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PubMed1994

The metabolism and availability of essential fatty acids in animal and human tissues.

Essential fatty acids (EFA), which are not synthesized in animal and human tissues, belong to the n-6 and n-3 families of polyunsaturated fatty acids (PUFA), derived from linoleic acid (LA, 18:2n-6) and alpha-linolenic acid (LNA, 18:3n-3). Optimal requirements are 3-6% of ingested energy for LA and 0.5-1% for LNA in adults. Requirements in LNA are higher in development. Dietary sources of LA and LNA are principally plants, while arachidonic acid (AA, 20:4n-6) is found in products from terrestrian animals, and eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) are found in products from marine animals. EFA are principally present in dietary triacylglycerols, which should be hydrolyzed by lipases in gastric and intestinal lumen. DHA seems to be released more slowly than the others. Its intestinal absorption is delayed but not decreased. Long-chain PUFAs are incorporated in noticeable amounts in chylomicron phospholipids. However, their uptake by tissues is no more rapid than uptake of shorter chain PUFA. In tissues, LA and LNA, which constitute the major part of dietary EFA, should be converted into fatty acids of longer and more unsaturated chain by alternate desaturation (delta 6, delta 5, delta 4)-elongation reactions. Animal tissues are more active in this biosynthesis than human tissues. Liver is one of the most active organs and its role is critical in providing less active tissues, particularly the brain, with long-chain PUFA secreted in VLDL (very low density lipoprotein). In liver, many nutritional, hormonal and physiological factors act on the PUFA biosynthesis. Dietary fatty acids exert a great influence and are often inhibitory. Dietary LNA inhibits delta 6 desaturation of LA. The desaturation products AA, EPA, and DHA inhibit delta 6 desaturation of LA and delta 5 desaturation of DGLA (dihomo-gamma-linolenic acid). With regard to hormones, insulin and thyroxin are necessary to delta 6 and delta 5 desaturation activities, whereas other hormones (glucagon, epinephrine, ACTH, glucocorticoids) inhibit desaturation. Concerning the physiological factors, the age of individuals is critical. In the fetus, the liver and the brain are capable of converting LA and LNA into longer-chain EFA, but these are also delivered by the mother, after synthesis in the maternal liver and placenta. Just after birth, in animals, the delta 6 desaturation activity increases in the liver and decreases in the brain. In aging, the capacity of the whole liver to desaturate LA and DGLA is equal at 1.5 and 25 months of age in rats fed a balanced diet throughout their life and the AA and DHA content of tissue phospholipids is unchanged in aging.(ABSTRACT TRUNCATED AT 400 WORDS)

Aging↗
PubMed1996

Protein utilization, growth and survival in essential-fatty-acid-deficient rats.

The relationship between essential fatty acids (EFA) deficiency and the utilization of dietary protein, growth rate and survival of offspring was investigated in rats during development and reproduction. EFA deficiency was induced by feeding a 200 g casein/kg-based diet containing 70 g hydrogenated coconut oil (HCO)/kg as the only source of fat. The conversion efficiency of dietary protein was assessed as net protein utilization (NPU), using a 10 d comparative carcass technique. Consumption of the deficient diet during the 10 d assay period induced biochemical changes characteristic of mild EFA deficiency in humans (triene:tetraene 0.27 (SD 0.04) compared with 0.026 (SD 0.004) for non-deficient controls), but there were no significant changes in growth rate or protein utilization. These variables were also unchanged when the deficient diet was fed for an additional 7 d before the assay, although triene:tetraene increased to 0.8 (SD 0.02). Feeding the deficient diet for 63 d before assay produced severe EFA deficiency (triene:tetraene 1.4 (SD 0.3) v. 0.036 (SD 0.005) for controls), a fall in growth rate (25% during assay period), and NPU (31.5 (SD 0.63) v. 39.0 (SD 0.93) for controls). These severely-EFA-deficient animals had a 30% higher fasting-resting rate of energy metabolism than that of age-matched controls. However, there was no change in the rate of endogenous N loss. Voluntary energy consumption was increased in animals fed on deficient diets, either with 200 g protein/kg, or protein free. The reduced efficiency of protein utilization could be entirely accounted for by the restricted amount of energy available for growth and protein deposition. Consumption of an EFA-deficient diet during pregnancy and lactation resulted in high mortality (11% survival rate at weaning compared with 79% for controls) and retarded growth in the preweaning offspring. It is concluded that animals are particularly sensitive to EFA deficiency during reproduction and pre- and post-natal stages of development. However, after weaning only severe EFA deficiency retarded growth, primarily through changes in energy balance.

Animals↗
PubMed1981

Essential fatty acid deficiency during total parenteral nutrition.

