroepiandrosterone on oleic acid accumulation in rat liver.

The purpose of the present study was to determine whether dehydroepiandrosterone (DHEA) affects de novo fatty acid synthesis, oleic acid formation, fatty acid oxidation, and very low density lipoprotein (VLDL) secretion, in relation to the accumulation of lipid containing oleic acid, in rat liver. The rates of hepatic de novo synthesis of both fatty acid and monounsaturated fatty acid, determined by incorporation of 3H from 3H(2)O into fatty acid, were increased markedly when rats were fed a diet containing 0.5% (w/w) DHEA for 14 days. The treatment of rats with DHEA also enhanced the conversion of [14C]stearic acid into oleic acid in the liver in vivo. DHEA did not suppress fatty acid degradation in the liver. Namely, mitochondrial palmitic acid oxidation in liver homogenates and isolated hepatocytes was increased approximately 1.9- and 5-fold, respectively, in DHEA-treated rats. Peroxisomal palmitic acid oxidation in isolated hepatocytes from rats treated with DHEA, however, was not significantly different from that of the control, despite the fact that peroxisomal degradation of palmitic acid in the liver homogenates was increased markedly. The rate of hepatic VLDL secretion in DHEA-treated rats was decreased markedly. These results indicate that the elevation of the hepatic fatty acid content, especially oleic acid, by DHEA feeding is due to an increase in both de novo fatty acid synthesis and the formation of oleic acid and to a decrease in the rate of hepatic VLDL secretion. Mitochondrial and peroxisomal fatty acid degradation does not appear to play a significant role in the accumulation of hepatic lipids.

Animal Feed↗

The interaction of albumin and fatty-acid-binding protein with membranes: oleic acid dissociation.

Bovine serum albumin or fatty-acid-binding protein rapidly lose oleic acid when incubated in the presence of dimyristoyl lecithin liposomes. The phenomenon is dependent on vesicle concentration and no measurable quantities of protein are found associated with liposomes. Upon gel filtration on Sepharose CL-2B of incubated mixtures of microsomes containing [1-14C] oleic acid and albumin or fatty-acid-binding protein, association of fatty acid with the soluble proteins could be demonstrated. Both albumin and fatty-acid-binding protein stimulated the transfer of oleic acid from rat liver microsomes to egg lecithin liposomes. These results indicate that albumin is more effective in the binding of oleic acid than fatty-acid-binding protein, which allows a selective oleic acid dissociation during its interaction with membranes.

Animals↗

The production of 10-hydroxystearic and 10-ketostearic acids is an alternative route of oleic acid transformation by the ruminal microbiota in cattle.

The formation of hydroxystearic acid (HSA) and ketostearic acid (KSA) from oleic acid transformation has been documented in a variety of microbial species, including several isolated from the rumen of domesticated ruminant species. However, their ruminal production rates have not been established as influenced by fatty acid source. Dosing continuous cultures of mixed ruminal microorganisms with 1-(13C)-oleic acid increased the 13C enrichment of both HSA and KSA at 24 h postdosing, and showed that the majority (96 and 85%, respectively) of the HSA and KSA present in the 24-h samples originated from oleic acid. Several experiments using batch cultures of ruminal microorganisms showed that production of HSA and KSA was directly related to oleic acid input but was not affected by elaidic acid input, and that HSA was further metabolized to KSA but not to other fatty acids. When continuous cultures of ruminal microorganisms were supplemented with soybean oil or canola oil, production of 10-HSA + 10-KSA was related to oleic acid input but not to linoleic acid input. Daily production of 10-HSA + 10-KSA across treatments was 14.4 micromol/100 micromol oleic acid input into the cultures or 31.1 micromol/100 micromol oleic acid net loss. The results of this study quantify the formation of 10-HSA and 10-KSA from oleic acid transformation by ruminal microorganisms, and show that their accumulation in ruminal contents is directly related to the extent of oleic acid input and biotransformation by the rumen microbiota.

Animals↗

Mechanism of the apparent regulation of Escherichia coli unsaturated fatty acid synthesis by exogenous oleic acid.

