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PubMed1967

The incorporation of long-chain fatty acids into phospholipids of respiring slices of rat cerebrum.

1. Respiring slices of adult rat cerebrum have been shown to incorporate long-chain (14)C-labelled fatty acids into phospholipid. 2. Labelling was almost entirely confined to lecithin and ethanolamine phospholipid, only traces being present in serine phospholipid. 3. Palmitic acid, oleic acid and linoleic acid were incorporated more actively into lecithin than into ethanolamine phospholipid, but the converse was found with stearic acid. 4. All four acids labelled the 1- and 2-positions of both lipids; palmitic acid, oleic acid and linoleic acid were approximately evenly distributed, but stearic acid was incorporated predominantly at the 1-position. 5. It is considered that incorporation is most likely brought about through acylation of endogenously derived lysophosphatides. 6. The possible implications of this pathway of lipid metabolism in nervous tissue are discussed.

Animals↗
PubMed2000

Polyunsaturated fatty acids reduce non-receptor-mediated transcellular permeation of protein across a model of intestinal epithelium in vitro.

BACKGROUND: Dietary polyunsaturated fatty acids influence the natural history of intestinal inflammatory diseases. Varying the types of long-chain fatty acids that are exposed to cells alters the physicochemical properties of cell membranes. This study aimed to determine whether such variations alter transcellular and paracellular permeability in intestinal epithelium. METHODS: Monolayers of Caco-2 cells, allowed to differentiate by culturing for 7 days following confluence, were used as the model for intestinal epithelium. Paracellular permeability was assessed by measurement of transepithelial resistance, while transcellular permeability was assessed by the transepithelial flux of horseradish peroxidase. RESULTS: Exposure of the cells to 100 micromol/L of palmitic acid, oleic acid, eicosapentaenoic acid, or linoleic acid, was not toxic to cells (measured by leakage of lactate dehydrogenase), and altered cell membrane fatty acid composition (as measured by gas chromatography). Flux of horseradish peroxidase was significantly affected by 24 h fatty acid exposure (P= 0.038, ANOVA), being decreased by 23 +/- 6% (mean +/- SEM) by eicosapentaenoic acid and 25 +/- 3% by linoleic acid. Oleic acid, palmitic acid and butyrate, had no effect. Transepithelial resistance also varied significantly across the treatment groups (P< 0.001) due to a 28 +/- 5% increase induced by butyrate. The long-chain fatty acids had no effect. CONCLUSIONS: Both omega-3 and omega-6 polyunsaturated fatty acids reduce transcellular, non-receptor-mediated permeation of proteins across differentiated Caco2 cell monolayers, without altering paracellular permeability. Alteration of intestinal barrier function should be considered as a possible mechanism of action of dietary polyunsaturated fatty acids.

Butyrates↗
PubMed2004

Decreased aortic early atherosclerosis and associated risk factors in hypercholesterolemic hamsters fed a high- or mid-oleic acid oil compared to a high-linoleic acid oil.

