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PubMed2002

In vitro mimicry of essential fatty acid deficiency in human endothelial cells by TNFalpha impact of omega-3 versus omega-6 fatty acids.

Severe endothelial abnormalities are a prominent feature in sepsis with cytokines such as tumor necrosis factor (TNF)alpha being implicated in the pathogenesis. As mimic to inflammation, human umbilical vascular endothelial cells (HUVEC) were incubated with TNFalpha for 22 h, in the absence or presence of the omega-6 fatty acid (FA), arachidonic acid (AA), or the alternative omega-3 FA eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). TNFalpha caused marked alterations in the PUFA profile and long chain PUFA content of total phospholipids (PL) decreased. In contrast, there was a compensatory increase in mead acid [MA, 20:3(omega-9)], the hallmark acid of the essential fatty acid deficiency (EFAD) syndrome. Corresponding changes were noted in phosphatidylcholine, phosphatidylethanolamine, phosphatidylserine, and phosphatidylinositol, but not in the sphingomyelin fraction. Supplementation with AA, EPA, or DHA markedly increased the respective FA contents in the PL pools, suppressed the increase in MA, and resulted in a shift either toward further predominance of omega-6 or predominance of omega-3 FA. We conclude that short-term TNFalpha incubation of HUVEC causes an EFAD state hitherto only described for long-term malnutrition, and that endothelial cells are susceptible to differential influence by omega-3 versus omega-6 FA supplementation under these conditions.

Cells, Cultured↗
PubMed1997

Delta-6-desaturase and delta-5-desaturase in human Hep G2 cells are both fatty acid interconversion rate limiting and are upregulated under essential fatty acid deficient conditions.

Essential fatty acids are interconverted by desaturases and elongases to eicosanoid precursors. In essential fatty acid deficiency (EFAD) an increased hepatic interconversion of linoleic acid (18:2) to arachidonic acid (20:4n-6) has been demonstrated in vivo. We now cultured Hep G2 cells under EFAD conditions. 20:3n-6 appeared in EFAD cells, but also in controls. After adding 14C-18:2 to the medium, interconversion products and their distribution in different lipids were studied by HPLC. When trace amounts 18:2 were incubated, 38% were converted by the EFAD cells after 21 h, vs 6% by controls. 20% was converted to 20:4 by EFAD cells vs 14% by controls. EFAD cells preferentially distributed more 18:2 and conversion products to neutral fats and to phosphatidyl ethanolamine, but less to cardiolipin than controls did, when incubated with trace amount 18:2, but not with 1 mM 18:2. A relative accumulation of radioactivity in 20:3 was observed. In conclusion; in EFAD Hep G2 cells delta-6- and delta-5-desaturase both were found to be upregulated and eicosanoid precursors were distributed more into phosphatidyl ethanolamine. Delta-5-desaturase had a rate limiting property as well as delta-6-desaturase.

Arachidonic Acid↗
PubMed1985

A unique cardiac cytosolic acyltransferase with preferential selectivity for fatty acids that form cyclooxygenase/lipoxygenase metabolites and reverse essential fatty acid deficiency.

The rabbit heart contains a cytosolic enzyme which selectively incorporates polyunsaturated fatty acids into phosphatidylcholine. This unique acyltransferase is selective for fatty acids, thus far tested, that are substrates for cyclooxygenase or lipoxygenase (i.e., arachidonic, eicosapentaenoic, linoleic and dihomo-gamma-linoleic acids) or which reverse the symptoms of essential fatty acid deficiency (columbinic acid). On the other hand, palmitic, oleic, 5,8,11-eicosatrienoic (n-9, Mead acid), and docosatetraenoic acid (n-6, adrenic acid) were not incorporated in phospholipids by the cytosolic acyltransferase. No such fatty acid selectivity was exhibited by the cytosolic acyl-CoA synthetase or by the acyltransferase activities present in cardiac microsomes and mitochondria.

Acyltransferases↗
PubMed1980

Essential fatty acids for the mosquito Culex pipiens.

