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PubMed1976

The repair of impaired epidermal barrier function in rats by the cutaneous application of linoleic acid.

Epidermal barrier function in rats was experimentally impaired by two separate means, namely, by rendering the animals deficient in essential fatty acids and by evoking a primary cutaneous irritant response by treating with a solution of sodium laurate. Impaired barrier function was manifested by a greatly increased rate of transepidermal water loss. Application to the skin of sunflower seed oil, which is rich in linoleic acid, rapidly restored to normal the abnormally high rates of transepidermal water loss in both experimental cases, and it was shown with the essential fatty acid-deficient rats that there was a concomitant incorporation of linoleic acid of the sunflower seed oil into epidermal lipids. Cutaneous application of olive oil, which is low in linoleic acid but rich in the non-essential oleic acid, did not influence epidermal barrier function. A close relationship of barrier function and essential fatty acids is indicated.

Animals↗
PubMed1996

Linoleic acid intake and susceptibility of very-low-density and low density lipoproteins to oxidation in men.

Lipoprotein peroxidation is thought to play an important role in atherogenesis. In the Kuopio Atherosclerosis Prevention Study (KAPS) the intake of fat and fatty acids, the oxidation susceptibility of the plasma very-low-density + low-density lipoprotein (VLDL+LDL) fraction (by induction with copper or hemin and hydrogen peroxide), and concentrations of plasma antioxidants, serum lipids, and lipoproteins were measured in 393 men. In the multivariate-regression model dietary linoleic acid was the most important determinant of the maximal oxidation velocity for the hemin assay (standardized regression coefficient = 0.294, P<0.0001). In the copper assay the association of dietary linoleic acid and maximal oxidation velocity was second in order of strength (standardized regression coefficient = 0.324, P< 0.0001). We conclude that high linoleic acid intake is associated with increased oxidation susceptibility of atherogenic lipoproteins in men.

Aged↗
PubMed2003

Purification of conjugated linoleic acid isomers through a process including lipase-catalyzed selective esterification.

A mixture of conjugated linoleic acids (CLAs) was prepared by alkali conjugation of high purity linoleic acid. The preparation contained 45.1 wt% cis-9, trans-11 (c9,t11)-CLA, 46.8 wt% trans-10, cis-12 (t10,c12)-CLA, and 5.3 wt% other CLAs. A process comprising Candida rugosa lipase-catalyzed selective esterification with lauryl alcohol, molecular distillation, and urea adduct fractionation under strict conditions in ethanol was very effective for purification of c9,t11- and t10,c12-CLAs. In particular, the urea adduct fractionation efficiently eliminated CLAs except c9,t11- and t10,c12-isomers. Purification of c9,t11- and t10,c12-CLAs from 1.0 kg of the CLA mixture increased the c9,t11-CLA purity to 93.1% with 34% recovery of the initial content, and increased the t10,c12-CLA purity to 95.3% with 31% recovery.

Candida↗
PubMed1994

Malondialdehyde concentration in plasma is inversely correlated to the proportion of linoleic acid in serum lipoprotein lipids.

It has been suggested that the susceptibility of low density lipoprotein (LDL) to oxidative stress depends on the balance between its contents of polyunsaturated fatty acids and antioxidants. In a healthy reference population (n = 103), the plasma concentration of malondialdehyde (MDA) (mean 0.86, range 0.50-1.27 mumol/l) was positively correlated to the serum concentrations of LDL cholesterol (r = 0.31, P = 0.001), very low density lipoprotein triglycerides (r = 0.25, P = 0.009) and apolipoprotein B (r = 0.23, P = 0.03), and negatively correlated to lipid corrected alpha tocopherol in serum (r = -0.22, P = 0.02) and lipoprotein(a) (Lp(a)) (r = -0.26, P = 0.01). Plasma MDA was negatively correlated to the content of linoleic acid in the serum lipoprotein phospholipids (r = -0.35, P = 0.0008). In a stepwise regression analysis 12% of the variation in plasma MDA was explained by variations in the content of linoleic acid and 27% after addition of Lp(a) and abdominal sagittal diameter. The significant negative relation between plasma MDA and the amount of linoleic acid in the lipoprotein lipids indicates that other factors, e.g. the availability of anti-oxidants and the lipoprotein metabolism, may be of greater importance for intravascular lipid peroxidation than the proportion of polyunsaturated fatty acids in the lipoprotein lipids.