Essential fatty acid (EFA) deficiency has become a clinical problem since the advent of fat-free total parenteral nutrition (TPN). The following study was done to determine the minimum fat requirements for patients receiving continuous TPN solution. Seventy-seven patients who had 97 courses of TPN of at least 14 days duration were prospectively studied. The following fat supplementation was given: a) none, b) 10% soybean oil emulsion intravenously at fixed dosage, c) fat from an oral diet, or d) intravenous and oral fat. No patient was EFA deficient before the onset of TPN. EFA deficiency was prevented when at least 3.2% of total calories were given as intravenous fat or at least 15% as oral fat. Lesser amounts of fat decreased the rate of EFA deficiency development but did not prevent it from occurring. The 7.7 g/day of linoleic acid provided in 1000 ml per week of 10% soybean oil emulsion provides adequate fat to prevent EFA deficiency.

8,11,14-Eicosatrienoic Acid↗
PubMed1990

Non-shivering thermogenesis and brown adipose tissue activity in essential fatty acid deficient rats.

The effects of essential fatty acid (EFA) deficiency on energetic metabolism and interscapular brown adipose tissue (BAT) activity were examined in the cold acclimated rat. Weanling male Long-Evans rats were fed on a low fat semipurified diet (control diet, 2% sunflower oil; EFA deficient diet, 2% hydrogenated coconut oil) for 9 weeks. They were exposed at 5 degrees C for the last 5 weeks. In EFA deficient rats, compared to controls, growth retardation reached 22% at sacrifice. Caloric intake being the same in the two groups, it follows that food efficiency was decreased by 40%. Resting metabolism in relation to body surface area was 25% increased. Calorigenic effect of norepinephrine (NE) in vivo (test of non-shivering thermogenesis) underwent a marked decrease of 34%. BAT weight was 21% decreased but total and mitochondrial protein content showed no variation. A 26% increase in purine nucleotide binding per BAT (taken as an index of thermogenic activity) was observed, suggesting that the enhancement in resting metabolism observed was mainly due to increased BAT thermogenesis. However, BAT mitochondria respiratory studies which are more direct functional tests showed a marked impairment of maximal O2 consumption of about 30% with palmitoyl-carnitine or acetyl-carnitine (both in presence of malate) or with alpha-glycerophosphate as substrate. It is likely that this impaired maximal BAT oxidative capacity may explain the impaired NE calorigenic effect in vivo. A possible increase in mitochondrial basal permeability is also discussed.

Acclimatization↗
PubMed1975

Nutritional regulation of lipid metabolism in rats. VII. Effect of overnight fasting on liver lipids of rats fed different levels of essential fatty acids.

Effect of dietary levels of essential fatty acid (EFA), 20% corn oil, 5% corn oil, 20% lard and no fat, on the overnight fasting-induced changes in the concentration and composition of liver lipids of rats was investigated. The increase due to fasting in triglyceride (TG) was not observed when the liver previously contained relatively large amounts of the glyceride. In contrast, phospholipid levels were similarly and significantly increased. Overnight fasting induced increases in percentage of linoleic acid in TG and arachidonic acid in TG and arachidonic acid in phosphatidylcholine, the extents of those being nearly paralleled with decreasing dietary levels of EFA. These changes are interpreted as a reflection of the compensatory action of the body.

Animals↗
PubMed1987

Sex-related differences in desaturation and chain elongation of essential fatty acids studied in isolated rat hepatocytes.

When [14C]linoleic acid (18:2(n-6)) or [14C]dihomogammalinolenic acid (20:3(n-6)) was incubated with isolated liver cells from rats fed an essential fatty acid deficient diet, delta 6- and delta 5-desaturation, chain elongation and synthesis of 14C-labelled C14-C18 fatty acids (from [14C]acetate) were enhanced in female cells compared with male ones. No sex difference in total secretion of very low density lipoproteins (VLDL) was observed. However, VLDL secreted from female cells contained significantly more C16-C18 fatty acids than male cells. It is suggested that the observed sex differences, at least in part, may be related to the different content of fatty acid binding proteins in female cells compared with males.

8,11,14-Eicosatrienoic Acid↗
PubMed1989

Essential fatty acids in clinical dermatology.

A deficiency of essential fatty acid intake can produce severe cutaneous abnormalities but is exceedingly rare in clinical practice. Recent research has shown that abnormalities in essential fatty acid metabolism may play a role in atopic eczema, acne, and psoriasis. Therapeutic innovations have already resulted from this knowledge, and more are likely to emerge.

Acne Vulgaris↗
PubMedDate not supplied

Effects of low-zinc status and essential fatty acid deficiency on growth and lipid composition of rat brain.

