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PubMed1997

Endogenous synthesis cannot compensate for absence of dietary oleic acid in rats.

It is important to know whether an organism is able to synthesize all the oleic acid it needs. To determine this, it is sufficient to feed animals a diet containing essential fatty acids but totally lacking oleic acid, and then determine whether tissue concentrations of fatty acids of the (n-9) series are altered due to insufficient endogenous synthesis of oleic acid from stearic acid. In fact, the effects of a total oleic acid deficiency have not previously been studied because all the vegetable oils used in human and animal nutrition contain this fatty acid in variable amounts. Thus, we fed rats semipurified diets whose lipids (triglycerides) were synthesized chemically. Female rats were fed the diets for 3 wk before mating, and their pups (fed the same diets) were killed when 21 and 60 d old. Generally speaking, oleic acid deficiency resulted in a lower level of this acid in the various organs examined (liver, kidney, testes, heart, muscle and sciatic nerve in 21-d-old rats and liver, kidney, heart, muscle and sciatic nerve in 60-d-old rats). Brain, myelin and nerve endings were not affected at either age. This lower level was accompanied by a higher level of 16:1(n-7) and, to a lesser extent, 18:1(n-7). Dietary supplementation with oleic acid (1666 mg/100 g diet) for up to 21 d resulted in normal levels of this fatty acid in some organs (liver, heart, sciatic nerve) but not in others (kidney, muscle, testes) and a decrease in 16:1(n-7), which returned to about the same levels as in the control group in all organs except liver. Adding small or large amounts of stearic acid to the oleic acid-deficient diet had little or no effect on oleic acid levels in the tissues. We conclude that rats (particularly in liver) do not have sufficient synthesizing potential to guarantee the normal fatty acid composition of certain organs if oleic acid is totally absent in the diet.

Animals↗
PubMed2001

Transcytosis of albumin in astrocytes activates the sterol regulatory element-binding protein-1, which promotes the synthesis of the neurotrophic factor oleic acid.

We have recently reported that albumin, a serum protein present in the developing brain, stimulates the synthesis of oleic acid by astrocytes, which promotes neuronal differentiation. In this work, we gain insight into the mechanism by which albumin induces the synthesis of this neurotrophic factor. Our results show that astrocytes internalize albumin in vesicle-like structures by receptor-mediated endocytosis. Albumin uptake was followed by transcytosis, including passage through the endoplasmic reticulum, which was required to induce the synthesis of oleic acid. Oleic acid synthesis is feedback-regulated by the sterol regulatory element-binding protein-1, which induces the transcription of stearoyl-CoA 9-desaturase, the key rate-limiting enzyme for oleic acid synthesis. In our research, the presence of albumin activated the sterol regulatory element-binding protein-1 and increased stearoyl-CoA 9-desaturase mRNA. Moreover, when the activity of sterol regulatory element-binding protein-1 was inhibited by overexpression of a truncated form of this protein, albumin did not affect stearoyl-CoA 9-desaturase mRNA, indicating that the effect of albumin is mediated by this transcription factor. The effect of albumin was abolished when traffic to the endoplasmic reticulum was prevented or when albumin was accompanied with oleic acid. In conclusion, our results suggest that the transcytosis of albumin includes passage through the endoplasmic reticulum, where oleic acid is sequestrated, initiating the signal cascade leading to an increase in its own synthesis.

Animals↗
PubMed1995

Oleic acid uptake into rat and rabbit jejunal brush border membrane.