Adult↗
PubMed1986

Retention of linoleic acid in carcass lipids of rats fed different levels of essential fatty acids.

Rats of an inbred Sprague-Dawley strain were fed purified diets with low (0.3% of total energy), normal (3%) or high (10%) content of essential fatty acids (EFA) for at least three generations. Two 30-day-old rats with similar weights were chosen from one litter. One was killed; weight increase and food consumption of the other rat was measured for 15 days. Total lipid content and fatty acid composition in total lipid and lipid classes were determined in both rats. Seven pairs of rats from each group were treated in the same way. Calculations based on amount of linoleic acid ingested and retained in the carcass lipids showed that 50% of the ingested linoleic acid was retained in the low EFA rats compared to 10-15% in the normal and high EFA rats.

Animals↗
PubMed1995

Effects of exogenous linoleic acid on fatty acid composition, receptor-mediated cAMP formation, and transport functions in rat astrocytes in primary culture.

We have examined the effects of culturing neonatal rat-brain astrocytes in medium containing delipidated serum, with or without added linoleic acid (LA, 18:2 omega 6), on membrane fatty-acid composition and functions. After 18-21 days in culture, polyunsaturated fatty acids (PUFA) constituted approximately equal to 24 mol% of the total fatty acids in the astrocytes grown in delipidated media ("controls'); these proportions were increased by 35-40% to approximately equal to 33 mol% when the cells were supplemented with 35 microM LA. Notable differences in the PUFA profiles of the cells cultured with or without added LA included: (a) higher proportions of omega 6 PUFA in the LA-supplemented astrocytes (approximately equal to 25%, relative to approximately equal to 10% in controls) that were accompanied by an increase in the ratio of omega 6/omega 3 PUFA (from < 2 in controls to approximately equal to 5), and (b) higher proportions of 20:3 omega 9 and 22:3 omega 9 in the control astrocytes (> 5%) relative to the LA-supplemented cells (approximately equal to 1%). The major metabolites in the omega 6 PUFA-enriched cells were arachidonic (20:4 omega 6), adrenic (22:4 omega 6) and docosapentaenoic (22:5 omega 6) acids (15, 5 & 3 mol%, respectively). Enrichment of the astrocytes in omega 6 PUFA did not alter basal levels of cAMP, nor did it affect the amounts of cAMP formed in response to forskolin, isoproterenol, adenosine or histamine. However, dopamine-dependent increases in cAMP formation in the presence of the phosphodiesterase inhibitor, Ro 20-1724, were reduced by approximately equal to 25% relative to those in controls. LA supplementation modified uptake of [3H]adenosine into the astrocytes; values for Kt for a high affinity transport were increased relative to controls, and maximum capacity of a lower affinity process was reduced. Uptake of [3H]glutamate was not altered in the omega 6 PUFA-enriched astrocytes. This study demonstrated that cultured astrocytes take up exogenous linoleic acid and incorporate its metabolites into phospholipid, and that the resulting changes in membrane PUFA composition modify only specific cell functional properties.

Animals↗
PubMed1990

Modulation of guinea pig airway reactivity by the linoleic acid metabolite 13-hydroxy-octadecadienoic acid (13-HODE).

The influence of the linoleic acid metabolite 13-hydroxy-octadecadienoic acid (13-HODE) on guinea pig tracheal reactivity to both contractile and relaxant agonists was investigated in vitro. 13-HODE induced an increased contraction of tracheal rings to histamine, whereas methacholine responsiveness was not significantly affected. Relaxant responses to isoprenaline and prostaglandin E2 were not influenced either.