Newly-hatched larvae of Culex pipiens grow well to adults in a chemically defined dietary medium containing cholesterol as the only lipid, but the adults cannot fly. Arachidonic acid (0.2 mg/100 ml medium) was previously shown to induce emergency from pupae of strong, flying adults, whereas linoleic and linolenic acids, which satisfy the essential fatty acid requirement of other insects, were inadequate. The effect of replacing arachidonic acid by other fatty acids is examined here. Saturated or monoenoic acids failed entirely to induce flight. Several polyunsaturated fatty acids, of both the omega 6 and omega 3 families, containing three double bonds in divinyl methane arrangement spanning carbons 6 to 13 from the methyl termination allowed the emergence of flying adults; besides arachidonic acid, these were gamma-linolenic (C18:3, delta 6,9, 1,2), homo-gamma-linolenic (C20:3, delta 8,11,14), eicosapentaenoic (C20:5, delta 5,8,11,14,17) and docosahexaenoic (C22:6, delta 4,7,10,13,16,19) acids. Certain other polyunsaturated fatty acids, including linoleic and linolenic acids, failed to support flight but allowed many adults to stand or hop on the medium surface. These findings are discussed in relation to essential fatty acid requirements of other insects and vertebrates.

Animals↗
PubMed1984

Development of hepatic steatosis and essential fatty acid deficiency in rats with hypercaloric, fat-free parenteral nutrition.

Intravenous (i.v.) infusion of excessive energy has been associated with hepatic steatosis. The time course of liver lipid accumulation was examined during 6 days of i.v. hyperalimentation with fat-free infusate. Adult male rats with indwelling superior vena cava cannulas received a dextrose-amino acid infusate for 0, 1/2, 1, 2, 4 or 6 days to provide 146% of nonprotein energy requirement [congruent to 350 non-protein kcal/(kg . day)] and 335% of nitrogen requirement [congruent to 2.7 g amino nitrogen/(kg . day)]. Significant hepatomegaly was apparent by day 1/2. Initially, glycogen deposition accounted for the liver enlargement, but after day 2, liver glycogen was declining and liver lipid was increasing. By day 4, liver lipid had increased fourfold and was the major contributor to hepatomegaly. Concurrent with fatty liver metamorphosis, hepatic essential fatty acid deficiency (EFAD) developed by day 4; liver linoleic acid levels had dropped from 20 to 1% of total fatty acids, and liver triene:tetraene ratio was 0.68. Similar changes in hepatic phospholipid fatty acids were observed. Enhanced lipogenesis and impaired lipid transport is known to accompany EFAD and may underlie the observed steatosis. A doubling of plasma cholesterol levels was also associated with steatosis. The mechanism leading to this increase in plasma cholesterol warrants further investigation.

Animals↗
PubMed1990

Protein and carbohydrate selection respond to changes in dietary saturated fatty acids but not to changes in essential fatty acids.

We previously reported differences in protein and carbohydrate selection patterns in post-weanling rats fed beef tallow or soybean oil-based diets. Two experiments were designed to determine the characteristic of the dietary fat which mediates the selection behavior. For each experiment, dietary fat was 20% (w/w) of diets and fatty acid profiles were obtained by blending fat sources. Rats were randomly assigned to diets (24% protein, 40% carbohydrate) which varied only in fatty acid composition. After 2 weeks, rats selected from 2 diets with the fat composition previously fed, but varying in their protein and carbohydrate composition (55% protein, 4% carbohydrate and 5% protein, 61% carbohydrate). Experiment 1 was designed to test the effect of relative (omega 6: omega 3 ratios of 1 and 20) and absolute (15% or 4% omega 6, 0.7% or 0.2% omega 3) differences in essential fatty acids on macronutrient selection patterns. Differences in dietary essential fatty acids had no effect on energy intake or the proportion of energy consumed as protein and carbohydrate. Experiment 2 examined the effect of differences in the level of saturated fat (3-10% diet (w/w] on protein and carbohydrate selection. Animals selecting from diets with higher levels of saturated fat consumed more energy as protein and less as carbohydrate than rats selecting from diets with lower levels of saturated fat (p less than 0.0001). Regression analysis was used to examine the relationship between percent protein or carbohydrate energy and classes of dietary fat. The strongest relationship existed between percent dietary saturated fat and percent protein or carbohydrate energy (p less than 0.0001). Polyunsaturated:saturated fat ratio was also weakly associated with percent protein and carbohydrate energy (p less than 0.05). Polyunsaturated, monounsaturated, omega 6 and omega 3 fatty acids were not significantly related to percent protein or carbohydrate energy. These results indicated that protein and carbohydrate selection patterns are altered in response to qualitatively different dietary fatty acids, and that the amount of saturated fat in the diet is the important characteristic of dietary fat mediating the behavioral alteration.

Analysis of Variance↗
PubMed1979

The effect of essential fatty acid deprivation on the metabolic transformations of [1(-14)C]linolenate in developing rat brain.

