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PubMed1993

Inhibition of thyroxine transport into cultured rat hepatocytes by serum of nonuremic critically ill patients: effects of bilirubin and nonesterified fatty acids.

We investigated bilirubin and oleic acid as causes of low plasma T3 in nonuremic critically ill patients with gross changes in serum thyroid hormone levels (T4, < or = 60; T3, < or = 1.1; rT3, > or = 0.45 nmol/L) and elevated bilirubin concentrations (> or = 33 mumol/L). Iodide production from [125I]T4 was inhibited by 42% when rat hepatocytes in primary cultures were incubated with 10% serum from these patients. The mean serum concentration of albumin was reduced by 41%, while the concentrations of bilirubin and nonesterified fatty acids (NEFA) were increased by 2022% and 115%, respectively, in the patients. The molar ratios of bilirubin/albumin and NEFA/albumin in the patients were 0.42 and 3.18, respectively. Addition of oleic acid (50-400 mumol/L) and bilirubin (3-130 mumol/L) to 10% normal human serum (albumin, 70 mumol/L; NEFA, 54 mumol/L; bilirubin, 1.1 mumol/L) progressively inhibited the production of iodide by rat hepatocytes. The decreased iodide production was presumed to be caused by inhibition of T4 transport into hepatocytes. The deiodination of rT3 by rat liver microsomes was unaltered by free bilirubin and free oleic acid concentrations up to 0.1 mumol/L. These free concentrations are at least 1 order of magnitude higher than that attained in nonthyroidal illness. The inhibition of iodide production by the sera of critically ill patients (n = 12) was significantly correlated with the molar ratios of bilirubin/albumin (r = 0.72; P < 0.01) and NEFA/albumin (r = 0.58; P < 0.05). Extensive dialysis or treatment of the sera with charcoal did not completely remove the inhibitory activity on iodide production. Serum concentrations of indoxyl sulfate, 3-carboxy-4-methyl-5-propyl-2-furan propanoic acid, and hippuric acid in the critically ill patients (other known T4 transport inhibitors into hepatocytes) were similar to those in the normal subjects. This study together with the well known effects of carbohydrate on T3 neogenesis suggest that elevated bilirubin and NEFA and the low albumin level in non-uremic critical illness may be at least partly responsible for the T4 transport inhibition in T3-producing tissues (e.g. the liver) and, thus, the low plasma T3 levels in these critically ill patients. The question of whether inhibitors of T4 transport into the hepatocytes are also present in other patients with nonthyroidal illness who show only mild changes in thyroid hormone levels and have low concentrations of bilirubin and NEFA remains to be determined.

Adsorption↗
PubMed1993

Increased proliferative response of lymphocytes from intestinal lymph during long chain fatty acid absorption.

The effect of long chain and medium chain fatty acid absorption on transport and mitogen-induced blast transformation of lymphocytes in intestinal lymphatics was investigated. Intestinal lymph was collected from mesenteric lymph duct cannulated rats maintained in Bollman's cage. Following the intraduodenal administration of oleic acid (long chain fatty acid) or octanoic acid (medium chain fatty acid), only oleic acid produced a significant increase in lymphocyte flux and enhanced proliferative response of lymphocyte in intestinal lymph, without significant alteration of lymphocyte subsets. These changes appeared to be closely correlated with the appearance of radiolabelled oleic acid. Absorption of a medium chain fatty acid, octanoic acid, most of which appeared to be transported to portal blood, did not produce a significant elevation of lymphocyte flux or increased proliferative response of lymphocyte in intestinal lymph. Pluronic L-81, which is a potent inhibitor of the intracellular formation and secretion of chylomicron, significantly attenuated the increased lymphocyte flux and suppressed the enhancement of lymphocyte responsiveness to PHA in intestinal lymph after stimulation by oleic acid administration. There is a possibility that lymphocyte transport and proliferative response in intestinal lymph during oleic acid absorption are closely related to the process of chylomicron formation and secretion to lymphatics in the intestinal mucosa.

Animals↗
PubMed1981

Fat inhibition of gastric acid secretion in man and plasma concentrations of neurotensin-like immunoreactivity.