Oleic acid uptake was studied using adult rabbit and rat jejunal brush border membrane vesicles. There was a reduction of oleic acid uptake following trypsin-treatment. Opposing Na+/H+ gradients (inward Na+ and outward H+ gradients) increased oleic acid uptake by about 40%, as compared with only an inward Na+ gradient, only an outward H+ gradient, or the absence of either Na+ or H+ gradients. The addition of mucin further increased the enhanced uptake of oleic acid observed in the presence of opposing Na+/H+ gradients. Amiloride, an inhibitor of the Na+/H+ exchanger, reduced by about 40% the uptake of oleic acid into sheets of rat jejunum, and this inhibitory effect was observed over a range of rates of stirring of the bulk phase. In rabbit jejunal brush border membrane vesicles, amiloride reduced oleic acid uptake in the presence but not in the absence of opposing Na+/H+ gradients, with a Ki of approx. 36 microM. Thus, oleic acid uptake occurs largely by partitioning of the lipid into the brush border membrane, influenced by a process which involves the activation of the brush border membrane Na+/H+ exchanger.

Amiloride↗
PubMed1983

Interactions of the carboxyl group of oleic acid with bovine serum albumin: a 13C NMR study.

The interactions of the carboxyl group of oleic acid with bovine serum albumin (BSA) were studied by 13C NMR spectroscopy at 50.3 MHz using 90% isotopically substituted [1-13C]oleic acid. 13C NMR spectra were obtained as a function of the mole ratio of oleic acid to BSA (from 0.5-10.0) and, for selected mole ratios, as a function of pH (between pH 3.0 and 10.6) and temperature (between 15 and 55 degrees C and thermally denatured at 95 degrees C). Except for spectra of highly acidic (pH less than or equal to 3.9) and denatured samples, spectra of oleic acid/BSA complexes showed multiple narrow resonances from the oleic acid carboxyl carbon in a region (179-184 ppm) downfield from protein carbonyl and carboxyl carbon resonances. At low oleic acid/BSA ratios (0.5 and 1.0), at least two oleic acid carboxyl carbon peaks were observed; at high ratios (greater than or equal to 3.0), at least four peaks were present. The intensities of individual peaks, but not their chemical shifts, varied with the oleic acid/BSA ratio. The chemical shift of individual oleic acid peaks was invariant between pH 6.0 and 10.6; below pH 6.0, one of the oleic acid resonances exhibited an NMR titration curve with an apparent pKa of approximately 4. Thus, BSA binding sites for oleic acid are heterogeneous as monitored by the magnetic microenvironment of the oleic acid carboxyl carbon. The number of different oleic acid environments and the relative population of oleic acid molecules in these environments is dependent on the mole ratio of oleic acid/BSA. Our results suggested that the anionic form of oleic acid is bound to BSA at physiological pH and that the multiplicity of NMR peaks for [1-13C]oleic acid resulted from, at least in part, different electrostatic and hydrogen bonding interactions between the oleic acid carboxyl group and specific amino acid residues of BSA.

Fourier Analysis↗
PubMed1991

Evidence that oleic acid exists in a separate phase within stratum corneum lipids.

Oleic acid is known to be a penetration enhancer for polar to moderately polar molecules. A mechanism related to lipid phase separation has been previously proposed by this laboratory to explain the increases in skin transport. In the studies presented here, Fourier transform infrared spectroscopy (FT-IR) was utilized to investigate whether or not oleic acid exists in a separate phase within stratum corneum (SC) lipids. Per-deuterated oleic acid was employed allowing the conformational phase behavior of the exogenously added fatty acid and the endogenous SC lipids to be monitored independently of each other. The results indicated that oleic acid exerts a significant effect on the SC lipids, lowering the lipid transition temperature (Tm) in addition to increasing the conformational freedom or flexibility of the endogenous lipid alkyl chains above their Tm. At temperatures lower than Tm, however, oleic acid did not significantly change the chain disorder of the SC lipids. Similar results were obtained with lipids isolated from the SC by chloroform:methanol extraction. Oleic acid, itself, was almost fully disordered at temperatures both above and below the endogenous lipid Tm in the intact SC and extracted lipid samples. This finding suggested that oleic acid does exist as a liquid within the SC lipids. The coexistence of fluid oleic acid and ordered SC lipids, at physiological temperatures, is consistent with the previously proposed phase-separation transport mechanism for enhanced diffusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Nature of pulmonary hypertension in canine oleic acid pulmonary edema.

