POSITION OF EICOSATRIENOIC ACID IN THE PHOSPHATIDYLCHOLINE AND PHOSPHATIDYLETHANOLAMINE FROM RATS DEFICIENT IN ESSENTIAL FATTY ACIDS.
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Fish oil supplementation and essential fatty acid deficiency reduce nitric oxide synthesis by rat macrophages.
Both fish oil-derived omega-3 polyunsaturated fatty acid (omega 3 PUFA) supplementation and essential fatty acid (EFA) deficiency have been shown to exert anti-inflammatory effects and, hence, to ameliorate immune-mediated glomerulonephritis. The mechanisms underlying these effects include alterations in the production of eicosanoids, cytokines (that is, tumor necrosis factor, TNF-alpha) and reactive oxygen species by blood borne cells. Because, in addition to these mediators nitric oxide (NO) is also implicated in glomerular injury, we have examined if both diets affected macrophage NO production as well. Rats were fed a standard chow, an omega 3 PUFA-supplemented diet, or an EFA-deficient diet for six weeks before resident peritoneal macrophages were isolated. These cells were exposed to lipopolysaccharide (LPS) and the NO metabolite, nitrite (NO2-), was measured in the medium using the Griess reagent. Release of NO2- was enhanced by LPS in a dose-dependent manner. With 10 ng/ml LPS challenge, NO2- release was reduced by 37% and 57% by omega 3 PUFA supplementation and EFA deficiency, respectively. NO2- returned to control levels two weeks after the end of diet. Macrophage production of TNF-alpha responded in a similar manner. Diet-induced reduction of NO2- release was neither attributable to a reduction of inducible NO synthase mRNA levels as shown by Northern blot analysis, nor to an increased competition of NO synthase and arginase for the substrate (L-arginine). Indeed, arginase activity of macrophages was even slightly reduced by both omega 3 PUFA-supplemented diet and EFA-deficient diet.(ABSTRACT TRUNCATED AT 250 WORDS)
Amino Acid Oxidoreductases↗
Magnesium deprivation or short-term essential fatty acid deficiency in rats: effects on serum lipids, platelet fatty acid composition and arachidonic acid incorporation into platelet phospholipids.
The aim of this study was to evaluate the effect of short-term magnesium or essential fatty acid (EFA) deficiencies on plasma lipids, platelet fatty acid composition and [1-14C] arachidonic acid incorporation into platelet phospholipids. Weanling rats were fed purified diets (casein 20%, sucrose 70.5%, lipid 5%) for two weeks. The control and magnesium-deficient diets included corn oil as lipid source. The EFA-deficient diet included hydrogenated coconut oil. The fatty acid composition of serum lipids confirmed the linoleic acid deprivation in the EFA-deficient group. Significant changes in platelet fatty acid composition occurred in this limited period of time and arachidonic acid incorporation into platelet lipids was markedly increased. Magnesium deficiency induced hyperlipaemia. A significant decrease in the percentage of arachidonic acid in total serum lipids was observed, but fatty acid profile appeared quite different in the two deficiencies. In magnesium-deficient rats, the alteration in fatty acid composition of serum lipids was not associated with similar changes in fatty acid composition of platelet lipids. Arachidonic acid incorporation into platelet lipids was markedly increased in magnesium deficient animals as compared to control group. Relatively more arachidonic acid was incorporated into phosphatidylcholine and phosphatidylinositol when magnesium-deficient or EFA-deficient animals were compared to the control group.
Animals↗
Enhancement of endocrine pancreatic secretions by essential fatty acids.