The effects of intraduodenal administration of oleic acid (5, 10, 20, and 40 ml) on gastric acid secretion stimulated by a submaximal intravenous pentagastrin infusion and on plasma concentrations on neurotensin-like plasma immunoreactivity (NTLI) were studied in 18 healthy subjects. Each volume of oleic acid or saline (controls) was tested in six subjects except the volume of 20 ml, which was given to ten subjects. Gastric acid secretion was studied for a 2-h period at 15-min intervals after intraduodenal infusion. Five milliliters oleic acid evoked a significant inhibition (29%) of gastric acid secretion. Maximal inhibition by oleic acid appeared after 20 ml (43%), which was significantly greater than after 10 ml. In seven duodenal ulcer (DU) patients 20 ml oleic acid evoked an inhibition of 20%, which was significantly lower than in the healthy subjects. Proximal gastric vagotomy (PGV) abolished the fat inhibition in DU patients. Basal and peak NTLI concentrations after 20 ml oleic acid were significantly lower in DU patients than in health subjects. In DU patients there was no significant difference in the integrated response of NTLI before and after PGV. The 2-h integrated NTLI response was dependent on the administered volume of oleic acid in healthy subjects. There was a correlation between acid inhibition and the integrated response ot NTLI in healthy subjects. This suggests that immunoreactive neurotensin may be involved in the oleic-acid-induced inhibition of gastric acid secretion. Neurotensin, or a neurotensin metabolite, apparently exerts its inhibitory effect at a synaptic level, which explains the finding that oleic acid did not inhibit gastric acid secretion after PGV. Neurotensin may have a physiological role as a hormone with enterogastrone functions.

Adult↗
PubMed1998

Effects of supplementation with unsaturated fatty acids on plasma and membrane lipid composition and platelet function in patients with cirrhosis and defective aggregation.

BACKGROUND/AIMS: Defective platelet aggregation and reduced platelet production of thromboxane A2, a metabolite of arachidonic acid, are common findings in patients with cirrhosis. We evaluated the effects of dietary supplementation with two combinations of unsaturated fatty acids on platelet function and plasma and membrane fatty acids in patients with liver cirrhosis. METHODS: In a double-blind study, 15 patients with cirrhosis and defective aggregation were randomized to receive a 6-week supplementation with gamma-linolenic and linoleic acid (1 g/day of each fatty acid) or with oleic acid and linoleic acid (groups GLA and OA, respectively). RESULTS: Under baseline conditions, patients showed elevated concentrations of monounsaturated fatty acids and a reduction in polyunsaturated fatty acids. The product/precursor ratios for delta6 and delta5 desaturases, two key enzymes in the pathway leading to arachidonic acid, were significantly reduced in the group of patients. In the GLA group, a significant increase in the levels of dihomo-gamma-linolenic acid (20:3omega6) was observed in plasma and membranes, together with a parallel decrease in the 20:4/20:3omega6 ratio after supplementation. No significant changes were observed in the OA group. The levels of arachidonic acid did not change significantly in either group of patients. Platelet aggregation to collagen was unchanged in the GLA group, but significantly improved in the OA group. CONCLUSIONS: These results show that supplementation with precursors of arachidonic acid is ineffective in elevating plasma or membrane arachidonate levels and does not improve platelet aggregation, suggesting that synthesis of arachidonic acid through the delta5 desaturase cannot be correspondingly activated or that incorporation/retention of the produced fatty acid into lipids is impaired. The increased platelet aggregation in the OA group is likely to be explained by the effect of oleic acid contained in the diet, the effects of which may have been counteracted by the elevation in 20:3omega6, a source of anti-aggregatory prostanoids, in the GLA group.

Aged↗
PubMed1999

Thioglycolate-elicited rat macrophages exhibit alterations in incorporation and oxidation of fatty acids.

Incorporation and oxidation of fatty acids (FA) were investigated in resident and thioglycolate-elicited (TG-elicited) rat macrophages (Mphi). Both cell types presented a time-dependent incorporation of [14C]-labeled palmitic acid (PA), oleic acid (OA), linoleic acid (LA), and arachidonic acid (AA) up to 6 h. The total amount of [14C]-FA incorporated by resident Mphi after 6 h was: AA > PA = LA > OA. TG-elicited cells presented a 50% reduction in the incorporation of LA, PA, and AA, whereas that of OA remained unchanged as compared to resident Mphi. The FA were oxidized by resident Mphi as follows: LA > OA > PA > AA. TG elicitation promoted a reduction of 42% in LA oxidation and a marked increase in AA oxidation (280%). The increased oxidation of AA in TG-elicited cells may account for the lower production of prostaglandins in Mphi under these conditions. The full significance of these findings for Mphi function, however, remains to be examined.