It has recently been suggested that pulmonary hypertension secondary to oleic acid lung injury mainly results from an increase in the critical closing pressure of the pulmonary vessels [Boiteau et al., Am. J. Physiol. 251 (Heart Circ. Physiol. 20): H1163-H1170, 1986]. To further test this hypothesis, we studied 1) the pulmonary arterial pressure- (Ppa) flow (Q) relationship with left atrial pressure (Pla) kept constant (n = 7) and 2) the Ppa-Pla relationship with Q kept constant (n = 9) in intact anesthetized and ventilated dogs before and after lung injury induced by oleic acid (0.09 ml/kg iv). Q was manipulated by use of a femoral arteriovenous bypass and a balloon catheter inserted in the inferior vena cava. Pla was manipulated with a balloon catheter placed by thoracotomy in the left atrium. Ppa-Q plots were rectilinear before as well as after oleic acid. Before oleic acid, the extrapolated pressure intercept of the Ppa-Q plots approximated Pla. Oleic acid administration resulted in a parallel shift of the Ppa-Q plots to higher pressure; i.e., the pressure intercept increased, whereas the slope was not modified. Increasing Pla at constant Q before oleic acid led to a proportional augmentation of Ppa. After oleic acid, however, changes in Pla over the same range affected Ppa only at the highest levels of Pla. These results suggest that oleic acid lung injury increases the critical closing pressure that exceeds Pla, becomes the effective outflow pressure of the pulmonary circulation, and is responsible for the pulmonary hypertension.

Animals↗
PubMed1981

Saturated fatty acid-starved cells of Saccharomyces cerevisiae grown in the presence of cerulenin and oleic acid.

Cell growth of Saccharomyces cerevisiae ATCC 12341 inhibited by the antibiotic cerulenin, a specific inhibitor of fatty acid synthesis, was restored by oleic acid (18 : 1) to give saturated fatty acid-starved cells, which could not grow when again transferred into a fresh synthetic medium containing the antibiotic and oleic acid. The growth of the saturated fatty acid-starved cells was restored when they were transferred into a medium supplemented with myristic acid (14 : 0), pentadecanoic acid (15 : 0), and palmitic acid (16 : 0) in the presence of cerulenin and oleic acid. Cellular saturated fatty acid content in the growth-restored cells was also restored to about two-thirds of that of the normal yeast cells. The DNA, RNA, and cell wall synthetic capabilities of the saturated fatty acid-starved cells were almost normal, but the L-leucine uptake and cytochrome pattern were severely impaired. These impairments were reversed on supplying palmitic acid. The decrease of L-leucine uptake of the yeasts was also caused by the addition of cerulenin alone. However, since the decrease occurred later than the inhibition of fatty acid synthesis, it was considered to be a secondary effect. These results, obtained by using the saturated fatty acid-starved cells, indicate that the membranes of S. cerevisiae require certain amounts of saturated fatty acid and that the membrane functions (energy metabolism, transport, and so on) are impaired by starvation of saturated fatty acids.

Antifungal Agents↗
PubMed1977

Effects of arachidonic, linoleic, linolenic and oleic acid on experimental arrhythmias in cats, rabbits and guinea-pigs.

Antiarrhythmic effects of the Prostaglandin (PG) precursors arachidonic and Linoleic acid were demonstrated on three models of experimental arrhythmias, whereas the fatty acids linolenic and oleic acid proved to be ineffective in these models. In ouabain-induced arrhythmias infusions of arachidonic acid (1, 0 mg/kg/min) caused a strong antiarrhythmic effect in 80 percent of the animals. On the same model linoleic acid showed a maximum effct in 40 percent of the animals. BaCl2-induced arrhythmias were abolished by arachidonic and linoleic acid in 60 percent and 66 percent of the rabbits, respectively. Pretreatment by indomethacin reduced the antiarrhythmic effects of linoleic acid from 40 percent to 9 percent on ouabain-induced arrhythmias in cats. The results suggest a participation of PG synthesis in the antiarrhythmic effect of PG precursors.

