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PubMed1994

Plasma cholesteryl ester transfer protein activity is increased when trans-elaidic acid is substituted for cis-oleic acid in the diet.

The trans isomer of oleic acid (elaidic acid) increases low density lipoprotein (LDL) cholesterol and decreases high density lipoprotein (HDL) cholesterol in man. One possible mechanism for this effect is that trans fatty acids increase plasma cholesteryl ester transfer protein (CETP) activity. We examined the effect of dietary trans fatty acids on activity of this protein in plasma from 27 men in a double blind crossover comparison. The background diet, containing 15% energy as fat from dairy products, meat, bread and cereals, was supplemented with oleic or elaidic acid providing a further 20% energy. The elaidic supplement provided about 6% energy as trans fatty acid. Activity of CETP in plasma was significantly higher (P < 0.001) after the elaidic acid-rich diet (23.95 +/- 1.26%) compared with the diet enriched with oleic acid (19.61 +/- 0.89%). A significant correlation between the change in plasma trans 18:1 fatty acids and the change in plasma CETP activity (r = 0.58, P < 0.002) was independent of changes in LDL-cholesterol. The increase in CETP activity was in turn significantly correlated with a fall in HDL-cholesterol among subjects during the elaidic acid-rich period (r = -0.57, P < 0.01). We have shown that CETP demonstrates substrate specificity and that the increase in activity with dietary trans fatty acids may contribute to a more atherogenic lipoprotein profile.

Adult↗
PubMed2005

Mitochondrial transporters involved in oleic acid utilization and glutamate metabolism in yeast.

Utilization of fatty acids such as oleic acid as sole carbon source by the yeast Saccharomyces cerevisiae requires coordinated function of peroxisomes, where the fatty acids are degraded, and the mitochondria, where oxidation is completed. We identified two mitochondrial oxodicarboxylate transporters, Odc1p and Odc2p, as important in efficient utilization of oleic acid in yeast [Tibbetts et al., Arch. Biochem. Biophys. 406 (2002) 96-104]. Yet, the growth phenotype of odc1delta odc2delta strains indicated that additional transporter(s) were also involved. Here, we identify two putative transporter genes, YMC1 and YMC2, as able to suppress the odc1delta odc2delta growth phenotype. The mRNA levels for both are elevated in the presence of glycerol or oleic acid, as compared to glucose. Ymc1p and Ymc2p are localized to the mitochondria in oleic acid-grown cells. Deletion of all four transporters (quad mutant) prevents growth on oleic acid as sole carbon source, while growth on acetate is retained. It is known that the glutamate-sensitive retrograde signaling pathway is important for upregulation of peroxisomal function in response to oleic acid and the oxodicarboxylate alpha-ketoglutarate is transported out of the mitochondria for synthesis of glutamate. So, citric acid cycle function and glutamate synthesis were examined in transporter mutants. The quad mutant has significantly decreased citrate synthase activity and whole cell alpha-ketoglutarate levels, while isocitrate dehydrogenase activity is unaffected and glutamate dehydrogenase activity is increased 10-fold. Strains carrying only two or three transporter deletions exhibit intermediate affects. 13C NMR metabolic enrichment experiments confirm a defect in glutamate biosynthesis in the quad mutant and, in double and triple mutants, suggest increased cycling of the glutamate backbone in the mitochondria before export. Taken together these studies indicate that these four transporters have overlapping activity, and are important not only for utilization of oleic acid, but also for glutamate biosynthesis.

Acetates↗
PubMedDate not supplied

Docosahexaenoic, arachidonic, palmitic, and oleic acids are differentially esterified into phospholipids of frog retina.