Animals↗
PubMed1996

Effect of insulin on triacylglycerol synthesis and secretion by chicken hepatocytes in primary culture.

A primary culture system of chicken hepatocytes was developed to study the effects of genetic, hormonal and nutritional factors on hepatic triglyceride (TG) secretion in the chicken, and the effect of insulin on TG synthesis and secretion examined. TG synthesis and secretion was measured using [3H]-glycerol incorporation into cellular and secreted TG. An additional step consisting of brief incubation of the monolayer with trypsin solution to improve harvesting the medium immediately adjacent to the cell monolayer, is also proposed. In our culture system, TG secretion occurred at least up to 75 hr of culture, showing a maximum between 40 and 60 hr of culture. No significant effect of insulin could be observed after 24 hr of culture. A clear stimulatory effect was observed with 10(-9) M insulin concentration after 48 hr. The mean ratio of the secretion rates in the presence or absence of insulin was 2.20 +/- 0.30 (SEM, n = 4). In contrast, the 10(-6) M concentration of insulin had no effect on TG secretion. The use of an additional trypsinization step enhanced the findings obtained by simple removal of the culture medium: a clear stimulatory effect of insulin on TG synthesis was observed after both 24 and 48 hr of culture. Analysis of TG fatty acid composition showed an imbalance of monoene versus saturated fatty acids between cellular and secreted TG, secreted TG being more monounsaturated than cellular TG. These results were obtained in the absence of exogenous fatty acid. An oleic acid supplement in the culture medium did not significantly influence TG secretion. In summary, a primary culture system for chicken hepatocyte was developed. A high level of TG secretion was seen in these cells with or without exogenous fatty acid and this secretion was stimulated by insulin. It was concluded that chicken hepatocytes in primary culture provide a useful model for studying regulation of TG secretion.

Animals↗
PubMed1977

Prevention of gallstone formation in rabbits by the oral administration of kanamycin.

Rabbits fed a diet containing 40 per cent casein, 15 per cent oleic acid and 45 per cent laboratory pellets developed glycoallodeoxycholic acid and glycodeoxycholic acid gallstones. The oral administration of kanamycin prevented allo bile acid stone formation in the oleic acid fed rabbit without leading to cholesterol gallstone formation. Kanamycin reduced the concentration of allodeoxycholic acid in the bile of oleic acid fed rabbits from 16.6+/-4.1 per cent of total bile acids to 1.1+/-1.1 per cent, with a reciprocal increase in deoxycholic acid concentration. The allodeoxycholate concentration was far below that found in control bile samples, 10.2+/-2.3 per cent. If the effect of kanamycin on the bile composition is by its antibiotic action, this eliminates the importance of a hepatic contribution to allodeoxycholate stone formation.

Administration, Oral↗
PubMed1990

Erucic acid metabolism in rat heart. A combined biochemical and radioautographical study.

Metabolism of Erucic Acid was studied in rat heart in comparison with that of oleic acid, particularly in relation with diet lipids. Rats were fed for 3 or 60 days a diet containing 30% of the calories of either Rapessed Oil, rich in erucic acid or sunflower seed oil rich in linoleic acid. They were I.V. injected with tritiated erucic or oleic acid. After 1 or 15 min the radioactivity recovered in heart lipids was very low whatever the diet (1 to 2%). One minute after injection of erucic acid the radioactivity was mainly recovered in the free fatty acid fraction and as untransformed erucic acid. After 15 min the major part of radioactivity was recovered in the triacylglycerol fraction which contained a high proportion of labelled oleic acid formed by shortening of erucic acid. When oleic was injected, the radioactivity was principally recovered in triacylglycerols as untransformed oleic acid whatever the experimental conditions. Electron microscopy showed that a much higher proportion of peroxisomes, was present in heart cells, following sunflower seed oil diet as compared to rapeseed oil diet. In all cases mitochondria supported the greater part of radioactivity, especially when erucic acid was injected in rats fed rapeseed oil. After sunflower seed oil, a noticeable radioactivity was observed in peroxisomes, most of them containing silver grains, especially when oleic acid was injected. According to the data reported, peroxisomes do not seem more implicated than mitochondria in the metabolism of erucic acid in myocardium.