Currently, diets higher in polyunsaturated fat are believed to lower blood cholesterol concentrations, and thus reduce atherosclerosis, greater than diets containing high amounts of saturated or possibly even monounsaturated fat. The present study was designed to investigate the effect of diets containing mid- or high-linoleic oil versus the typical high-linoleic sunflower oil on LDL oxidation and the development of early atherosclerosis in a hypercholesterolemic hamster model. Animals were fed a hypercholesterolemic diet containing 10% mid-oleic sunflower oil, high-oleic olive oil, or high-linoleic sunflower oil (wt/wt) plus 0.4% cholesterol (wt/wt) for 10 weeks. After 10 weeks of dietary treatment, only the animals fed the mid-oleic sunflower oil had significant reductions in plasma LDL-C levels (-17%) compared to the high-linoleic sunflower oil group. The high-oleic olive oil-fed hamsters had significantly higher plasma triglyceride levels (+41%) compared to the high-linoleic sunflower oil-fed hamsters. The tocopherol levels in plasma LDL were significantly higher in hamsters fed the mid-oleic sunflower oil (+77%) compared to hamsters fed either the high-linoleic sunflower or high-oleic olive oil. Measurements of LDL oxidation parameters, indicated that hamsters fed the mid-oleic sunflower oil and high-oleic olive oil diets had significantly longer lag phase (+66% and +145%, respectively) and significantly lower propagation rates (-26% and -44%, respectively) and conjugated dienes formed (-17% and -25%, respectively) compared to the hamsters fed the high-linoleic sunflower oil. Relative to the high-linoleic sunflower oil, aortic cholesterol ester was reduced by -14% and -34% in the mid-oleic sunflower oil and high-oleic olive oil groups, respectively, with the latter reaching statistical significance. Although there were no significant associations between plasma lipids and lipoprotein cholesterol with aortic total cholesterol and cholesterol esters for any of the groups, the lag phase of conjugated diene formation was inversely associated with both aortic total and esterified cholesterol in the high-oleic olive oil-fed hamsters (r = -0.69, P < 0.05). The present study suggests that mid-oleic sunflower oil reduces risk factors such as lipoprotein cholesterol and oxidative stress associated with early atherosclerosis greater than the typical high-linoleic sunflower oil in hypercholesterolemic hamsters. The high-oleic olive oil not only significantly reduced oxidative stress but also reduced aortic cholesterol ester, a hallmark of early aortic atherosclerosis greater than the typical high-linoleic sunflower oil.

Animals↗
PubMed1992

Replacement of the aliphatic chains of Clostridium acetobutylicum by exogenous fatty acids: regulation of phospholipid and glycolipid composition.

The membrane lipid aliphatic chains of Clostridium acetobutylicum ATCC 4259 have been extensively modified by growth in biotin-free medium containing vitamin-free casein hydrolysate supplemented with either elaidic acid, oleic acid, or mixtures of palmitic and oleic acids. Growth with elaidic acid resulted in polar lipids containing 88.6% 18:1 acyl chains and 94.5% 18:1 ether-linked chains. Growth with oleic acid resulted in comparable levels of enrichment of the lipids with 18:1 chains and C19 chains containing cyclopropane rings. When cells were grown with mixtures of palmitic and oleic acids, the ether-linked chains of the plasmalogens were greater than or equal to 64% 18:1 plus C19 chains containing cyclopropane rings at all ratios of oleic to palmitic acid in the medium. The acyl chains reflected the palmitic acid content of the medium more closely. Marked changes were observed in both phospholipid and glycosyldiglyceride compositions as the lipid acyl and ether-linked chains became more enriched with unsaturated and cyclopropane chains. The ratio of the glycerol acetal of plasmenylethanolamine to phosphatidylethanolamine increased, the ratio of cardiolipin to phosphatidylglycerol decreased, and the ratio of diglycosyldiglyceride to monoglycosyldiglyceride increased. However, the monoglycosyldiglyceride/diglycosyldiglyceride ratio was lower for cells grown on 100% oleic acid than for cells grown on 60 or 80% oleic acid. In the membranes of cells grown on 100% oleic acid, the ratio of glycolipids to phospholipids was lower than that found in cells grown on 60% oleic acid. These results indicate that C. acetobutylicum regulates its polar lipid composition in a complex manner involving phospholipids and glycosyldiglycerides. These changes can affect the equilibria between those lipids that form bilayers and those lipids that tend to form nonlamellar phases when enriched with unsaturated aliphatic chains. Phosphoglycolipids of unknown structure were also observed in cells grown either with biotin or with fatty acids. The content of the most abundant phosphoglycolipid also varied with the degree of unsaturation of the cellular lipids.

Biotin↗
PubMed1986

Protein kinase C activation by cis-fatty acid in the absence of Ca2+ and phospholipids.