Docosahexaenoic acid (22:6n-3) is highly enriched in the retina. To determine if retinal cells take up and metabolize fatty acids in a specific manner, retinas from Rana pipiens were incubated for 3 h with an equimolar mixture of tritiated 22:6n-3, arachidonic acid (20:4n-6), palmitic acid, and oleic acid. The radiolabeling of retinal lipids was determined and compared to the endogenous fatty acid content of the lipids. The results showed that in most, but not all, cases, the relative labeling with the four precursor fatty acids was similar to their relative abundance in each glycerolipid. Thus, during retinal glycerolipid synthesis, either through de novo or acyl exchange reactions, fatty acids are incorporated in proportions reflecting their steady-state mass levels. Since other studies with labeled glycerol have shown greater differences between early labeling patterns and molecular species mass, the final incorporation we report may be due primarily to acyl exchange reactions.

Animals↗
PubMed2006

Linoleic and oleic acids alter the licking responses to sweet, salt, sour, and bitter tastants in rats.

The free fatty acids (FFAs), linoleic and oleic acids, commonly found in dietary fats can be detected by rats on the basis of gustatory cues following conditioned taste aversion pairings. FFAs depolarize the membrane potential of isolated rat taste receptor cells by inhibiting delayed rectifying potassium channels. This study examined the licking response of rats to sweet, salt, sour, and bitter taste solutions when 88 muM linoleic acid, 88 muM oleic acid, or an 88 muM linoleic-oleic acid mixture was added to the solutions. The presence of linoleic, oleic, and the linoleic-oleic acid mixture in sweet solutions produced increases in the licking responses, whereas adding linoleic, oleic, and the linoleic-oleic acid mixture to salt, sour, or bitter taste solutions produced decreases in licking responses when compared with the licking responses to the solutions in the absence of the FFAs. We conclude that FFAs may act in the oral cavity to depolarize taste receptor cells and therefore to increase the perceived intensity of concomitant tastants, thus contributing to the enhanced palatability associated with foods containing high dietary fat.

Animals↗
PubMed2004

Solid-liquid phase behavior of binary fatty acid mixtures 3. Mixtures of oleic acid with capric acid (decanoic acid) and caprylic acid (octanoic acid).

Solid-liquid phase behavior of binary mixtures of oleic acid (OA)/capric acid (C10A) and OA/caprylic acid (C8A) were investigated by means of differential scanning calorimetry (DSC), Fourier transform infrared spectroscopy (FT-IR), and X-ray diffraction. The phase diagram of OA/C10A mixture constructed from the DSC results suggested that a molecular compound with the composition of OA:C10A = 3:2 is formed in a solid phase, and OA and the molecular compound are miscible, while C10A and the molecular compound are completely immiscible. The formation of the molecular compound was supported by the IR spectroscopic observation, and a possible model of the structure was proposed on the basis of X-ray diffraction spectrum in small angle region. This compound formation is characteristic of the OA/C10A mixture, and may be attributed to the similarity of the acyl chain length of C10A to the lengths of Delta- and omega-chains of OA (i.e., the chain segments divided by cis-double bond). The mixture of OA and C8A, whose chain length is close to but shorter than the two chain segments of OA, provided a eutectic-type phase diagram showing a partial mixing of the two components in OA-rich region. Thermodynamic analysis of the liquidus line in the phase diagram exhibits a systematic trend for the non-ideality parameter of mixing with the variation of the chain length difference between OA and saturated fatty acid species.

Calorimetry, Differential Scanning↗
PubMed1996

Formyl-methionyl-leucyl-phenylalanine and a calcium ionophore A23187 reverse the inhibition of phorbol myristate acetate-induced oxidative burst by linoleic and oleic acid anilides.