Animals↗
PubMedDate not supplied

Fluoro-fatty acids and the impairment of cardiac function in the rat in vivo and in vitro.

Dichapetalum toxicarium seeds contain long chain fluoro-fatty acids, particularly fluoro-oleic acid, which in doses as low as 10 mg/kg can cause death. We have used the rat heart both in vivo and in vitro to assess the cardiovascular effects of various doses of the fluoro-oleic acid extract of the seeds of Dichapetalum toxicarium. Intraperitoneal administration of 0.25 ml of seed extract solution/kg body weight (estimated to be equivalent to 10 mg fluoro-oleic acid/kg body weight) or 0.5 ml/kg body weight (equivalent to 20 mg fluoro-oleic acid/kg body weight) resulted in death in all animals (n = 6 in each group). The mean time from administration to death was 36.4 +/- 4 h and 21.0 +/- 2 h, respectively. Death was attributable to severe bradycardia which developed progressively throughout the experiment. Thus, during the first 6 h, heart rate fell by 32.2% from 450 +/- 7 beats/min to 305 +/- 36 beats/min (p less than 0.01) in the 0.25 ml/kg group and by 66 +/- 10% to 150 +/- 20 beats/min (p less than 0.001) in the 0.5 ml/kg group. Administration of the extract solution alone or oleic acid alone (equivalent to 0.5 ml/kg seed extract) to control rats had no effect. Investigating the effects of the seed extract in vitro, hearts (n = 6 in each group) were perfused with buffer containing 0.5 ml/l seed extract (equivalent to 20 mg fluoro-oleic acid/l) or with buffer containing extract solution alone.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Total cellular fatty acid composition of cultured Pneumocystis carinii.

Oleic acid makes up > 50% of the total fatty acids of Pneumocystis carinii grown on WI-38 cells. Oleic acid levels increased in parallel with increasing trophozoites over 7 days in culture. The fatty acid composition of P. carinii resembles that of certain fungi but differs from those of lung surfactant lipid, host cells, and fetal bovine serum.

Animals↗
PubMed1987

Cyclooxygenase metabolites contribute to oleic acid-induced lung edema by a pressure effect.

We investigated the role that lung-derived arachidonic acid metabolites play in the acute changes in pulmonary hemodynamics, airway function, and lung fluid balance following oleic acid-induced injury in the isolated blood free perfused lung. A bolus injection of oleic acid (OA) emulsion (12 mg) into the pulmonary artery caused a rapid increase in pulmonary arterial pressure, inspiratory pressure, and weight gain. These pathophysiologic changes were not due to emboli per se, but were correlated with release of the vaso- and broncho-constrictive prostanoids, thromboxane A2 (measured as thromboxane B2) and prostaglandin F2 alpha. The leukotrienes (C4, D4, and E4) and prostacyclin (measured as 6 keto-prostaglandin F1 alpha) were not released by OA injury. Ibuprofen, a cyclooxygenase inhibitor, blocked the release of the vasoconstrictive prostanoids and also attenuated the rise in pressures and the development of edema indicating an important functional role for the prostanoids in the fluid imbalance. Ibuprofen also attenuated the increase in bronchoalveolar lavage protein but the protein leak was not completely prevented, suggesting that OA-induced increases in protein permeability occurred independently of prostanoid or leukotriene action. These data indicate that OA-induced edema formation was greatly amplified by arachidonic acid mediated pressure increases.

Animals↗
PubMed2005

Cloning and expression of a lipoxygenase from Pseudomonas aeruginosa 42A2.

In order to produce (S) 10-monohydroxy-8E-octadecenoic acid (MHOD) from oleic acid, a full-length probable lipoxygenase cDNA from Pseudomonas aeruginosa 42A2 was cloned and expressed in Escherichia coli BL21(DE3). The recombinant protein was purified by affinity chromatography to electrophoretic homogeneity and specifically stained. Its molecular mass was 70 kDa. The activity of the rec-LOX with oleic acid was about 30% of that of the preferred substrate, linoleic acid (100%). Bacterial LOX forms a new subfamily in the lipoxygenase phylogenetic tree.