Starvation of strains of Escherichia coli which are glycerol auxotrophs and are also defective in beta oxidation results in the accumulation of large amounts of free fatty acid (Cronan, J. E., Jr., Weisberg, L. W., and Allen, R. G. (1975) J. Biol. Chem. 250, 5835-5840). We now report that addition of exogenous oleic acid to these cultures results in no decrease in the synthesis of the unsaturated acids of the free fatty acid fraction although a 40 to 60% decrease of [14C]acetate incorporation into phospholipid unsaturated acyl moieties occurs under these conditions. This result indicates that the decreased synthesis of phospholipid unsaturated acyl moieties observed by others during oleic acid supplementation can be attributed to competition between exogenous and endogenously synthesized unsaturated fatty acids rather than a curtailment of unsaturated fatty acid synthesis per se.

Acetates↗

Pretreatment with oleic acid accelerates the entrance into the mitotic cycle of EGF-stimulated fibroblasts.

We have previously demonstrated that pretreatment of several cell lines with cis-unsaturated fatty acids, like oleic acid, blocks epidermal growth factor (EGF)-induced early ionic signals, and in particular the [Ca2+]i rise. In the present work we show that this blockade does not alter EGF-stimulated cellular proliferation evaluated by direct cell counting, but induces a powerful enhancement in the pulsed thymidine incorporation assay. The lack of effect of oleic acid on EGF-stimulated cellular proliferation was confirmed by repeated cell counts, cumulative thymidine incorporation, and protein synthesis, but a clear synergistic effect between oleic acid and EGF was again obtained by means of time course experiments with pulsed thymidine. Combined flow cytometry analysis and cell counts at earlier times in EGF-stimulated cells showed that oleic acids accelerates the entrance of cells into the replicative cycle leading to an earlier cell division. Afterward, these oleic acid-pretreated cells became delayed by an unknown compensatory mechanism in such a way that at 48 h post-EGF, the cell count in control and oleic acid-pretreated cells was equal. In conclusion (a) oleic acid accelerates or enhances the EGF mitogenic action and (b) in the long term cells compensate the initial perturbation with respect to untreated cells. As a side observation, the widely employed pulsed thymidine incorporation method as a measure of cell division could be extremely misleading unless experimental conditions are well controlled.

3T3 Cells↗

Effect of chronic incubation of CaCo-2 cells with eicosapentaenoic acid (20:5, n-3) and oleic acid (18:1, n-9) on triacylglycerol production.

CaCo-2 monolayers, cultured for 1 week after reaching confluence, were incubated with micellar solutions of fatty acids for up to 7 days. These conditioned cells were incubated acutely (5 h) with eicosapentaenoic acid and oleic acid, and the levels of cell-associated and secreted triacylglycerol were determined. With acute addition of oleic acid, both cell-associated and secreted triacylglycerol were decreased in cells chronically exposed to eicosapentaenoic acid. This effect was observed after as little as 2 days of chronic incubation with eicosapentaenoic acid. A further decrease was found when these cells were incubated acutely with eicosapentaenoic acid, regardless of which radioisotopes were used to label precursors in the incubation media. The secretion of both labelled and total triacylglycerol and apolipoprotein B was reduced approximately 50% in cells incubated chronically with eicosapentaenoic acid. The amounts of triacylglycerol and apolipoprotein B within the cells were not decreased by chronic exposure to eicosapentaenoic acid. Our data indicate that CaCo-2 cells chronically incubated with eicosapentaenoic acid secrete significantly less triacylglycerol than cells incubated chronically with oleic acid. When eicosapentaenoic acid was also included acutely, triacylglycerol secretion was reduced even more. We conclude that chronic exposure of eicosapentaenoic acid to this intestinal cell type reduces the rate of chylomicron secretion and may help explain the decreased postprandial lipaemia observed in humans taking fish oil supplements.

Adenocarcinoma↗

Bacterial DNA evokes epithelial IL-8 production by a MAPK-dependent, NF-kappaB-independent pathway.