Recent studies have suggested the beneficial effects of essential fatty acids in postoperative patients receiving total parenteral nutrition. While there is abundant information on the role of glucose and amino acids on insulin release, the effect of essential fatty acids on endocrine pancreatic secretions is not clear. Since linoleic and linolenic acids are constituents of TPN solutions as well as dietary fat, our aim was to examine their effect on the endocrine pancreatic function, using isolated islets. In each experiment, six islets microdissected from three mice were preperifused at the rate of 1 ml/min with Krebs-Ringer bicarbonate (KRB) buffer pH 7.4 containing 2% bovine albumin and 5.5 mM glucose (basal) with continuous supply of 95%/5%, O2/CO2 for 1 hr, after which basal samples were collected on ice every minute. The perifusion was continued for 20 min after the addition of a mixture of 10 mM linoleic acid and 5 mM linolenic acid to the KRB. During each perifusion phase, effluent samples were also collected for insulin and glucagon assay. The mean integrated area under the curve/20 min showed an increase in both insulin and glucagon secretions with the addition of fatty acids. Hence insulin increased from a basal 3154.8 +/- 953.7 to 8393.0 +/- 2073.1 pg (P less than 0.025, n = 6) and glucagon increased from 193.7 +/- 46.9 to 1566.1 +/- 411.2 pg (P less than 0.0025, n = 5). The fatty-acid-induced insulin but not glucagon secretion was blocked by the addition of 2 mM palmoxirate an inhibitor of fatty acid oxidation.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Essential fatty acid requirements in infancy.
The infant's requirements for essential fatty acids (EFA) have been calculated by different workers from the same limited number of observations which depended on the use of butterfat, linoleic acid, and its esters as the source of EFA. The linoleic acid content of the butterfat employed was determined by a method of known not to be specific for the biologically active linoleic acid (cis cisC18:2omega6). The assay reported (3.3%) is about double that (1+01.6%) usually anticipated. If the butterfat used was actually of average linoleic acid content, then estimates of requirements are about twice the true values. In some tests, linoleic acid or its esters were used rather than fat or triglycerides. In other tests the total fat content of the diet was very low, and the tocopherol content of the diet was not controlled. All of these factors could adversely affect linoleic acid utilization and so exaggerate EFA requirements. If minimum EFA needs are as high as those suggested (1.0%) of cal), deficiency should be commoner than it in fact is. For the reasons noted above it is believed that the minimum requirements for EFA have been set far too high and are in fact less than 0.5% of cal, so that a daily allowance of 65 mg/100 cal (about 0.6% cal) should provide an ample margin of safety.
Animals↗
Retinoic acid stimulates essential fatty acid-supplemented human keratinocytes in culture.
The effect of all-trans retinoic acid on the proliferation of essential fatty acid (EFA)-deficient and of EFA-supplemented adult human keratinocytes was investigated. EFA-deficient cell strains were supplied with one of four different fatty acid-supplemented media at the P0 to P1 passage. All-trans retinoic acid at 0.5 or 1.0 microM was added to the cultures at the P1 to P2 passage. At passage P3, and 3 and 7 d thereafter, the cell growth rate was determined. The fatty acid content of cultures grown in each medium was measured using gas chromatography. All the EFA media "normalized" the cellular fatty acid composition and drastically decreased the cell number and total DNA and protein of the cultures. All-trans retinoic acid at 1 microM prevented the loss of cell viability and growth usually associated with EFA supplementation but did not affect the control (EFA deficient) or 18:1 fatty acid-supplemented cultures. All-trans retinoic acid at 1 microM altered the fatty acid content of the EFA-supplemented cultures. A statistically significant increase in 14:0, 14:1, 16:1, 18:1, and 20:4 fatty acids occurred, whereas the amounts of 18:0 and 18:2 fatty acids decreased. The largest changes were in 16:1 fatty acid (8-14%) and 18:2 fatty acid (12-5%). All-trans retinoic acid at 0.5 microM also affected both cell growth and fatty acid composition without induction of the CRABP II message. These studies demonstrate that all-trans retinoic acid stimulates the growth of EFA-supplemented keratinocyte cultures while also altering the fatty acid composition of the cells.
Adult↗
[Essential-fatty-acid deficiency syndrome in man].
The syndrome of essential fatty acid deficiency was first described in rats in 1929. Not before 1958, a corresponding syndrome was observed in infants after administration of cow's milk over longer periods of time. Until recently, the syndrome of essential fatty acid deficiency in adults was completely unknown. In 1970, it was reported in a 44-year-old male patient who had received fatfree parenteral nutrition for 70 days. In its course, a desquamative exanthema developed which completely remitted after administration of linoleic acid. Between 1970-1973, we observed two patients who developed hyperkeratotic dermatoses after long-term administration of a synthetic formula diet (Vivasorb). The lack of essential fatty acids could also be demonstrated in gas-chromatographic studies of the course of the process.