Animals↗
PubMed1994

Ratios of linoleic acid to alpha-linolenic acid in formulas for term infants.

Commercial infant formulas with a ratio of linoleic acid (LA) to alpha-linolenic acid (ALA) of 10:1 or higher are nutritionally inadequate; the tissue levels of docosahexaenoic acid (DHA) are lower and the visual function indices are reduced in infants who are fed these formulas. All the evidence points to using LA:ALA ratios of less than 8:1, but there has been only one study in infants that used formulas with reduced LA:ALA ratios, and only biochemical indices were monitored. There is a need for both short-term studies to establish the ratios of LA to ALA that will make possible the accumulation of DHA to levels close to those in breast-fed infants and long-term trials to determine the effects of such fat blends on growth and development.

Breast Feeding↗
PubMed2003

Dietary linoleic acid suppresses gene expression of rat liver alpha-amino-beta-carboxymuconate-epsilon-semialdehyde decarboxylase (ACMSD) and increases quinolinic acid in serum.

Hepatic ACMSD [EC4.1.1.45] plays a key role in regulating NAD biosynthesis from tryptophan. We previously reported that ingestion of polyunsaturated fatty acids by rats leads to a decrease in their hepatic ACMSD activity. We purified ACMSD and cloned cDNA encoding rat ACMSD. Therefore, in this study, we examined whether dietary linoleic acid altered ACMSD gene expression and its protein level. Moreover we measured the tryptophan catabolite quinolinic acid level in rats. In the rats fed with linoleic acid, ACMSD mRNA and its protein levels in the liver were strongly suppressed and serum quinolinic acid was significantly increased as compared with the rats fed on a fat-free diet. These results suggest that the transcription level of ACMSD is modulated by linoleic acids or their metabolites and probably there is an inverse relationship between ACMSD activity and the production of quinolinic acid converted from tryptophan.

Animals↗
PubMed2004

Effect of conjugated linoleic acid on Delta-5 desaturase activity in yeast transformed with fungal Delta-5 desaturase gene.

Conjugated linoleic acid (CLA), a mixture of positional and geometric isomers derived from linoleic acid (LA: delta9, 12-18:2), has been shown to exhibit various biological functions based on studies using cell culture and animal models. It was postulated that the beneficial effects of CLA were exerted through suppression of production of arachidonic acid (AA; delta5,8,11,14-20:4) and consequently, production of pro-inflammatory eicosanoids. In this study, we used the baker's yeast, Saccharomyces cerevisiae, transformed with fungal delta5-desaturase gene as a model, to study whether CLA affects the activity of delta5-desaturase, a rate-limiting step which converts dihomo-gamma-linolenic acid (DGLA; delta8,11, 14-20:3) to AA. The activity of delta5-desaturase was examined in the transformed yeast incubated in a medium supplemented with DGLA and one of four different CLA isomers (c9, t11-, t10, c12-, c9, c11- and t9, t11). Results show that all four isomers were taken up readily by the yeast, and all of them suppressed the conversion of DGLA to AA. The degree of suppression, which varied significantly among four isomers was modulated by the level of CLA isomers added in the medium. Since portions of these CLA isomers could be converted to form delta5-CLA metabolites (delta5, c9, t11-, delta5, t10, c12-, delta5, c9, c11- and delta5, t9, t11-18:3), it is suggested that CLA suppressed the delta5-desaturation of DGLA to AA through substrate competition between DGLA and CLA isomers.

Arachidonic Acid↗
PubMed1986

Apparent in vivo retroconversion of dietary arachidonic to linoleic acid in essential fatty acid-deficient rats.