Recognition of bacterial products by the innate immune system is dependent on pattern-recognition receptors: toll-like receptor 9 (TLR-9) in the case of bacterial DNA. We hypothesized that bacterial DNA can directly affect enteric epithelial cells. RT-PCR revealed constitutive TLR-9 mRNA expression in three human colonic epithelial cell lines (T84, HT-29, Caco-2) and THP-1 monocytes. Epithelial cells, in six-well culture plates or on filter supports, were exposed to E. coli DNA (1-50 microg/ml), synthetic CpG-rich oligonucleotides, or calf thymus DNA for 6-48 h. Exposure to E. coli DNA resulted in an increase in IL-8 mRNA, and a time- and dose-dependent increase in IL-8 secretion. Also, CpG oligonucleotides induced epithelial IL-8 production, whereas calf thymus DNA did not. Exposure to E. coli DNA resulted in phosphorylation of ERK 1/2 MAPK and inhibitors of ERK activity (PD98059, UO126) significantly reduced the evoked IL-8 production. In contrast, inhibitors of NFkappaB activity (PDTC, SN50) did not block E. coli DNA-induced IL-8 production. Electrophoretic mobility shift assays revealed that E. coli DNA stimulated epithelial AP-1 but not NFkappaB activation. The barrier (i.e., transepithelial resistance) and ion transport parameters of epithelial monolayers (assessed in Ussing chambers) were unaltered following E. coli DNA exposure. Thus model gut epithelia express TLR-9 mRNA and, while maintaining their barrier function, can respond to E. coli DNA by increased IL-8 production.

Caco-2 Cells↗

Displacement of sulphobromophthalein from albumin and fatty-acid-binding protein by oleic acid.

The absorption of sulphobromophthalein changes upon addition of bovine serum albumin or fatty-acid-binding protein at pH 8.4. The sulphobromophthalein spectrum is changed most drastically after the addition of albumin than in the presence of fatty-acid-binding protein isolated from rat liver, suggesting as a first approximation that binding capacity of albumin is much higher than that of fatty-acid-binding protein. When both soluble proteins are saturated with oleic acid it is observed a decrease in the binding of sulphobromophthalein which suggests that the presence of fatty acids in those soluble proteins may affect the binding of other ligands.

Animals↗

Effects of dihydroxy bile acids and hydroxy fatty acids on the absorption of oleic acid in the human jejunum.

Perfusion studies of the normal human jejunum were performed to test whether dihydroxy bile acids and hydroxy fatty acids inhibit the absorption of oleic acid, since previous reports documented their inhibitory effects on the absorption of several other organic solutes. 3 mM deoxycholate and 7 mM glycodeoxycholate inhibited the absorption of 3 mM oleic acid in isotonic micellar solutions while inducing net fluid secretion. Similarly, fractional absorption of oleic acid decreased in the presence of hydroxy fatty acids. However, only the changes induced by 2 mM ricinoleic acid could be distinguished from changes induced by an increase in total fatty acid concentration. Under all experimental conditions, close linear relationships existed between net water movement and fractional absorption of glucose, xylose, and fatty acids, as well as between the absorption rates of these solutes. In contrast, net fluid secretion induced by hypertonic D-mannitol (450 mosmol/liter) had no effect on solute absorption. Our data and observations in the literature do not allow formulation of a hypothesis which would adequately define all effects of dihydroxy bile acids and fatty acids on intestinal transport processes. The observations help explain the malabsorption of fat and other nutrients in patients with the blind loop syndrome.

Adult↗

Adrenoleukodystrophy: oleic acid lowers fibroblast saturated C22-26 fatty acids.

Monounsaturated fatty acids, especially oleic acid (C18:1), decreased the content of saturated very-long-chain fatty acids (VLFA) in cultured skin fibroblasts from patients with adrenoleukodystrophy (ALD) and controls. When confluent ALD fibroblasts were incubated with oleic acid for 5 days in lipid-free medium, which eliminates uptake of exogenous VLFA, the mean cell content of C26:0 was decreased by 33.7 +/- 10.1%. Oleic acid inhibited C26:0 synthesis in ALD fibroblasts by 58% and total fatty acid synthesis by 68 to 78%. Therefore, the elevated C26:0 levels in ALD cells may be lowered by inhibiting fatty acid biosynthesis, and inhibition of saturated VLFA synthesis by oleate may be useful in treating ALD.

Adrenoleukodystrophy↗