Animals↗
PubMed1986

Mechanisms involved in acute lung edema induced in dogs by oleic acid.

We investigated mechanisms related to the development of acute lung edema, as induced by oleic acid in adult mongrel dogs. The intravenous injection of oleic acid (0.04 ml/kg) was considered to induce a permeability edema, as an enhancement of transvascular protein clearance was observed after the injection. The effects of oleic acid injection on systemic blood pressure (SBP), pulmonary arterial pressure (PAP), pulmonary arterial wedge pressure (PAWP), cardiac output (CO) and airway pressure (AWP) were measured. A significant decrease in CO and increase in AWP were evident after the injection, but there were no changes in SBP, PAP and PAWP. Treatment of the animals with prostaglandin I2 (PGI2) did not alter the induction of edema by oleic acid. However, the decrease in CO and increase in AWP were normalized by treatment with PGI2. Blood platelet count was not affected by oleic acid given in a dose of 0.04 ml/kg. To determine the direct effect of oleic acid on the vascular endothelium, the agent was injected through a catheter placed in the pulmonary artery. Electron microscopic examination revealed severe vacuolation on the endothelium of the pulmonary artery after only 1 min of exposure to oleic acid. Increased permeation of Evans blue into the subendothelial tissue was also observed with oleic acid treatment, compared with findings in the controls. These results indicate that the lung edema induced by oleic acid is due to an increased protein clearance, probably through a direct toxic effect on the vascular endothelium rather than an indirect toxic effect of chemical mediators released from the aggregated platelets.

Airway Resistance↗
PubMed2005

Interactions of oleic acid and model stratum corneum membranes as seen by 2H NMR.

We have investigated the mechanism through which the penetration enhancer oleic acid acts on stratum corneum (SC) model membranes (bovine brain ceramide:cholesterol:palmitic acid, 1:1:1 molar ratio). We used solid state deuterium nuclear magnetic resonance to monitor such multilamellar SC dispersions containing either cholesterol-d(6), palmitic acid-d(31), or oleic acid-d(2) as a function of both fatty acid concentration (2:2:1:1 and 1:1:1:1 bovine brain ceramide:cholesterol:palmitic acid:oleic acid) and temperature (18-75 degrees C). Our results show that below 40 degrees C, oleic acid (OA) is in an 'isotropic' phase, indicating that it has not incorporated into the lamellar membrane phase. At and above the SC model membrane's crystalline to liquid crystalline melting temperature, T(m)=40-42 degrees C, OA interacts with lamellar SC membranes with a slight dependence on OA concentration. T(m) does not change upon the exposure of the SC model membrane to OA, nor do we see any significant change in membrane chain disorder as monitored by the labelled PA. However, the spectra of both the palmitic acid (PA) and cholesterol SC model membrane components contain an isotropic peak that grows with increasing temperature. Our results thus indicate that oleic acid extracts a fraction of the endogenous SC membrane components, promoting phase separation in the SC membrane system. Reducing the proportion of crystalline lipids and creating more permeable OA-rich domains is a plausible mechanism that explains how OA enhances transdermal penetration.

Animals↗
PubMed1983

Intestinal exsorption of oleic acid: influence of aging, bile, pH and ethanol.

The transfer of oleic acid from the circulation into the intestinal lumen perfusate (exsorption) was investigated in vivo in male Sprague-Dawley rats. Following intravenous infusion of oleic acid, its appearance in the intestinal perfusate was assessed over a 3-hour period. The relationship between exsorption rate and the amount of infused oleic acid delineated a linear plot. Oleic acid exsorption rate increased as the taurocholate concentration was raised to 10 mM in the intestinal perfusate. In contrast, oleic acid exsorption rate decreased following decrease in the intestinal perfusate pH, or increase in the intestinal perfusate's concentrations of oleic, butyric and octanoic acids or following the additions of increasing concentrations of ethanol to the intestinal perfusate. Increase in the age of the animals from 3 to 21 months resulted in a decrease of oleic acid exsorption. These data indicate that exsorption of oleic acid into the intestinal perfusate is not simply a process of "leakiness" of the intestinal epithelium. Rather, exsorption of this fatty acid is modified by factors that change the characteristics of the perfusate or modify the characteristics of the intestinal epithelium or the unstirred water layer at the luminal surface of the small intestine.