Essential fatty acid-deficient rats were fed ethyl [U-14C]arachidonate (308 dpm/nmol) and when a decrease in the transepidermal water loss was seen, the epidermal sphingolipids, acylglucosylceramide and acylceramide were isolated. [14C]Linoleic acid (approx. 130 dpm/nmol) was present in both lipid classes, while the substrate was only detected in the former. These results intimate that in vivo retroconversion of arachidonic to linoleic acid can be induced in the rat.

Animals↗
PubMedDate not supplied

[K+-dependent swelling of Ehrlich ascitic carcinoma cells in the presence of linoleic acid hydroperoxides and Fe2+ ions].

EFfect of linoleic acid hydroperoxide (I) and Fe++ on viscous elastic properties of cell membranes of Ehrlich ascite carcinoma was studied by the method of K+-dependent swelling. It has been shown that the action of 1 and Fe++ is of similar character, and the effect depends on the incubation time and concentration of agents in the incubation mineral solutions. After 2 h incubation the concentration relationships have two patterns characterized by increased swelling at concentrations 10(-6)-10(-5) M and inhibition of this process at concentrations above 10(-5) M. After 4 incubation only the inhibition effect of observed, which seems to reflect the increase of cell membranes rigidity conditioned by the formation of "joints" resulting from the interaction between the products of lipid peroxide oxidation and membrane macromolecules.

Animals↗
PubMed1990

Direct cardiovascular actions of two metabolites of linoleic acid.

Two newly discovered oxidation products of linoleic acid (i.e., 9,10-epoxy-12-octadecenoate termed Leukotoxin A, and 12,13-epoxy-9-octadecenoate termed Leukotoxin B) are produced by neutrophils in a variety of species. These substances appear to combat bacterial infection although they also have detrimental effects on normal organ function. Administration of Leukotoxin A or B to isolated cat papillary muscles decreased developed force, an index of myocardial contractility, in a concentration-dependent manner. Leukotoxin B was more active in decreasing the developed force than Leukotoxin A at high concentrations. Leukotoxin A or B, when added to isolated perfused cat carotid arteries, produced a significant vasoconstriction which in vivo would result in an increased vascular resistance. Thus, leukotoxins exert significant direct effects on the cardiovascular system in cats. Leukotoxins A and B are both cardiodepressant and vasoactive independent of release of other blood borne mediators.

Animals↗
PubMed2004

Hepatic steatosis is not due to impaired fatty acid oxidation capacities in C57BL/6J mice fed the conjugated trans-10,cis-12-isomer of linoleic acid.

Decreased body fat mass and liver steatosis have been reported in mice fed diets containing the conjugated linoleic acid trans-10,cis-12-C18:2 (CLA2), but not in those fed diets containing cis-9,trans-11-C18:2 (CLA1). Because the decrease in fatty acid (FA) oxidation may cause fat accumulation, we questioned whether the effects of both CLAs on enzyme activities and mRNA expression were related to liver FA oxidation. To address this question, 7-wk-old male C57BL/6J mice were fed for 4 wk a diet supplemented with 1% CLA1, CLA2, or cis-9-C18:1 (control) esterified as triacylglycerols. In CLA2-fed mice, the proportions of CLA2 in the total FA of liver lipids were substantially lower than those of CLA1 in mice fed CLA1. The mitochondrial protein content per total liver was about 56% greater in CLA2-fed mice than in CLA1-fed mice and controls. Mitochondrial carnitine palmitoyltransferase I (CPT I) and carnitine-dependent palmitate oxidation activities were also significantly greater in CLA2-fed mice than in the two other groups. The amounts of malonyl-CoA per gram of liver and the sensitivity of CPT I to malonyl-CoA inhibition were greater in both groups of CLA-fed mice than in the controls. L-CPT I mRNA expression doubled in CLA2-fed mice and was 3 and 2 times greater for M-CPT I in the CLA1 and CLA2 groups, respectively, compared with controls. Peroxisomal FA oxidation-related activities and acyl-CoA oxidase mRNA expression were increased in CLA1-fed mice, and to a larger extent in CLA2-fed mice, relative to controls. These data indicate that FA oxidation capacities were increased in mice fed CLA2, but were likely depressed in vivo through malonyl-CoA inhibition.