Adult↗
Polyethenoid fatty acid metabolism. VI. Effect of pyridoxine on essential fatty acid conversions.
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Fatty Acids↗
Importance of essential fatty acids and their derivatives in poultry.
More than thirty-five years have passed since essential fatty acid requirements were demonstrated for poultry. Subsequent studies were conducted to establish a recommended level of linoleic acid for growing poultry. Although a requirement of 1% linoleic acid is suggested, a critical evaluation of the nutritional and metabolic significance of essential fatty acids is lacking. Perhaps alpha-linolenic acid is also essential, but direct evidence is not yet available. Recent literature indicates that several individual fatty acids, including the polyunsaturates derived from essential fatty acids, are biologically active. Furthermore, the numerous eicosanoids biosynthesized from specific polyunsaturates act as either cellular autocrine or paracrine signaling agents. Formation of eicosanoids is ubiquitous in tissues and organs, and these compounds influence nearly all systems in mammalian species. However, although such compounds have been studied extensively in mammalian systems, the formation of polyunsaturates, the biosynthesis of eicosanoids and the biological effects of these compounds have not been intensely studied in domestic poultry.
Animal Nutritional Physiological Phenomena↗
Essential fatty acid metabolism in cultured human airway epithelial cells.
To characterize essential fatty acid metabolism of human airway epithelium, we examined the capacity of epithelial cells to incorporate and desaturate/elongate 18:2(n - 6) and the turnover of phospholipid fatty acyl chains in these cells. Epithelial cells were cultured for 5-7 days and incubated with [1-14C]18:2(n - 6) (1 microCi, 100 nmol). The essential fatty acid profile of the cells was readily modified by 18:2(n - 6) supplementation to culture medium. After 4 h incubation, 32 +/- 5.6 nmol of [1-14C]18:2(n - 6) was incorporated into phospholipids (65 +/- 9.5%, of which 74% was incorporated into phosphatidylcholine (PC)) and neutral lipid (31 +/- 10%) per mg protein of cultured cells. 30 +/- 8% of [1-14C]18:2(n - 6) incorporated, was converted to homologous trienes, tetraenes and pentaenes, the major products being 20:3(n - 6) and 20:4(n - 6). The conversion of 18:2(n - 6) was time-dependent and donor age-related. A higher proportion of 20:3(n - 6) and 20:4(n - 6) was incorporated into phosphatidylinositol (PI) and phosphatidylethanolamine (PE). About 10-15% of total products formed from 18:2(n - 6) was released from membrane to culture medium. Both 20:4(n - 6) and 20:5(n - 3) inhibited 18:2(n - 6) incorporation and desaturation. Rate of incorporation of 18:2(n - 6) was more than either 18:1(n - 9) or 16:0. With pulse-chase studies, the half-life of 18:2(n - 6) in PC, PI and PE was estimated to be 5.5, 6.0 and 7.3 h, respectively. These data indicate active metabolism of essential fatty acids in human airway epithelial cells. This metabolism may play a key role in the regulation of membrane properties and function in these cells.
Carbon Radioisotopes↗
Do essential fatty acids play a role in brain and behavioral development?
The membrane phospholipids of the brain contain high levels of polyunsaturated fatty acids (PUFA), particularly arachidonic acid, 20:4n-6 and docosahexaenoic acid, 22:6n-3. These long-chain PUFA are synthesized from their respective essential fatty acid (EFA) precursors, linoleic acid, 18:2n-6 and linolenic acid, 18:3n-3. Although the necessity of n-6 fatty acids for optimum growth has been established, a similar requirement for those of the n-3 family is less clear. The rapid accumulation of the long-chain n-3 PUFA in the brain during prenatal and preweaning development suggests that the provision of n-3 fatty acids to the developing brain may be necessary for normal growth and functional development. The intent of this review is to assess the experimental work which addresses this question, most of which has been conducted on rodents. The emphasis will be on studies which measure behavioral outcomes, and particular attention will be paid to methodological issues which affect the interpretation of these data. An integration of the research findings will be presented and discussed in light of possible implications for therapeutic interventions.
Animals↗
Essential fatty acid deficiency profiles in idiopathic immunoglobulin A nephropathy.