Linolenic acid undergoes rapid metabolism in the brain of 21-day-old rats. Radioactivity is rapidly transferred from linolenic acid to the C20 (n--3) fatty acids while that in docosapentaenoic acid (22 : 5 n--3) and docosahexaenoic acid (22 : 6 n--3) gradually increases. A greater proportion of the radioactivity is associated with the polyunsaturated and less with saturated and monounsaturated fatty acids in essential fatty acid-deprived rats relative to controls.

Animals↗
PubMed1990

Free radical generation, lipid peroxidation and essential fatty acids in uncontrolled essential hypertension.

Vascular endothelium produces prostacyclin (PG12) and endothelium-derived vascular relaxing factor (EDRF), which are potent vasodilators and hence, may have a role in the regulation of blood pressure. Both PG12 and EDRF are readily degraded by free radicals, especially superoxide anion. Hence, we studied free radical generation and lipid peroxidation in patients with uncontrolled essential hypertension. It was observed that superoxide anion and hydrogen peroxide production by polymorphonuclear leukocytes (PMN) and the levels of lipid peroxides (measured by thiobarbituric acid assay) were higher in uncontrolled hypertensives compared to controls. Both free radical generation and the levels of lipid peroxides reverted to normal values when assayed after the control of hypertension. The calcium antagonist, verapamil, and beta-1 blocker, metoprolol, at the doses used inhibited free radical generation by phorbolmyristate acetate-stimulated PMNs. On the other hand, angiotensin II augmented free radical generation in normal PMN. In addition, it was also observed that both linoleic acid and arachidonic acid levels are low in the plasma of patients with hypertension compared to controls. These results suggest that increase in free radical generation by PMN and alterations in the plasma concentrations of essential fatty acids are closely associated with uncontrolled hypertension.

Angiotensin II↗
PubMed1999

Fatty acid uptake by cultured human keratinocytes grown in medium deficient in or supplemented with essential fatty acids.

Epidermal linoleic acid, i.e. essential fatty acid (EFA), is essential for cutaneous barrier function. Cultured human keratinocytes, routinely used for studies of lipid metabolism, are grown in a keratinocyte serum-free medium (KSFM), under conditions that reveal EFA-deficient cells. Here, fatty acid (FA) uptake was analysed in human adult keratinocytes grown either under EFA-deficient conditions [KSFM supplemented with 10% FCS (A) or 1% UltroserG (B)] or EFA-supplemented conditions [KSFM supplemented with a devised FA cocktail (C) or evening primrose oil (D)]. The FA composition of the total cellular lipid and major lipid fractions was analysed by gas chromatography. Cells grown with supplements A or B balanced their EFA-deficient state primarily with oleic acid. Cells grown with supplements C or D normalized to the epidermal FA composition in vivo with raised linoleic and lower oleic acid contents. When cells were grown longer than 48 h with supplements C or D decreased cell growth was observed. FA uptake was curvilinear with preference for linoleic over oleic acid under all culture conditions. The uptake of linoleic acid by cells cultured with supplement B was twice the uptake of those cultured with supplement A, while the uptake of oleic acid was similar under both culture conditions. Oleic acid uptake of cells cultured with supplement C or D was lower. These results show that the uptake of linoleic, but not that of oleic acid, is influenced by the extracellular FA composition, and that EFA-supplemented keratinocytes compared to EFA-deficient cells might serve as an in vitro model for the study of EFA metabolism.

Adult↗
PubMed1993

Essential fatty acid deficiency in parenterally fed preterm infants.

To determine the incidence of essential fatty acid (EFA) deficiency during short term fat-free parenteral nutrition, the authors investigated prospectively the EFA status of nine low birthweight (1145 +/- 343 g) preterm (28.2 +/- 1.9 weeks) infants, in whom delivery of dietary fat was delayed postnatally for 2-9 days. Serial determinations of plasma fatty acids showed that during fat-free alimentation, the major EFA, linoleic acid (LA), decreased rapidly (-0.75% total fatty acids per day), accompanied by a rise in endogenously produced non-essential fatty acid, eicosatrienoic acid (Mead acid). Essential fatty acid deficiency was confirmed biochemically by an elevation in the triene-tetraene ratio in six of the infants, only one of whom developed clinical symptoms. Abnormal fatty acid profiles were corrected within a few days of fat delivery by either intravenous or enteral routes. Essential fatty acids and their metabolites are involved in a wide range of physiological functions vital to postnatal growth and development. Depletion of these nutrients can be corrected by providing a minimum of 0.25 g LA/kg per day (equivalent to 0.50 g/kg per day of 20% intralipid or 30-50 mL/kg per day of breast milk).