Protein kinase C has been shown to be a phospholipid/Ca2+-dependent enzyme activated by diacylglycerol (Nishizuka, Y. (1984) Nature 308, 693-697; Nishizuka, Y. (1984) Science 225, 1365-1370). We have reported that unsaturated fatty acids (oleic acid and arachidonic acid) can activate protein kinase C independently of Ca2+ and phospholipid (Murakami, K., and Routtenberg, A. (1985) FEBS Lett. 192, 189-193). This study shows that other cis-fatty acids such as linoleic acid also fully activate protein kinase C in the same manner. None of the saturated fatty acids (C:4 to C:18) nor the detergents (sodium dodecyl sulfate and Triton X-100) tested here were as effective as oleic acid. Unlike oleic acid, these detergents strongly inhibited protein kinase C activity induced by Ca2+/phosphatidylserine (PS) and diacylglycerol. Lowering the critical micelle concentration of oleic acid by increasing ionic strength also strongly inhibited oleic acid activation of protein kinase C activity. Dioleoylphosphatidylserine activated protein kinase C effectively (Ka = 7.2 microM). On the other hand, dimyristoylphosphatidylserine, which contains saturated fatty acids at both acyl positions, failed to activate protein kinase C even in the presence of Ca2+. These observations suggest that: protein kinase C activation by free fatty acid is specific to the cis-form and is not due to their detergent-like action, cis-fatty acid activation is due to the direct interaction of protein kinase C with the monomeric form of cis-fatty acids and not with the micelles of fatty acids, and cis-fatty acids at acyl positions in PS are also important for Ca2+/PS activation of protein kinase C.

Animals↗
PubMed1984

Inhibition of chymase activity by long chain fatty acids.

The activity of chymase was markedly inhibited by fatty acids with carbon chain lengths of 14-22 at doses greater than 0.02 microM, irrespective of the number of double bonds. Cis acids with a carbon chain length of 18, such as stearic acid, oleic acid, linoleic acid, and linolenic acid were potent inhibitors, whereas the trans isomer of oleic acid, elaidic acid, showed less inhibitory activity. The extent of inhibition by oleyl alcohol was almost the same as that by oleic acid, suggesting that the acid moiety itself was not necessary for the inhibition; but a fatty acid with a terminal functional amide, oleamide, showed little inhibitory activity. The inhibition was noncompetitive and was reversible, and the Ki value of oleic acid was 2.7 microM. Stearic acid and oleic acid inhibited all chymotrypsin-type serine endopeptidases tested. The ID50 values of these fatty acids for atypical mast cell protease were higher than those for the other chymotrypsin-type serine endopeptidases tested. Other proteases, such as papain, trypsin, collagenase, and carboxypeptidase A, except cathespin D, were not affected by stearic or oleic acid.

Animals↗
PubMed1999

Fatty acid block of the transient outward current in adult human atrium.

Fatty acids represent an essential source of fuel for the heart and play an important role in the mechanical, electrical, and synthetic activities of cardiac cells. Under pathological conditions, such as ischemia followed by reperfusion, the myocardium is exposed to very high levels of fatty acids, in particular the monounsaturated fatty acid, oleic acid. Elevated plasma fatty acids have been linked to an increased risk for cardiac arrhythmias. In other species, fatty acids have been shown to modulate several cardiac ion channels, most notably potassium channels. Virtually nothing is known about the actions of oleic acid on potassium channels in human heart. We therefore characterized the effects of oleic acid on the transient outward current, sustained current, and inwardly rectifying current, some of the major potassium channels present in human atrium, using the whole-cell patch clamp method. Exposure of cells to oleic acid (5 microM) reduced the transient outward potassium current to 3.7 +/- 0.8 pA/pF (n = 4) compared with 7.0 +/- 0.7 pA/pF (n = 4) (P <. 05) for cells not exposed. In contrast, oleic acid had little effect on either the sustained current (4.3 +/- 0.3 pA/pF, n = 4 for oleic acid versus 4.8 +/- 0.5, n = 5 for control) present after the decay of the transient outward current or on the amplitude of IK1 measured at -100 mV (1.4 +/- 0.4 pA/pF, n = 4 for oleic acid versus 1.3 +/- 0. 4 pA/pF, n = 6 for control). In addition, oleic acid significantly slowed the rate of recovery of the transient outward current, which is predicted to result in a use-dependent reduction in current amplitude in the beating heart. These results suggest a possible contributing role for oleic acid block of the transient outward current in the pathological consequences of myocardial ischemia.