Chromatography, Affinity↗
PubMed2005

Effects of unsaturated fatty acids on calcium-activated potassium current in gastric myocytes of guinea pigs.

AIM: To investigate the effects of exogenous unsaturated fatty acids on calcium-activated potassium current (I(K(Ca))) in gastric antral circular myocytes of guinea pigs. METHODS: Gastric myocytes were isolated by collagenase from the antral circular layer of guinea pig stomach. The whole-cell patch clamp technique was used to record I(K(Ca)) in the isolated single smooth muscle cells with or without different concentrations of arachidonic acid (AA), linoleic acid (LA), and oleic acid (OA). RESULTS: AA at concentrations of 2,5 and 10 micromol/L markedly increased I(K(ca)) in a dose-dependent manner. LA at concentrations of 5, 10 and 20 micromol/L also enhanced I(K(Ca)) in a dose-dependent manner. The increasing potency of AA, LA, and oleic acid (OA) on I(K(Ca)) at the same concentration (10 micromol/L) was in the order of AA>LA>OA. AA (10 micromol/L)-induced increase of I(K(ca)) was not blocked by H-7 (10 micromol/L), an inhibitor of protein kinase C (PKC), or indomethacin (10 micromol/L), an inhibitor of the cyclooxygenase pathway, and 17-octadecynoic acid (10 micromol/L), an inhibitor of the cytochrome P450 pathway, but weakened by nordihydroguaiaretic acid (10 micromol/L), an inhibitor of the lipoxygenase pathway. CONCLUSION: Unsaturated fatty acids markedly increase I(K(ca)), and the enhancing potencies are related to the number of double bonds in the fatty acid chain. The lipoxygenase pathway of unsaturated fatty acid metabolism is involved in the unsaturated fatty acid-induced increase of I(K(ca)) in gastric antral circular myocytes of guinea pigs.

Animals↗
PubMed1970

Pathways of fatty acid metabolism in human platelets.

The metabolic fate of (14)C-labeled fatty acids which have been incubated with human platelets, has been traced. The following has been shown. (a) Intact platelets have a considerable capacity to oxidize fatty acids. (b) When tracer amounts of four of the most common fatty acids in normal plasma were incubated with platelets, each showed a distinctive pattern of uptake among neutral lipids and phospholipids. With regard to the latter, it was shown that these distribution patterns were, in most cases, similar to those of the fatty acids found in natural platelet phospholipids. (c) By increasing the time of incubation or the amount of added oleic acid, the distribution of oleic acid uptake between lecithin and other phosphoglycerides was altered so that a larger share was incorporated into the latter. (d) The effects of added lysolecithin or lysoethanolamine phosphoglycerides on oleic acid incorporation into platelet phosphoglycerides are quite variable. At low concentrations, added lysolecithin functions chiefly as a reaction partner for oleic acid. Added adenosine triphosphate and CoASH augment the incorporation of oleic acid into lecithin over a wide range of added lysolecithin (12.5-500 mumoles/liter). At higher concentrations of added lysolecithin, in the absence of ATP and CoASH, oleic acid incorporation into lecithin is considerably reduced. Also, added lysolecithin and lysoethanolamine phosphoglycerides, in the absence of ATP and CoASH, are able, at certain concentrations, to stimulate oleic acid incorporation into all except the serine phosphoglycerides. (e) Platelets appear to have a de novo pathway for renewal of lecithin.

Adenosine Triphosphate↗
PubMed1997

Efficacy of inhaled nitric oxide in oleic acid-induced acute lung injury.