Linoleic and oleic acid anilides profoundly inhibited the production of reactive oxygen metabolites (ROM) in human polymorphonuclear leukocytes (PMNL) induced by a tumor promoter, phorbol myristate acetate (PMA). The addition of a Ca2+ ionophore, A23187, or a chemotactic peptide, formyl-methionyl-leucyl-phenylalanine (fMLP), readily reversed linoleic and oleic acid anilide-induced inhibiton of PMA-evoked respiratory burst in PMNL without affecting PMA-induced respiratory burst. fMLP or A23187 caused a marked increase in the production of ROM in PMNL that did not produce ROM after their co-exposure to PMA and cis-fatty acid anilides. This suggests a role for Ca2+ in this restoration of respiratory burst activity in PMNL. Oleic and linoleic acid anilides enhanced also respiratory burst in PMNL subsequent to their stimulation with fMLP. Interestingly, corresponding fatty acids, linoleic and oleic acid, also inhibited PMA-induced production of ROM in PMNL, but this inhibition was not reversed by A23187 or fMLP. These findings suggest that the aniline moiety of cis-fatty acids significantly modifies the effects of linoleic and oleic acids in the production of ROM in PMNL. Moreover, free intracellular Ca2+ may play a critical role in the activation of PMNL to produce ROM, and in the modulation of the effects of cis-fatty acid anilides.

Anilides↗
PubMed1994

Potentiation of canine pancreatic bicarbonate output by oleic acid is not neurally dependent.

To study neural involvement in potentiation of acid-induced pancreatic bicarbonate output, six dogs underwent extrapancreatic denervation and pancreatic fistula creation. Pancreatic responses to secretin (16 and 32 ng/kg/h) and cholecystokinin (50 ng/kg/h) were then assessed. The duodenum was then perfused with three sets of perfusates. The first set contained hydrochloric acid with either D- or L-phenylalanine. The second set contained bovine serum albumin and hydrochloric acid with or without oleic acid; the albumin and acid were varied so that each 50 ml contained 1, 2, or 4 meq titratable acid (pH 2.0-4.5). The third set was identical to the second except for initial pH of 3.5. Pancreatic responses predicted upon addition of cholecystokinin to secretin, L-phenylalanine to hydrochloric acid, or oleic acid to bovine serum albumin were compared with observed responses. At both doses, secretin-induced bicarbonate output was increased by cholecystokinin (16 ng/kg/h: 0.88 +/- 0.29 meq/15 min; 32 ng/kg/h: 1.01 +/- 0.23 meq/15 min). The latter significantly exceeded predicted output (16 ng/kg/h: 0.38 +/- 0.10 meq/15 min; 32 ng/kg/h: 0.58 +/- 0.15 meq/15 min), verifying potentiation. L-phenylalanine failed to potentiate bicarbonate output evoked by acidified D-phenylalanine. In contrast, addition of oleic acid to pH 2.0 or 3.5 bovine serum albumin potentiated bicarbonate output. These data suggest that enteropancreatic reflexes mediate potentiation of acid-induced pancreatic bicarbonate output by amino acids, but not by fatty acids.

Animals↗
PubMed1991

Interactions between oleic acid and drug competitors influence specific binding of thyroxine in serum.

Long chain nonesterified fatty acids and various drugs may share albumin-binding sites in common. We questioned whether serum binding of T4 could be indirectly influenced by displacement of drug competitors from these sites by nonesterified fatty acids. The influence of oleic acid on drug-induced inhibition of [125I]T4 binding was measured by equilibrium dialysis, using undiluted serum in order to avoid dilution-related artefacts. Oleic acid (1 mmol/L) alone did not inhibit serum protein binding of T4, but this concentration augmented the inhibitory effects on T4 binding of diflunisal, mefenamic acid, meclofenamic acid, and aspirin. This effect increased with increasing concentrations of mefenamic acid, meclofenamic acid, and furosemide. The T4-displacing effect of fenclofenac was not augmented by oleic acid. The mechanism of these interactions was studied by examining 1) oleic acid effects on drug binding, and 2) drug effects on oleic acid binding in undiluted serum. Increments in added oleic acid (0.5-2.0 mmol/L) progressively increased the mean unbound fractions of [14C]aspirin, [14C] diflunisal, and [14C]furosemide, but did not displace [14C]fenclofenac. At the relevant total and free drug concentrations, the inhibitory effect of oleic acid on drug binding and its influence on drug-induced displacement of T4 were concordant in the order: meclofenamic acid greater than aspirin greater than mefenamic acid greater than diflunisal greater than furosemide greater than fenclofenac. In contrast, drug-induced increases in the unbound fraction of [14C]oleic acid did not correlate with augmentation of T4 displacement. We conclude that synergistic effects of oleic acid and drugs on T4 binding result from drug displacement by oleic acid, rather than the reverse effect. Hence, substances that increase the unbound concentration of a competitor by displacing it from albumin can increase its T4-displacing potency. Interactions between various ligands may exert a greater hormone-displacing effect than the sum of each alone.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1994