The profiles of fatty acids (FAs) of plasma phospholipids (the compartment reflecting the essential FA status of tissue lipids), nonesterified FAs (the precursor pool for autacoid synthesis), urine protein excretion, and glomerular filtration rate were measured before and after supplementation with fish oil in 15 patients with immunoglobulin A nephropathy. In the FA profiles, there was deficient 18:3 omega 3 (alpha-linolenic acid), the parent compound of omega 3 polyunsaturated FA, and deficient chain elongation products of both omega 3 and omega 6 polyunsaturated FAs with replacement by saturated and monounsaturated short-chain, odd-chain, and branched-chain FAs, producing significant loss of omega 3 FA. These alterations indicate nutritional or functional (omega 3) and metabolic (omega 6) deficiencies. Additionally, the mean melting point of the FAs was significantly increased, implying an inherent decrease in cell membrane fluidity. Enhancement of 20: 5 omega 3 (eicosapentaenoic acid) and 22:6 omega 3 (docosahexaenoic acid) and suppression of 20:4 omega 6 (arachidonate) after supplementation with fish oil were accompanied by important decreases in proteinuria and improved glomerular filtration rate. Omega-3 polyunsaturated FAs may favorably influence immunoglobulin A nephropathy through a modulation of the pathologic actions of the omega 6 eicosanoids and other diverse actions on various mediators produced by an initial immune injury.
Adult↗
Essential fatty acids are antagonists of the leukotriene B4 receptor.
A series of essential fatty acids and fatty acid derivatives were evaluated for their ability to inhibit [3H] leukotriene B4 (LTB4) binding to pig neutrophil membranes. The fatty acids varied in chain length, extent of unsaturation, position of unsaturation, and isomerization. Generally, fatty acids with two or more unsaturated sites and chain lengths of 18-22 were potent inhibitors of [3H]LTB4 binding; both n-3 and n-6 fatty acids were inhibitory. The most potent compounds tested were homogammalinolenic acid and ricinelaidic acid which gave Ki values of 1 microM and 2 microM in the binding assay. Ricinelaidic acid was also tested for its ability to inhibit LTB4-mediated chemotaxis (IC50 = 10 microM) and LTB4-induced calcium fluxes (IC50 = 7 microM) in isolated human neutrophils. Ricinelaidic acid did not show agonist activity in these assays. In an in vivo model of LTB4-induced bronchoconstriction, ricinelaidic acid and homogammalinolenic acid gave 46% and 53% inhibition, respectively, at a 1 mg/kg i.v. dose. These results indicate that essential fatty acids are LTB4 receptor antagonists, which may account in part for their reported anti-inflammatory activities.
8,11,14-Eicosatrienoic Acid↗
Effect of corticosteroids and eicosapentaenoic acid/docosahexaenoic acid on pro-oxidant and anti-oxidant status and metabolism of essential fatty acids in patients with glomerular disorders.
It is known that the concentrations of essential fatty acids and their metabolites including eicosanoids, free radicals and anti-oxidants are altered in glomerular disorders. Both corticosteroids and n-3 fatty acids--eicosapentaenoic acid and docosahexaenoic acid (EPA and DHA respectively)--are useful in the management of glomerular disorders. In the present study, the altered plasma concentrations of lipid peroxides, nitric oxide and the metabolites of essential fatty acids and anti-oxidants--superoxide dismutase, glutathione peroxidase and vitamin E--in the RBC membranes of patients with glomerular disorders (nephrotic syndrome) reverted to normalcy following corticosteroids or EPA/DHA administration. This suggests that the beneficial actions of corticosteroids and EPA/DHA in glomerular disorders can be attributed to their action on the pro-oxidant and anti-oxidant concentrations and metabolism of essential fatty acids.
Adrenal Cortex Hormones↗
The essential fatty acid status in phenylketonuria patients under treatment.