1. Nineteen-day old female weanling rats were maintained on diets deficient in essential fatty acids, low in zinc (6 p.p.m.) or both deficient in essential fatty acids and low in zinc; the weights of their brains were 25.6, 35.0 and 43.2% respectively, less than those of rats on control diets. 2. In essential fatty acid deficiency, the myelin lipids cerebrosides and sphingomyelin were considerably reduced in proportion whereas zinc deficiency had no significant effect on the proportions of the lipids. 3. Essential fatty acid deficiency was also characterized by the appearance of a high proportion of eicosatrienoic acid (20:3) and the reduction of arachidonic acid (20:4) and the other essential fatty acids. In zinc deficiency, however, there was an accumulation of arachidonic acid. 4. The low-zinc status aggravated essential fatty acid deficiency causing a higher reduction in the proportion of the myelin lipids and the accumulation of both eicosatrienoic and arachidonic acids. 5. It is considered that zinc plays some role in the metabolism of essential fatty acids in brain lipids and the pathological effect of the double deficiency of essential fatty acids and zinc causes a greater impairment to brain development and maturation than either of the single deficiencies.

Animals↗
PubMed1992

A high-density-lipoprotein receptor appears to mediate the transfer of essential fatty acids from high-density lipoprotein to lymphocytes.

It has been shown previously that a specific high-density lipoprotein (HDL) receptor exists on human lymphocytes that recognizes apoprotein (apo) A1 as its ligand, and may be responsible for utilization of HDL lipids to respond optimally to mitogenic stimulation when cultured in serum-free medium supplemented with HDL. To clarify further the relationship between various HDL lipids used by lymphocytes and HDL receptor activity, the lipid composition of the cells and the regulation of HDL and low-density lipoprotein (LDL) receptors on freshly isolated lymphocytes and mitogen-activated T-blasts after treatment with lipoproteins, liposomes or fatty acids were investigated. Our data show that the linear increase in cell proliferation correlates with the presence of HDL in fatty-acid-free culture medium in the concentration range of HDL receptor saturation. Decreased binding/uptake of dioctadecylindocarbocyanine (DiI)-fluorescence-labelled HDL by freshly isolated lymphocytes was observed in the presence of unlabelled HDL in 4-day culture, whereas T-blast binding/uptake was down-regulated by preincubation not only with HDL but also with LDL. T-blasts pretreated with HDL showed increased cellular contents of phosphatidylcholine, oleic acid (C18:1,n-9) and linoleic acid (C18:2,n-6), which are essential for optimal proliferation of mitogen-stimulated lymphocytes. Furthermore, DiI-HDL binding on lymphocytes was down-regulated by up to 20% (resting T cells) and 50% (T-blasts) when cultured in the presence of apoA1-phosphatidylcholine liposomes (T-blasts only), oleic acid or linoleic acid, but not by stearic acid (C18:0). The results indicate that HDL provide lymphocytes with essential fatty acids, which in turn regulate HDL receptor activity.

Adult↗
PubMed1982

Effect of essential fatty acid deficiency on lipids of rat Sertoli and germinal cells.

The effect of essential fatty acid deficiency on lipids of separated rat Sertoli and germinal cells was determined at various time intervals after the animals were placed on a fat-free diet. Alterations in the fatty acid composition typical of essential fatty acid deficiency were noted in the Sertoli cells as well as in germinal cells as early as Days 9-14 on the fat-free diet. These changes included increased concentrations of oleic acid (18:1W9)2 and the appearance of 20:3W9. In some of the rats there were also decreases in linoleic (18:2W6) and arachidonic acids ((20:4W6), but no significant differences were found between Sertoli and germinal cells. Feeding a corn oil diet to rats previously maintained on a fat-free diet for 4 weeks reversed the changes in fatty acid composition of both Sertoli and germinal cells at the times studied. Lipid changes in phospholipids closely reflected those observed in the total lipids. These early changes in Sertoli cell lipids caused by an essential fatty acid deficiency may have important consequences since the Sertoli cell lipids caused by an essential fatty acid deficiency may have important consequences since the Sertoli cells play a significant role in the spermatogenic process.

Animals↗
PubMed1978

Essential fatty acid requirements in infancy.

The view expressed by Cuthbertson that essential fatty acid needs of human infants have been overestimated is contested. In our view Cuthbertson's assessment of essential fatty acid requirements of infants is too low because 1) consideration of the omega3 fatty acids is omitted; 2) the biological value of long-chain essential fatty acids is wrongly assessed; and 3) the significance of variations in composition of random human milk samples is misunderstood.

Animals↗
PubMed1984

Effects of essential fatty acids on prostaglandin biosynthesis.