Aged↗
PubMed2004

Growth temperature affects accumulation of exogenous fatty acids and fatty acid composition in Schizosaccharomyces pombe.

The incorporation of exogenously supplied fatty acids, palmitic acid, palmitoleic acid, oleic acid and linoleic acid, was examined in the yeast Schizosaccharomyces pombe at two growth temperatures, 20 degrees C and 30 degrees C. Fatty acids supplied to S. pombe in the growth medium were found to be preferentially incorporated into the cells, becoming a dominant species. The relative increase in exogenous fatty acids in cells came at the expense of endogenous oleic acid as a proportion of total fatty acids. Lowering the temperature at which the yeast were grown resulted in decreased levels of incorporation of the fatty acids palmitic acid, palmitoleic acid and linoleic acid compared to cells supplemented at 30 degrees C. In addition, the relative amount of the endogenously produced unsaturated fatty acid oleic acid, while greatly reduced compared to unsupplemented cells, was increased in cells supplemented with fatty acids at 20 degrees C compared to supplemented cells at 30 degrees C. The differential production of oleic acid in S. pombe cells indicates that regulation of unsaturated fatty acid levels, possibly by control of the stearoyl-CoA desaturase, is an important control point in membrane composition in response to temperature and diet in this species.

Culture Media↗
PubMed1985

16,16-Dimethyl PGE2 and fatty acids protect hepatocytes against CCl4-induced damage.

16,16-Dimethyl PGE2 (dmPGE2) has previously been shown to protect the in vivo rat liver against CCl4-induced damage. These studies were undertaken to determine if this protection could be demonstrated in vitro where factors of absorption, secretion, and blood flow are not present. Primary hepatocyte cultures were established by perfusing rat liver with collagenase. Hepatocytes were plated at a density of 2 X 10(4) cells/cm, allowed 90 min to attach, then stabilized in L15 medium for 18 h. Hepatocytes were then challenged with CCl4 with concomitant exposure to 10(-9) to 10(-5) M dmPGE2, stearic acid, oleic acid, or ethanol vehicle (0.00001 to 0.1%). After 1 h, challenge was aspirated and cells were stained with 0.04% trypan blue to determine viability. Hepatocytes in the vehicle groups took up more trypan when exposed to CCl4 than those treated with dmPGE2, stearic acid, or oleic acid at concentrations of 10(-9) to 10(-7) M. At 0.1% ethanol vehicle protected as well as all other treatments. Protection against CCl4 by dmPGE2, stearic, and oleic acids as well as high concentrations of ethanol may occur by altering the metabolism of CCl4.

16,16-Dimethylprostaglandin E2↗
PubMed2000

Comparison of an oleic acid enriched-diet vs NCEP-I diet on LDL susceptibility to oxidative modifications.

OBJECTIVE: The objective of this trial was to compare the effect on the susceptibility of plasma Low Density Lipoprotein (LDL) to oxidative modifications of consumption of two oleic rich diets, prepared with two different plant oils, virgin olive oil (OL)1 and refined high monounsaturated fatty acids (MUFA sunflower oil (SU)), with the susceptibility of plasma LDL to oxidation after an National Cholesterol Education Program step 1 (NCEP-I) phase diet. DESIGN: A randomized crossover design. SUBJECTS AND INTERVENTIONS: Twenty-two healthy normolipidemic young males consumed an NCEP-I diet for a 4-week period. Subjects were then assigned to two diets each of 4-weeks duration. Group one was placed on an olive oil enriched diet (40% fat, 22% MUFA) followed by a 4-week period of a MUFA diet enriched in sunflower oil (40% fat, 22% MUFA). In group two, the order of the diets was reversed. RESULTS: Both MUFA diets induced a decrease in saturated (14:0, 16:0, and 18:0) and an increase in monounsaturated and polyunsaturated n-6 (18:2, 20:3, and 20:5) plasma LDL-phospholipid fatty acids, compared to the NCEP-I diet (P<0.01). No significant differences in lag times were observed between the olive oil and the NCEP-I diet periods. However there was a greater inhibition time (P<0.001) when subjects consumed the MUFA rich sunflower oil diet compared to the NCEP-I diet. These differences were probably related to the relative enrichment of plasma LDL particles in alpha-tocopherol due to the high vitamin E content of the MUFA-rich sunflower oil. Indeed, the alpha-tocopherol content was positively correlated with lag time (r=0.338; P<0.008). CONCLUSION: Our findings suggest that changes in plasma LDL alpha-tocopherol content with practical solid-food diets can decrease its susceptibility to oxidation. SPONSORSHIP: This work has been supported by grants from the Investigaciones de la Seguridad Social (FIS 92/0182, to Francisco Pérez Jiménez); and from Koype Co, Andújar, Jaén, Spain. European Journal of Clinical Nutrition (2000) 54, 61-67