Phenylketonuric patients are on a special diet that lacks certain essential fatty acids. This study evaluates the essential fatty acid status of a group of phenylketonuric patients in the Netherlands undergoing dietary treatment. To this end, the essential fatty acid status of nine phenylketonuria patients was studied. On the basis of age and gender, two control subjects were selected for each patient. The essential fatty acid composition of duplicate food portions and the essential fatty acid status of plasma and erythrocytes were analyzed. Phenylketonuria subjects had a different essential fatty acid profile from their peers, especially concerning the n-3 fatty acids. N-6 and n-3 fatty long-chain polyenes were hardly consumed by phenylketonuria subjects, in contrast to the control subjects. Linoleic acid, on the other hand, was consumed in significantly higher amounts by phenylketonuria subjects and made up about 40% of their daily fat consumption. The essential fatty acid consumption pattern of the phenylketonuria subjects is mirrored by the essential fatty acid concentrations in blood. The essential fatty acid status of the phenylketonuric diet should be improved in order to prevent deficiency in n-3 fatty acids.
Journal Article↗
Modification of fluidity and lipid-protein relationships in pig intestinal brush-border membrane by dietary essential fatty acid deficiency.
The effect of dietary essential fatty acid (EFA) deficiency on the dynamic molecular organization of pig intestinal brush-border membrane (BBM) was studied using purified BBM vesicles. A 6 week dietary treatment of weaning piglets induced a typical EFA-deficient pattern in the lipid composition of both plasma and epithelial membranes. In pigs fed on the EFA-deficient diet, the plasma 20:3(n - 9)/20:4(n - 6) ratio progressively increased and reached a stable value after 3 weeks of experiment, whereas it remained low (less than 0.2) in controls. In the intestinal BBM, the cholesterol/protein, phospholipid/protein and consequently the cholesterol/phospholipid ratios, as well as the phospholipid class distribution, were unchanged. In particular, the sphingomyelin/phosphatidylcholine (SM/PC) molar ratio was not affected. However, the fatty acid composition of phospholipid main classes was markedly modified, leading to decreased lipid fluidity and to a large change in membrane protein behaviour with EFA deficiency. These findings could be interpreted in terms of reduced lipid-protein interactions. Moreover, the increasing gradient of fluidity which took place within the lipidic matrix from its surface was modified by the dietary treatment, as fluidity was lowered by EFA deficiency at different depths of the layer.
8,11,14-Eicosatrienoic Acid↗
Pancreatic function in the essential fatty acid deficient rat.
The influence of essential fatty acid (EFA) deficiency on pancreatic endocrine and exocrine function was studied in 120-day-old rats. The plasma insulin response was determined after in vivo administration of glucose and arginine. The plasma glucagon response was assessed after infusion of arginine. Islet peptides were examined by immunocytochemistry. The exocrine function of pancreas was studied by amylase secretion in isolated pancreatic acinar cells after stimulation with the cholinergic agonist carbacholine chloride. The EFA-deficient (EFAD) rats showed higher basal plasma insulin concentrations and lower basal glucose levels than control rats (P less than .01 and P less than .01, respectively). The plasma insulin response to glucose was potentiated in the EFAD rats (P less than .001). Both insulin and glucagon responses to arginine were normal. The isolated pancreatic acinar cells showed a low basal amylase secretion, but a normal response to carbacholine chloride. There were no overt morphological changes seen in the pancreas and the immunocytochemical staining pattern of insulin, glucagon, somatostatin, and pancreatic polypeptide cells did not differ from controls. The results of the study show that the secretory function of the endocrine and exocrine pancreas is operational in EFA deficiency. The EFA deficiency was accompanied by a basal hyperinsulinemia and hypoglycemia and an exaggerated insulin response to glucose, the pathophysiology of which has to be further studied.
Amylases↗
Normalization by dietary cod-liver oil of reduced thrombogenesis in essential fatty acid deficient rats.
Rats, deficient in essential fatty acids (EFA), were given diets containing 5 energy% sunflowerseed oil (SO, rich in linoleic acid), cod-liver oil (CLO, rich in timnodonic acid and cervonic acid), or hydrogenated coconut oil (HCO), containing no EFAs at all. SO and CLO feeding resulted in normalization of the reduced arterial thrombus formation in EFA-deficient animals. SO feeding was associated with the normalization of the arachidonic acid content of platelet phospholipids. CLO feeding did not have this effect but greatly increased the availability of timnodonic acid (EPA) and cervonic acid (DHA). Further research is required to investigate whether these changes in fatty acid composition can be hold responsible for the normalizing effect of dietary CLO on the disturbed arterial thrombosis tendency in EFA deficient rats, possibly via the formation of eicosanoids.
Animals↗