Fatty acid composition of salmonid muscle changes in response to a high oleic acid diet.

Substitution of high oleic acid sunflower oil for herring oil in formulated salmonid diets affected the fatty acid composition of muscle, liver and visceral fat from coho salmon (Oncorhynchus kisutch) and rainbow trout (O. mykiss). Fish were fed diets containing either high oleic acid sunflower oil or herring oil as the supplemental lipid source (12.4 g/100 g diet) for 1-2 mo. Muscle from fish fed the sunflower oil diet had twice the concentration of oleic acid (approximately 25 g/100 g lipid) as muscle from fish fed the herring oil diet (approximately 12 g/100 g lipid). The maximum concentration of oleic acid in the muscle was obtained after only 2 wk of feeding the sunflower oil diet. Oleic acid concentrations in liver and visceral fat of fish fed the sunflower oil diet were significantly higher than in fish fed the herring oil diet. Rainbow trout fed the sunflower oil diet for 4 wk maintained the higher oleic acid concentrations in muscle and liver when deprived of feed for 2 wk compared with fish fed the herring oil diet. These data indicated that accumulation of oleic acid in coho salmon and rainbow trout muscle was fairly rapidly achieved when a high oleic acid diet was fed. The differences between the fish receiving the two dietary treatments in fatty acid composition and in concentrations of thiobarbituric acid-reactive substances in muscle stored at refrigerated temperatures were consistent with previously reported differences in aroma perceived by a sensory panel.

Adipose Tissue↗
PubMedDate not supplied

Astrocyte-synthesized oleic acid behaves as a neurotrophic factor for neurons.

Unlike in the adult brain, the newborn brain specifically takes up serum albumin during the postnatal period, coinciding with the stage of maximal brain development. Here we shall summarize our knowledge about the role played by albumin in brain development. The role of this protein in brain development is intimately related to its ability to carry fatty acids. Thus, albumin stimulates oleic acid synthesis by astrocytes from the main metabolic substrates available during brain development. Astrocytes internalize albumin in vesicle-like structures by receptor-mediated endocytosis, which is followed by transcytosis, including passage through the endoplasmic reticulum (ER). The presence of albumin in the ER activates the sterol regulatory element-binding protein-1 (SREBP-1) and increases stearoyl-CoA 9-desaturase (SCD) mRNA, the key enzyme in oleic acid synthesis. Oleic acid released by astrocytes is used by neurons for the synthesis of phospholipids and is specifically incorporated into growth cones. In addition, oleic acid promotes axonal growth, neuronal clustering, and the expression of the axonal growth associated protein, GAP-43. All of these observations indicate neuronal differentiation. The effect of oleic acid on GAP-43 synthesis is brought about by the activation of protein kinase C. The expression of GAP-43 is significantly increased by the presence of albumin in neurons co-cultured with astrocytes, indicating that neuronal differentiation takes place by the presence of oleic acid synthesized and released by astrocytes in situ. In conclusion, during brain development the presence of albumin could play an important role by triggering the synthesis and release of oleic acid by astrocytes, thereby inducing neuronal differentiation.