Dietary Fats↗
PubMed1980

Glutamic acid transport in cortical synaptosomes from essential fatty acid deficient rats.

the sodium dependence of the high-affinity transport of glutamic acid in rat brain synaptosomes has been studied in animals maintained on a diet deficient in essential fatty acids (EFAD), and the results compared to similar studies with animals on a normal diet. Although the data give best fit to the same kinetic model as for control data, there are differences in the constants that describe the model. Except at low sodium concentrations, uptake is lower for the EFAD gorup. As a consequence of the differences in constants for the two groups, there are quantitative differences in the transport mechanism. The rate equation for the best fit model has been utilized to define certain functions in terms of dissociation and translocation constants, glutamate, sodium, and total carrier concentrations. These functions were calculated and utilized to compare the transport mechanism for the two groups. Although there are differences between these functions for control and EFAD animals, these differences are small and therefore of doubtful physiological significance.

Animals↗
PubMed1997

Essential fatty acid metabolism in cardiomyocytes grown in media enriched with different N-6/N-3 fatty acid combinations.

We have evaluated the effects of three different 18:3n-6, 20:5n-3 and 22:6n-3 fatty acid combinations on essential fatty acid (EFA) metabolism in rat cultured cardiomyocytes. The desaturating/elongating activities for linoleic (LA) and alpha-linolenic acid (ALA) were evaluated by radiolabeling the cells with 1-[14C]LA or 1-[14C]ALA and the fatty acid pattern of cardiomyocytes was assessed by gas chromatography. LA and ALA conversion to more unsaturated metabolites was reduced by increasing respectively n-3 and n-6 fatty acid concentration in the media. The all three combinations used reduced the saturated and increased the polyunsaturated fatty acid content of cardiomyocytes. The n-6/n-3 fatty acid ratio did not change compared to control cells in cardiomyocytes receiving the highest amount of 18:3n-6 and the lowest amounts of n-3 fatty acids. This combination may be suitable for modifying EFA desaturating/elongating activities without altering the physicochemical parameters which are related to the correct balance between n-6 and n-3 fatty acid content.

Animals↗
PubMed1987

Interaction of (n-3) and (n-6) fatty acids in desaturation and chain elongation of essential fatty acids in cultured glioma cells.

Recent research in various biological systems has revived interest in interactions between the (n-6) and (n-3) essential fatty acids. We have utilized cultured glioma cells to show that linolenic acid, 18:3(n-3), is rapidly desaturated and chain elongated; 20:5(n-3) is the major product and accumulates almost exclusively in phospholipids. We examined effects of various (n-6), (n-3), (n-9) and (n-7) fatty acids at 40 microM concentration on desaturation and chain elongation processes using [1-14C]18:3(n-3) as substrate. In general, monoenoic fatty acids were without effect. The (n-6) fatty acids (18:2, 18:3, 20:3, 20:4 and 22:4) had little effect on total product formed. There was a shift of labeled product to triacylglycerol, and in phospholipids, slightly enhanced conversion of 20:5 to 22:5 was evident. In contrast, 22:6(n-3) was inhibitory, whereas 20:3(n-3) and 20:5(n-3) had much less effect. At concentrations less than 75 microM, all acids were inhibitory. Most products were esterified to phosphatidylcholine, but phosphatidylethanolamine also contained a major portion of 20:5 and 22:5. We provide a condensed overview of how the (n-6) and (n-3) fatty acids interact to modify relative rates of desaturation and chain elongation, depending on the essential fatty acid precursor. Thus, the balance between these dietary acids can markedly influence enzymes providing crucial membrane components and substrates for biologically active oxygenated derivatives.

Animals↗
PubMed1980

The permeability barrier in essential fatty acid deficiency: evidence for a direct role for linoleic acid in barrier function.