Aging↗
PubMed1991

Oleic acid as an inhibitor of gastric H+, K(+)-ATPase.

A study was made of the effects of oleic acid on gastric H+, K(+)-ATPase. Oleic acid inhibited both H+, K(+)-ATPase and K(+)-pNPPase from pig gastric mucosa. The concentrations for 50% inhibition were 7.8 x 10(-6) M and 5.0 x 10(-6) M respectively. Oleic acid also inhibited Na+, K(+)-ATPase with an IC50 value of 1.2 x 10(-5) M. Double reciprocal plots demonstrated the inhibition of gastric H+, K(+)-ATPase by oleic acid to be noncompetitive with respect to K+ and competitive with respect to ATP. A proton transport experiment also showed oleic acid to inhibit H+, K(+)-ATPase mediated acid secretion. Oleic acid may thus possibly be a potent inhibitor of gastric H+, K(+)-ATPase and that the inhibition of H+, K(+)-ATPase may be responsible for the antisecretory effect of oleic acid.

4-Nitrophenylphosphatase↗
PubMed2004

Dimorphecolic acid is synthesized by the coordinate activities of two divergent Delta12-oleic acid desaturases.

Dimorphecolic acid (9-OH-18:2Delta(10)(trans)(,12)(trans)) is the major fatty acid of seeds of Dimorphotheca species. This fatty acid contains structural features that are not typically found in plant fatty acids, including a C-9 hydroxyl group, Delta(10),Delta(12)-conjugated double bonds, and trans-Delta(12) unsaturation. Expressed sequence tag analysis was conducted to determine the biosynthetic origin of dimorphecolic acid. cDNAs for two divergent forms of Delta(12)-oleic acid desaturase, designated DsFAD2-1 and Ds-FAD2-2, were identified among expressed sequence tags generated from developing Dimorphotheca sinuata seeds. Expression of DsFAD2-1 in Saccharomyces cerevisiae and soybean somatic embryos resulted in the accumulation of the trans-Delta(12) isomer of linoleic acid (18: 2Delta(9)(cis)(,12)(trans)) rather than the more typical cis-Delta(12) isomer. When co-expressed with DsFAD2-1 in soybean embryos or yeast, DsFAD2-2 converted 18:2Delta(9)(cis)(,12)(trans) into dimorphecolic acid. When DsFAD2-2 was expressed alone in soybean embryos or together with a typical cis-Delta(12)-oleic acid desaturase in yeast, trace amounts of the cis-Delta(12) isomer of dimorphecolic acid (9-OH-18:2Delta(10)(trans,)(12)(cis)) were formed from DsFAD2-2 activity with cis-Delta(12)-linoleic acid [corrected]. These results indicate that DsFAD2-2 catalyzes the conversion of the Delta(9) double bond of linoleic acid into a C-9 hydroxyl group and Delta(10)(trans) double bond and displays a substrate preference for the trans-Delta(12), rather than the cis-Delta(12), isomer of linoleic acid. Overall these data are consistent with a biosynthetic pathway of dimorphecolic acid involving the concerted activities of DsFAD2-1 and DsFAD2-2. The evolution of two divergent Delta(12)-oleic acid desaturases for the biosynthesis of an unusual fatty acid is unprecedented in plants.

Calendula↗
PubMed1985

Regulation of jejunal blood flow and oxygenation during glucose and oleic acid absorption.