OBJECTIVE: To assess the efficacy of inhaled nitric oxide in improving pulmonary hypertension and gas exchange following oleic acid-induced acute lung injury. DESIGN: Prospective, pharmacologic study. SETTING: Surgical research laboratory at the University of Pittsburgh, Pittsburgh, PA. SUBJECTS: Instrumented, intubated pigs weighing 16 to 27 kg. INTERVENTIONS: Intravenous oleic acid and inhaled nitric oxide. MEASUREMENTS AND MAIN RESULTS: All pigs treated with intravenous oleic acid (0.11 mL/kg) developed a severe lung injury with pulmonary hypertension, accompanied by impaired oxygenation, intrapulmonary shunting, and increased extravascular lung water (p < .05 compared with baseline). Following nitric oxide inhalation, although pulmonary hypertension decreased in a dose-dependent fashion, no amelioration in pulmonary gas exchange was observed, as reflected by PaO2 and intrapulmonary shunt. Plasma nitrite and nitrate concentrations, the stable end products of nitric oxide metabolism, did not increase following nitric oxide exposure in this model of severe lung injury. CONCLUSIONS: The effect of inhaled nitric oxide, restricted to relieving pulmonary vasoconstriction in this model of lung injury, may have limited benefit in improving pulmonary gas exchange when diffusion is impaired by severe lung injury and inflammatory thickening of the alveolar-capillary barrier. Nitric oxide inhalation may have better results when used at an earlier, less severe stage of acute lung injury.

Administration, Inhalation↗
PubMed1994

[Protective effect of putrescine on oleic acid-induced respiratory distress syndrome (RDS)].

The effect of putrescine on oleic acid-induced RDS were studied in rat, it was found that preadministration of putrescine to rat with RDS significantly improved its hypoxemia, pulmonary edema and histologic injury; inhibited the leakage of protein from plasma; lowered increase of pulmonary lipid peroxidation products (malondialdehde, MDA). The result suggests that putrescine could have significant potential for clinical treatment of acute pulmonary injury.

Animals↗
PubMed1989

Intervesicular exchange of lipids with weak acid and weak base characteristics: influence of transmembrane pH gradients.

Transmembrane pH gradients have previously been shown to induce an asymmetric transmembrane distribution of simple lipids that exhibit weak acid or basic characteristics (Hope, M.J. and Cullis, P.R. (1987) J. Biol. Chem. 262, 4360-4366). In the present study we have examined the influence of proton gradients on the inter-vesicular exchange of stearylamine and oleic acid. We show that vesicles containing stearylamine immediately aggregate with vesicles containing phosphatidylserine and that disaggregation occurs subsequently as stearylamine equilibrates between the two vesicle populations. Despite visible flocculation during the aggregation phase, vesicle integrity is maintained. Stearylamine is the only lipid to exchange, fusion does not occur and vesicles are able to maintain a proton gradient. When stearylamine is sequestered to the inner monolayer in response to a transmembrane pH gradient (inside acidic) aggregation is not observed and diffusion of stearylamine to acceptor vesicles is greatly reduced. The ability of delta pH-dependent lipid asymmetry to modulate lipid exchange is also demonstrated for fatty acids. Oleic acid can be induced to transfer from one population of vesicles to another by maintaining a basic interior pH in the acceptor vesicles. Moreover, it is shown that the same acceptor vesicles are capable of depleting serum albumin of bound fatty acid. These results are discussed with respect to the mechanism and modulation of lipid flow between membranes both in vitro and in vivo.

Acids↗
PubMed1986

Alveolar epithelial damage. A critical difference between high pressure and oleic acid-induced low pressure pulmonary edema.

The present study was designed to compare high pressure pulmonary edema (HPPE) and oleic acid-induced low pressure pulmonary edema (OAPE) in dogs when similar amounts of extra vascular water were present in the lung. The high pressure edema was produced by intravenous fluid overload and by inflating an aortic balloon catheter (n = 6). The low pressure edema was produced by the injecting 0.08 mg/kg oleic acid suspended in 5 ml saline (n = 6). Comparison of the difference between initial control measurements and final measurements in the edematous states showed that the animals with OAPE had a greater fall in percent oxygen saturation and a greater increase in shunt fractions. The light microscopic studies showed that OAPE was associated with greater amounts of alveolar flooding than HPPE where the edema fluid was located to a greater extent in the peribronchial interstitial space. The electron microscopy studies showed that the alveolar flooding in OAPE was associated with epithelial disruption, and tracer studies carried out in rabbits showed that dextran (150,000 mol wt) could pass from blood to airspace and that dextran (40,000 mol wt) could pass from air-space to blood in OAPE. We conclude that epithelial disruption is responsible for the excessive alveolar flooding in OAPE and that this results in a greater impairment in gas exchange.

Animals↗