Animals↗
PubMed1993

Oleic acid blocks epidermal growth factor-activated early intracellular signals without altering the ensuing mitogenic response.

In EGFR-T17 cells, which express high levels of the epidermal growth factor (EGF) receptor, addition of a saturating dose of EGF (10 nM) leads to an increase in Ins(1,4,5)P3/diacylglycerol and also to cytosolic calcium [Ca2+]i due to both intracellular redistribution and influx from extracellular medium. Pretreatment of cells with cis-unsaturated nonesterified fatty acids such as oleic acid (1 to 100 microM) inhibited EGF-stimulated Ins(1,4,5)P3 generation and Ca2+ release from intracellular stores. Furthermore, such a treatment completely suppress Ca2+ influx in a dose-dependent manner. At doses capable of suppressing such early signals, oleic acid did not alter the process of EGF-mediated internalization of the EGF/EGF-receptor complex, suggesting that [Ca2+]i rise did not mediate receptor internalization. EGF-induced cell proliferation assessed by either thymidine incorporation into DNA, direct cell counting, and microscopic observation was not altered by oleic acid, at doses able to block EGF-mediated early signals. In conclusion, suppression of Ins(1,4,5)P3 generation and [Ca2+]i rises by oleic acid did not alter EGF-receptor internalization nor EGF-induced cell mitosis. Such results suggest that [Ca2+]i rise is not instrumental for EGF-stimulated cell proliferation.

Animals↗
PubMed1993

ATP leakage from ELD cells after exposure to stearic, monochlorostearic, dichlorostearic, and oleic acids.

The capacity of stearic, monochlorostearic, dichlorostearic and oleic acids to cause membrane damage was measured as their ability to induce leakage of adenosine triphosphate (ATP) from mammalian tumour cells in vitro. Chlorinated stearic acids, and oleic acid, caused ATP leakage at lower concentrations than normal stearic acid. The membrane disturbing properties are suggested to be a result of the different molecular geometries of the chlorinated stearic acids, and oleic acid, compared to non-chlorinated stearic acid.

Adenosine Triphosphate↗
PubMed2001

Fat-specific satiety in humans for fat high in linoleic acid vs fat high in oleic acid.

OBJECTIVE: To investigate the effect of 2 week use of oils high in linoleic (LA), gamma-linolenic (GLA) and oleic acid (OA) on energy intake (EI), macronutrient composition, parameters of appetite and taste perception. DESIGN: A randomized placebo-controlled 2-week treatment, followed by a test day. SETTING: Two-week treatments, daily life; test day, laboratory restaurant. SUBJECTS: Eight overweight men and eight overweight women (body mass index 27.4+/-1.5 kg/m(2)). INTERVENTIONS: Three 2 week treatments, in which subjects replaced their habitual fat products by three different oils (relatively) high in LA (66.8%), GLA (20.2%) or OA (79.6%, placebo). The wash-out periods were 2 weeks. Before each intervention period, taste perception and sensory specific satiety was tested. RESULTS: Even though energy intake was higher during dinner, subjects ate relatively less fat with LA (45.0+/-9.4 E%, P<0.05) than with OA (48.3+/-8.3 E%). Subjects did not distinguish the oils with the different fatty acids from each other. There was no relation between satiety or fat-specific satiety and taste characterization without as well as with sucrose. Although no differences were seen for the AUC of the appetite profile, aet 15:00 h subjects were less satiated with LA (46.1+/-6.2 mm, P<0.05) or GLA (45.1+/-5.8 mm, P<0.01) than after treatment OA (62.5+/-4.8 mm). 24 h EI on the test day was 7.6--8.0 MJ and did not differ between treatments. CONCLUSIONS: Fat-specific satiety during dinner with LA vs OA was shown after a 2-week treatment of each oil, but no change in general satiety. Fat specific satiety was not related to taste perception or characterization of the oils.

Adult↗
PubMed2000

Possible relevance of abnormal fatty acid metabolism in undernutrition: the relationship between oleic acid and growth.