To differentiate the mechanisms whereby actively absorbed glucose and passively absorbed oleic acid increase blood flow and oxygen uptake during their absorption, the effects of these two nutrients on jejunal blood flow, arteriovenous oxygen difference [(a-v)O2], O2 uptake, absorption, rubidium extraction, and capillary permeability-surface area product (PS) were compared in anesthetized dogs. Oleic acid (37 mM) produced significantly greater hyperemia (+28.2%) than glucose (270 mM) did (+12.5%). As estimated by (a-v)O2, tissue oxygen extraction was decreased by oleic acid (-12%) but increased by glucose (+6.5%); the increases in O2 uptake by these two nutrients did not differ significantly. Glucose absorption was accompanied by an increase in rubidium extraction and capillary PS (+11.3%), whereas oleic acid absorption was not. Unlike glucose, intra-arterial infusion of oleic acid decreased vascular resistance and increased blood flow equally to the mucosa and muscularis layers. A significant relation existed between oleic acid absorption and blood flow but not between glucose absorption and blood flow. The enhancement of glucose-induced hyperemia by bile was not related to glucose absorption. Unmasking of oleic acid-induced hyperemia by bile is unrelated to oleic acid absorption but is related to solubility of oleic acid in aqueous solution. The above findings suggest that glucose absorption affects both resistance and exchange vessels, whereas oleic acid absorption affects primarily resistance vessels.

Animals↗
PubMed1991

Oleic acid reversibly opens the blood-brain barrier.

This study examined the effect of intracarotid oleic acid infusion on blood-brain barrier permeability. Oleic acid was infused for 30 s at a rate of 6 ml/min into the right internal carotid artery at concentrations of 10(-6), 10(-5), 2 x 10(-5) and 5 10(-5) M. Extensive Evans blue-albumin extravasation was observed 15 min after the administration of 2 x 10(-5) M oleic acid. The permeability surface area product for alpha-aminoisobutyric acid (AIB), determined 1-11 min following the infusion of oleic acid was increased 10-fold following infusion of 10(-5) M oleic acid and 20-fold following the administration of 5 x 10(-5) M oleate. The blood-brain barrier opening to AIB proved to be reversible 80-90 min after the infusion of 2 x 10(-5) M oleic acid. The possible mechanisms of the oleic acid effect are discussed.

Aminoisobutyric Acids↗
PubMed1969

Simple liquid-liquid partition system for isolation of labeled oleic acid from mixtures with glycerides.

Oleic acid has a partition coefficient, upper phase/lower phase, of 1.9 (22 degrees C) in the liquid-liquid partition system described herein. Tri-, di-, and monoolein are found almost exclusively in the lower (organic) phase. Oleic acid can be quantitatively removed from mixtures of triglyceride and partial glycerides by means of this partition system under conditions resembling those in a lipase assay.

Animals↗
PubMed2004

Oleic acid modulates the post-translational glycosylation of macrophage ApoE to increase its secretion.

There has been increasing interest in a potential role for fatty acids in adversely affecting organismal substrate utilization and contributing to the cardiovascular complications in insulin resistance. Fatty acids have already been implicated in regulating the expression of a number of genes in resident cells of the vessel wall. In the current studies, we evaluated a potential role for fatty acids in the regulation of macrophage apoE expression. Incubation in oleic acid increased the synthesis and secretion of apoE by human monocyte-derived macrophages. Part of this stimulation was mediated at a post-translational locus. Oleic acid increased the secretion of apoE from macrophages that constitutively expressed a human apoE3 cDNA. Incubation in palmitic acid decreased apoE secretion from these cells. The effect of oleic acid on apoE secretion could not be accounted for by the known effect of fatty acid on cellular sterol, because incubation in oleic acid did not suppress the degradation of nascent apoE. Incubation in oleic acid for at least 6 h was required to observe an effect on apoE secretion. Oleic acid altered the glycosylation pattern of cellular and secreted apoE, with a loss of the most heavily sialylated isoform. Oleic acid had no effect on the glycosylation of interleukin 6 secreted from macrophages. Elimination of apoE glycosylation, by substitution of threonine 194 with alanine, eliminated oleic acid-mediated stimulation of apoE secretion. These results indicate that oleic acid increases apoE secretion from macrophages at a locus involving post-translational glycosylation.

Apolipoproteins E↗