Essential fatty acid (EFA) deficient rodents demonstrate abnormal epidermal permeability barrier function and differentiation, defects which can be corrected by either topical or systemic administration of linoleic acid. Since linoleic acid is a precursor of prostaglandins, correction of the defect in barrier function may either reflect a prostaglandin-mediated return toward normal epidermal differentiation, or, instead, a direct effect of linoleic acid. To test these possibilities severely EFA-deficient mice were pretreated daily with indomethacin and/or 5,8,11,14-eicosatetrayeonic acid, and then placed on normal (lineolic acid-supplemented) diets. Endogenous formation of prostaglandin E2 was determined by thin-layer chromatography after transformation into prostaglandin B2 with ethanolic-hydrochloric acid. Animals treated with both indomethacin and TYA DEMONSTRATED SUBSTANTIAL REDUCTIONS IN PROSTAGLANDIN E2 levels in liver and skin. Animals replenished with linoleic acid invariably demonstrated a rapid return of barrier function toward normal whether or not they were blockaded, while nonreplenished animals, with or without inhibition of prostaglandin biosynthesis, demonstrated continued deterioration in barrier function. In other experiments, topically applied linoleic acid rapidly reversed the defect in barrier function at the sites of application prior to systemic correction of the EFA deficient state. These results suggest that: (1) defective cutaneous barrier function in EFA deficiency can be corrected locally without prior systemic reversal of the deficiency state; and (2) that linoleic acid may play a direct role in the epidermal permeability barrier independent of its role in prostaglandin metabolism.

Animals↗
PubMed1981

[Studies of the effects of cis, cis and trans, trans-octadecadienoic acids on lipid metabolism in essential fatty acid deficient rats (author's transl)].

The effect of an essential fatty acid [EFA] deficiency in male Sprague-Dawley rats and its excerbation by inclusion of trans fatty acids in the diet were observed from the level and composition of serum lipoproteins. Male Sprague-Dawley rats were fed from weaning diet containing all essential nutrients and 10% of a fat supplement as safflower oil (SAFF] or hydrogenated coconut oil [HCO] for 28 weeks. At the end of 28 weeks, the blood was withdrawn from the retro-ocular plexes of 4 animals of each group, and lipoprotein lipid and fatty acids were analyzed. Another 5 animals of each group were switched to a 5% supplement of ethyl linolelaidate [TRANS]. In addition, the remaining 5 animals of HCO group were switched to SAFF diet. Lipoprotein lipid and fatty acid analyses were performed on the pooled serum in each group at 3, 7 and 14 days after switching the diet, and after 21 days serum was analyzed on the individual animal of each group. The results obtained were as follows: [1] With the development of an EFA deficiency in HCO group, there was a decrease in the high density lipoprotein [HDL] and increase in the very low density lipoprotein [VLDL] plus low density lipoprotein [LDL] fraction. [2] In a switching group from the SAFF to the TRANS supplement, the level of arachidonate in the serum lipid was decreased with a corresponding decrease in HDL, whereas linoleate, at least for the initial 3 weeks, decreased only in triglyceride fraction. [3] In a EFA deficient rat [HCO group] after switched to the TRANS supplement, HDL was further decreased and increase o VLDL-LDL was progressed. Consequently, the HDL: VLDL-LDL ratio was lowered strikingly. These changes in the EFA deficiency were accompanied by a large increase in monoenoic acids and a decrease in eicosatrienoic acid converted from oleic acid. [4] The administration of SAFF diet to the EFA deficient group induced a rapid increase in arachidonate in HDL, and decrease in eicosatrienoic acid and oleic acid. These changes were accompanied by a marked decrease in VLDL-LDL. It is suggested that the normal HDL might play an important role on catabolism of VLDL-LDL. These results suggest that polyunsaturated fatty acid, especially arachidonic acid rather than linoleic acid is essential to the formation and the function of HDL in the rats.

Animals↗
PubMed1987

Alpha-linolenic acid deficiency in man: effect of essential fatty acids on fatty acid composition.

Alpha-linolenic acid deficiency (ALAD) is described in five adults receiving long-term gastric tube feeding with a commercially available powdered formula mixed with water and/or skimmed milk. Three patients receiving the same powder mixed with whole milk showed no signs of essential fatty acid deficiency (EFAD). The patients showed scaly dermatitis and skin atrophy. In four patients, supplementing with cod liver oil and soya oil for 4 weeks normalized n-3 acids in plasma and red cells, while n-6 acids remained unchanged or decreased slightly. At the same time, skin changes were normalized. In the fifth patient, supplementing with ethyl linolenate started to normalize skin changes within 5 days, and after 2 weeks had increased the red cell concentration of 22:6n-3 threefold. Simultaneously, 20:4n-6 increased twofold, to above control level. Minimal daily requirement of alpha-linolenic acid and of long-chain n-3 acids is estimated to be 0.2% to 0.4% and 0.1% to 0.2% of calories, respectively.

Adult↗