Prostaglandins (PGs) are derived from dietary essential fatty acids (EFAs) by relatively short biochemical pathways. PG synthesis can be manipulated by modifying EFA intake. PGs and related compounds of the 1 and 3 series have desirable or neutral actions while those of the 2 series are mixed, some being desirable but others being highly undesirable. Methods for selectively increasing 1 and 3 series products while simultaneously reducing the formation of arachidonic acid derivatives are described.

Animals↗
PubMed2001

Studies on the metabolism of essential fatty acids in isolated human testicular cells.

The essential fatty acid 22:6(n-3) is a minor component of the Western diet, but a major fatty acid in human testis and semen. In mature spermatozoa, the physical and fusogenic properties of the plasma membrane are probably influenced by its particular fatty acid composition. In this study, the synthesis of 22:6(n-3) and 22:5(n-6) was investigated in isolated human testicular cells. [1-(14)C]20:4(n-6), [1-(14)C]20:5(n-3), [1-(14)C]22:4(n-6) and [1-(14)C]22:5(n-3) were incubated in a 'crude' cell suspension (consisting of a mixture of the cells in the seminiferous tubule), and in fractionated pachytene spermatocytes and round spermatids. The esterification of fatty acids in lipid and phospholipid classes and the fatty acid chain elongation and desaturation were measured. The crude cell suspension metabolized the fatty acids more actively than did the fractionated germ cell suspension, indicating that types of cell other than the germ cells are important for fatty acid elongation and desaturation and thus the production of 22:6(n-3). This finding is in agreement with previous results in rats that indicated that the Sertoli cells are the most important type of cell for the metabolism of essential fatty acids in the testis. Some [1-(14)C]20:5(n-3) was elongated to [(14)C]22:5(n-3) in the fractionated germ cells, but very little was elongated further to [(14)C]24:5(n-3),possibly restricting the formation of [(14)C]22:6(n-3). In the fractionated germ cells, the fatty acid substrates were recovered primarily in the phospholipid fraction, indicating an incorporation in the membranes, whereas in the crude cells, more substrates were esterified in the triacylglycerol fraction. In the phospholipids, more radioactivity was recovered in phosphatidylcholine than in phosphatidylethanolamine and more radioactivity was recovered in phosphatidylethanolamine than in phosphatidylinositol or phosphatidylserine.

Esterification↗
PubMed1984

Essential fatty acid status and characteristics associated with colostrum-deprived gnotobiotic and conventional lambs. Growth, organ development, cell membrane integrity and factors associated with lower bowel function.

A factorial experiment involving gnotobiotic (GN) and conventional (CV) colostrum-deprived lambs and diets formulated to be adequate or deficient in linoleic acid was conducted to determine the effect(s) of the intestinal microflora on the essential fatty acid (EFA) status of the host and subsequent physiological consequences, i.e., growth, organ development, cell membrane integrity and lower bowel function. Lambs were obtained by sterile surgical procedures and housed in sterile isolators or in conventional metabolism stalls for 60 d. Skimmed cow's milk with 6% hydrogenated coconut oil and vitamins A, D and E added with and without .32% of the total calories as linoleic acid was homogenized, bottled and autoclaved, then fed to appetite three to four times daily. The GN lambs supplemented with linoleic acid gained significantly faster between 13 and 41 d of age and more efficiently between 27 and 41 d than the other treatment groups. The absence of dietary linoleic acid decreased liver and spleen weights and, in general, suppressed development of organs except the brain. Red blood cell hemolysis was not affected by treatment. Although showing signs of chronic mild diarrhea, the GN neonatal ruminant differed in Cl- concentration and dry matter percentage of its lower bowel contents from the "classic rodent model." The results indicate that neonatal colostrum-deprived lambs have an EFA requirement, as evidenced by decreased growth and performance characteristics in the GN linoleic deficient vs GN supplemented group, and suggests that the required level is in excess of .32% of the total caloric intake as linoleic acid.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Essential fatty acid deficiency in rats: effects on arachidonate metabolism, generation of cyclooxygenase products and functional responses in neutrophils.

Linoleic and arachidonic acid concentrations in neutrophils from rats maintained on a diet with only 0.3% of the energy content as essential fatty acid (EFA, EFAD group) were reduced by 70 +/- 2.2% and 34.8 +/- 5.2%, respectively, compared with controls fed a diet with a normal 3% EFA content. Neutrophil chemiluminescence and aggregation induced by f-Met-Leu-Phe was substantially reduced in the EFAD group. Production of 6-keto-prostaglandin F1 alpha and thromboxane B2 were significantly lower in the EFAD neutrophils when stimulated by the ionophore A23187, whereas there was no difference when leukotriene B4 was used as stimulus.

Animals↗