Animals↗
PubMed1996

Increasing dietary linoleic acid in young rats increases and then decreases docosahexaenoic acid in retina but not in brain.

The accumulation of fatty acids in retina, brain, liver, and plasma of 30-day-old rat pups consuming various levels of linoleic acid (LA, 18:2n-6) and constant alpha-linolenic acid (ALA, 18:3n-3) is reported. Dams were fed graded levels of LA during gestation and lactation, and the pups were maintained on the diet of their dams until the end of the brain growth spurt at 30 d of life. Milk, and pup brain, retina, liver, and plasma were analyzed quantitatively for fatty acid profile. The percentage of docosahexaenoic acid (DHA, 22:6n-3) in retina increased from an LA-deficient dietary level, peaked at the 9:1 (LA/ALA) level, then fell for the 41:1 and 69:1 levels. In contrast, the brain DHA percentage was unaffected by dietary LA levels. Retinal unsaturated fatty acid levels paralleled liver and plasma levels. The milk fatty acid composition mirrored the diets. These data show that the retinal fatty acid composition responds sensitively to dietary fatty acid composition, similar to liver and plasma, while the brain unsaturate composition is nearly independent of dietary composition.

Animals↗
PubMed2005

Incorporation and metabolism of c9,t11 and t10,c12 conjugated linoleic acid (CLA) isomers in rat brain.

Conjugated linoleic acid (CLA) has been shown to exert several biological activities in different organs, in particular organs such as adipose and mammary tissue where CLA accumulates preferentially because of its high incorporation into neutral lipids. However, despite numerous studies carried out in different experimental models, both in vivo and in vitro, very little is known about the accumulation and metabolism of CLA in the brain. In this communication we present data showing that the two CLA isomers c9,t11 and t10,c12 are actively incorporated and metabolised in rat brain, and in cultures of astrocytes in vitro with patterns remarkably similar to those previously reported to occur in other tissues and cells. However, beta oxidation of CLA was found to be more efficient in brain than in other tissues, with t10,c12 a better substrate than the c9,t11 isomer. CLA incorporation and metabolism have been linked to antiinflammatory and antiproliferative activities in experimental models. Therefore, CLA activity in brain could have a positive impact on neurological disorders, such as Alzheimer's disease, Parkinson's disease and adrenoleukodystrophy, where an observed increase in inflammatory responses seems to contribute heavily to the pathogenesis.

Animals↗
PubMed2004

Metabolic effects of conjugated linoleic acid in humans: the Swedish experience.

Conjugated linoleic acid (CLA) comprises a group of unsaturated fatty acid isomers with a variety of biological effects. CLA reduces body fat accumulation in animal models and has been ascribed significant effects on lipid and glucose metabolism. It has been suggested that the trans-10,cis-12 isomer is the active isomer with regard to antiobesity and insulin-sensitizing properties. The metabolic effects in humans are not well characterized. We have investigated and published the effects of CLA (given as the commercially available mixture and as the purified trans-10,cis-12 isomer) on anthropometry, lipid and glucose metabolism, and markers of lipid peroxidation. The results from those studies indicate that CLA might slightly decrease body fat in humans, particularly abdominal fat, but there is no effect on body weight or body mass index. There is no simultaneous improvement in lipid or glucose metabolism. Rather, the trans-10,cis-12 CLA isomer unexpectedly caused significant impairment of the peripheral insulin sensitivity as well as of blood glucose and serum lipid concentrations. In addition, CLA markedly elevated lipid peroxidation. Thus, the metabolic effects of CLA in humans seem complex, and further studies, especially of specific isomers and of longer duration, are needed.

Adipose Tissue↗