Adult↗
PubMed1990

Binding of unsaturated fatty acids to Na+, K(+)-ATPase leading to inhibition and inactivation.

The effects of free fatty acids on the mechanism of action of Na+, K(+)-ATPase were studied. Unsaturated free fatty acids (palmitoleic acid, oleic acid, linoleic acid and arachidonic acid) inhibited the Na+, K(+)-ATPase activity within a narrow range, while saturated and methylated fatty acids had little or no effect. The following effects of oleic acid were found: (1) The affinity for K+ on the overall ATPase and the p-nitrophenylphosphatase reaction as well as the maximal activities were decreased. (2) The Na(+)-ATPase activity was also inhibited but the '0'-ATPase activity was hardly changed. (3) The steady-state ATP phosphorylation level in the presence of Na+ was not influenced. (4) The dephosphorylation rate constant of the phosphointermediate was slightly decreased, resulting in elevated phosphorylation levels in the absence of Na+. (5) The inhibitory effect of ATP on the dephosphorylation rate was not affected. (6) The K+ sensitivity of the phosphoenzyme in the presence as well as in the absence of Na+ was decreased. (7) Ouabain binding was inhibited. Both the affinity and the number of binding sites were lowered. In addition it was found that Na+, K(+)-ATPase binds oleic acid linearly with the fatty acid concentration up to more than 100 mol oleic acid per mol alpha beta oligomer of Na+, K(+)-ATPase. Prolonged incubation with oleic acid led to irreversible inactivation of the enzyme. This inactivation was dependent on the reaction conditions: ligands, temperature, enzyme concentration, time and fatty acid concentration. The combined presence of inactivation (long term effects) and the effects on the (K(+)-activated) dephosphorylation (short term effects) explain the mixed type inhibition of free fatty acids as observed in assays for K(+)-activated ATPase, K(+)-activated p-nitrophenylphosphatase and ouabain binding. It also explains the sharp inhibition curve in the Na+, K(+)-ATPase activity test.

Adenosine Triphosphate↗
PubMed2004

Removal of copper(II) from some environmental samples by sorptive-flotation using powdered marble wastes as sorbents and oleic acid as surfactant.

A simple and economic experimental sorptive -flotation procedure is presented for the removal of copper(II) species from aqueous solutions. It is based on using powdered marble wastes (PMW), which are widespread and inexpensive and may represent an environmental problem, as the effective inorganic sorbent and oleic (HOL) as the surfactant. The main parameters (i.e. initial solution pH, sorbent, surfactant and copper concentrations, stirring times, ionic strength, temperature and the presence of foreign ions) influencing the flotation of PMW and /or Cu(II) were examined. Nearly, 100% of PMW and Cu(II) were removed from aqueous solutions at pH7 after stirring for 10 min and at room temperature, (approximately 25 degrees C). The procedure was successfully applied to recover Cu(II) spiked to some natural water samples. A mechanism for sorption and flotation is suggested.

Calcium Carbonate↗
PubMed2003

Effect of iontophoresis and fatty acids on permeation of arginine vasopressin through rat skin.