Energy, protein, essential fatty acids, vitamins and minerals are all necessary for normal growth and development of children. In undernutrition, there is evidence for abnormal fatty acid metabolism. High levels of oleic acid and low levels of docosahexaenoic acid in plasma phosphatidylcholine have been associated with weight-for-age Z-score shifts to the left (increased prevalence of underweight) and vice versa (reduced prevalence of underweight). An alternative hypothesis is proposed, which describes a possible physiological mechanism whereby omega3 fatty acids contribute to growth. High blood oleic acid levels under conditions of undernutrition are proposed to be an adaptation to conserve glucose in the form of glycogen. Replacement with docosahexaenoic acid under conditions of adequate nutrition enhances membrane functioning so that glucose and energy become available for muscle formation.

Child↗
PubMed2006

Effects of salvianolic acids on erythrocyte deformability in oleic acid induced acute lung injury in rabbits.

The present study was to investigate the protective effects of salvianolic acids (SA) on deformability of red blood cells (RBCs) and its mechanism during the development of acute lung injury (ALI) induced by oleic acid (OA) in rabbits. 32 rabbits were randomized into four groups, normal control group, OA-treated group (0.15 ml/kg), SA-treated group and OA+SA treated group. The blood samples were collected at 0, 10, 30, 60, 90, 120 and 180 min after OA injection. The RBC deformation index, Orientation index and small deformation index were measured by ektacytometry. The concentration of malondialdehyde (MDA) in RBCs was detected by the assay kit. Meanwhile, the pulmonary pathological examination and the blood gas analysis were also performed. The results showed that the deformation index, orientation index and small deformation index decreased during the early phase of ALI, while the concentration of MDA in RBCs increased during the course. Pre-treatment with SA increased the deformability and orientability of RBC significantly and decreased the concentration of MDA in RBCs compared with OA group. Meanwhile, the hypoxia and pulmonary pathological damage were much improved. These results suggest that there were erythrocyte deformability changes in the early phase of ALI. SA has the protective effects on erythrocyte deformability during the development of ALI induced by OA, which might be due to its antioxidant effect. These results are valid in rabbits and in a model of ARDS, it would be interesting to see the effects of SA in patients.

Acute Disease↗
PubMed2006

Oleic acid inhibits amyloid formation of the intermediate of alpha-lactalbumin at moderately acidic pH.

The effects of oleic acid on amyloid formation of Ca2+-depleted bovine alpha-lactalbumin (apo-BLA) at low pH and the biological impact of the effects were investigated by using thioflavin T, Congo red, far-UV circular dichroism, atomic force microscopy, transmission electron microscopy, and other biophysical methods. The results from the phase diagram method of fluorescence show that two intermediates exist in the conformational transition of apo-BLA induced by low pH. One intermediate populated at pH 3.0 is characterized as a molten globule state and the other accumulates with stable secondary structure and exposed hydrophobic surface at pH 4.0-4.5. Amyloid formation of apo-BLA takes place upon decreasing the pH to 4.5 and is accelerated remarkably as the pH is decreased further. However, amyloid fibrils of apo-BLA are not observed in the pH range of 5.0-7.0 on a time-scale of 30 days. The lag time of fibrillation at pH 4.0 is greatly elongated by the presence of oleic acid, accompanied by a remarkable decline of the maximum thioflavin T intensity. Furthermore, amyloid formation of apo-BLA at pH 4.5 is inhibited completely by oleic acid, and insoluble aggregates are observed. In contrast, the effects of oleic acid on amyloid formation are not remarkable at pH 3.0 or at pH 2.0. Our data demonstrate that oleic acid specifically induces the intermediate of apo-BLA at pH 4.0-4.5 to form insoluble amorphous aggregates, which is responsible for the inhibition of amyloid formation of the protein by oleic acid in this range of pH values.

Amyloid↗