The aim of this study was to assess the effects of fatty acids and iontophoretic mode of penetration enhancement on transdermal delivery of Arginine Vasopressin (AVP). Sprague-Dawley (SD) rat skin was pretreated with fatty acids (e.g. 5% w/v, lauric acid, oleic acid, and linoleic acid in ethanol:water (EtOH:W, 2:1 system) for 2h and iontophoresis in vitro, separately or together. The results indicate that all fatty acids studied increased (P<0.05) the flux of AVP in comparison to control (not pretreated with enhancer) and their effectiveness in flux enhancement was comparable. Further, oleic acid in combination with iontophoresis significantly increased the permeation of AVP both in comparison to pretreatment with fatty acids and iontophoresis alone. However, iontophoresis did not further increase the permeation of AVP through linoleic acid pretreated skin. Fourier transform infrared (FT-IR) spectroscopic studies revealed that EtOH:W (2:1) system is not effective in lipid extraction. The shift to higher wavenumbers of the symmetric and asymmetric stretching peaks at 2850 and 2920cm(-1) revealed that at the concentration used, oleic acid and linoleic acid caused fluidization of stratum corneum (SC) lipids. This study provides direct evidence that oleic acid in EtOH:W (2:1) system causes disruption of the SC lipid lamellae and that a combination of oleic acid with iontophoresis further enhances the effects of oleic acid in a synergistic manner.

Administration, Cutaneous↗
PubMed2004

Hypothalamic responses to long-chain fatty acids are nutritionally regulated.

Central administration of the long-chain fatty acid oleic acid inhibits food intake and glucose production in rats. Here we examined whether short term changes in nutrient availability can modulate these metabolic and behavioral effects of oleic acid. Rats were divided in three groups receiving a highly palatable energy-dense diet at increasing daily caloric levels (below, similar, or above the average of rats fed standard chow). Following 3 days on the assigned diet regimen, rats were tested for acute biological responses to the infusion of oleic acid in the third cerebral ventricle. Three days of overfeeding virtually obliterated the metabolic and anorectic effects of the central administration of oleic acid. Furthermore, the infusion of oleic acid in the third cerebral ventricle failed to decrease the expression of neuropeptide Y in the hypothalamus and of glucose-6-phosphatase in the liver following short term overfeeding. The lack of hypothalamic responses to oleic acid following short term overfeeding is likely to contribute to the rapid onset of weight gain and hepatic insulin resistance in this animal model.

Agouti-Related Protein↗
PubMedDate not supplied

Oleic acid-induced cholelithiasis in the rabbit: conversion of dietary oleic acid to cholestanol as a cause of calcium-bile salt gallstones.

Rabbits fed a diet rich in oleic acid develop gallstones consisting of calcium salts of (5 alpha)-glyco-allodeoxycholic acid. To study the metabolic pathway of oleic acid, we followed the changes in plasma, hepatic and biliary lipids in this animal model. In addition, to also determine the role played by intestinal microflora on biliary lipid metabolism, we added kanamycin to the oleic acid diet. Oleic acid-fed rabbits rapidly developed hypercholesterolemia. This was associated with an increase in liver 3-hydroxy-3-methylglutaryl coenzyme A reductase activity, accumulation of cholesterol as well as cholestanol in the liver and progressive saturation of cholesterol in bile. [14C]oleic acid fed orally to rabbits was recovered in liver extracts as both cholesterol and cholestanol. With oleic acid feeding, there was a progressive increase in glyco-allodeoxycholic acid culminating in the formation of gallstones. Kanamycin supplement to the oleic acid diet resulted in the same changes in plasma and hepatic sterol metabolism compared with oleic acid-fed rabbits. There was, however, a striking difference in the biliary bile acid profile. Kanamycin supplementation dramatically reduced the proportion of 5 alpha-dihydroxy bile acids, increased the proportion of 5 beta-trihydroxy bile acids and completely abolished gallstone formation. We postulate that, in the rabbit, oleic acid is used as a carbon source for cholesterol synthesis, and a high oleic acid diet increases hepatic cholesterogenesis. Hepatic cholesterol is then metabolized to form cholestanol, followed by (5 alpha)-glyco-allocholic acid which is secreted into bile and transformed by gut bacteria to form (5 alpha)-allodeoxycholic acid. Kanamycin abolished gallstone formation by inhibiting intestinal bacterial dehydroxylation.

Animals↗