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At least 19 recordsLinked to original sources
PubMed1988

Reversible phenotypic modulation induced by deprivation of exogenous essential fatty acids.

Essential fatty acid deficiency, produced by deprivation of omega-6 and omega-3 fatty acids, is a condition characterized by renal disease, dermatitis, and infertility. Although many of the biochemical aspects of this disorder have been investigated, little is known about the ultrastructural changes induced by essential fatty acid deficiency. Using a unique fatty acid-deficient cell line (EFD-1), which demonstrates the in vivo fatty acid changes of essential fatty acid deficiency, and the prostaglandin E2-producing mouse fibrosarcoma line from which it was derived (HSDM1C1), we correlated ultrastructural and biochemical changes induced by prolonged deprivation of all exogenous lipids and subsequent repletion of selected essential fatty acids. We found that in cells deprived of all exogenous lipids, there was dilation of rough endoplasmic reticulum and an associated defect in protein secretion; these changes were specifically reversed by arachidonate. There was also an accumulation of secondary lysosomes containing degraded membranes in these cells with an associated increase in phospholipids relative to parent HSDM1C1 cells. Cytoplasmic lipid bodies present in parent cells disappeared, with an associated decrease in triacylglycerol. After just 2 days in lipid-free medium, all these changes were apparent, and prostaglandin E2 production was markedly impaired despite normal amounts of cellular arachidonate. Incubation of EFD-1 cells with arachidonate, the major prostaglandin precursor fatty acid, induced a reversion to the HSDM1C1 phenotype, whereas other fatty acids were totally ineffective. These results indicate changes in fatty acid metabolism in essential fatty acid deficiency are associated with marked alterations in ultrastructure and secretion of protein from cells.

Animals↗
PubMed1976

Rat testicular lipids and dietary isomeric fatty acids in essential fatty acid deficiency.

Weanling rats were fed essential fatty acid-deficient diets, either completely fat-free, or with partially hydrogenated fish oil (PHFO, 28 wt %), or with fractions derived from PHFO containing primarily positional isomers of trans-eicosenoate (20:1, 3 wt %) or trans-docosenoate (22:1, 3 wt %). Control animals were fed a peanut oil-containing diet (28 wt %). After 5 or 15 weeks on the diet, the content of neutral and phosphorus-containing lipids in the testes was determined. The fatty acid distribution in major lipid classes was analyzed for animals fed the diets for 15 weeks. The testicular stage of maturation or degeneration was assessed by histology. The group fed PHFO exhibited signs of complete testicular degeneration, or lack of maturation, already after 5 weeks, whereas the animals on the diets with the very long chain monoenoic acids suffered severe degenerations only after 15 weeks. In the PHFO-fed rats, a sharp decline in the concentration of testicular triacylglycerols was observed. In all of the essential fatty acid-deficient groups, an increase in testicular sphingomyelin was observed. Cholesterol levels were fairly similar among all dietary groups. The total testicular fatty acids of the PHFO-fed animals contained somewhat more eicosadienoic acid than found in the other groups, and somewhat less (n-9)-acids. In all EFA-deficient groups, (n-6)-acids were lowered, in particular in triacylglycerols and phosphatidyl cholines. The PHFO group did not show a lower (n-6)-concentration than the other deficient groups, in spite of the more severe symptoms of deficiency. There was no evidence of a major accumulation of long chain isomeric fatty acids in the degenerated testes of the PHFO-, 20:1-, and 22:1-fed groups.

Animals↗
PubMed1990

Role of the blood-brain barrier in the formation of long-chain omega-3 and omega-6 fatty acids from essential fatty acid precursors.

Elongated, more highly polyunsaturated derivatives of linoleic acid (18:2 omega-6) and linolenic acid (18:3 omega-3) accumulate in brain, but their sites of synthesis and mechanism of entry are not well characterized. To investigate the role of the blood-brain barrier in this process, cultured murine cerebromicrovascular endothelia were incubated with [1-14C]18:2 omega-6 or [1-14C]18:3 omega-3 and their elongation/desaturation products determined. The major metabolite of 18:2 omega-6 was 20:4 omega-6, whereas the primary product from 18:3 omega-3 was 20:5 omega-3. Although these products were found primarily in cell lipids, they were also released from the cells and gradually accumulated in the extracellular fluid. Eicosanoid production was observed from the 20:4 omega-6 and 20:5 omega-3 that were formed. No 22:5 omega-6 or 22:6 omega-3 fatty acids were detected, suggesting that these endothelial cells are not the site of the final desaturation step. Although the uptake of 18:3 omega-3 and 18:2 omega-6 was nearly identical, 18:3 omega-3 was more extensively elongated and desaturated. Competition experiments demonstrated a preference for 18:3 omega-3 by the elongation/desaturation pathway. These findings suggest that the blood-brain barrier can play an important role in the elongation and desaturation of omega-3 and omega-6 essential fatty acids during their transfer from the circulation into the brain.

Acetyltransferases↗
PubMed1987

Selective incorporation of n-3 and n-6 fatty acids in essential fatty acid deficient rats in response to short-term oil feeding.

Essential fatty acid deficient male Sprague Dawley rats were fed for 7 days a fat-free semi-synthetic diet supplemented with 10% by weight of different oil supplements. The oil supplement was a mixture of olive, safflower and linseed oils prepared at different proportions so the dietary n-9/n-6/n-3 ratios were approximate 2/1/1, 1/2/1, 1/1/2, and 1/1/1. The fatty acid compositions of plasma and liver lipids were then examined. Our results show polyunsaturated n-6 and n-3 fatty acids were selectively incorporated into plasma and liver phospholipids, and also into plasma cholesteryl esters. A preferential incorporation of n-6 over n-3 fatty acids into plasma cholesteryl esters and phospholipids was also observed.

Animals↗
PubMed1989

Effects of dietary long-chain polyunsaturated fatty acids on the essential fatty acid status of premature infants.

The effect of different diets on the percentage content of long-chain polyunsaturated fatty acids (LCP; metabolites of linoleic and alpha-linolenic acids) in plasma lipids was studied in 29 premature infants on days 4 and 21 of life. Eleven infants were fed human milk which supplies LCP (1.7% of the fatty acids), 10 a commercially available milk formula without LCP, and 8 a new formula enriched with LCP of the omega-6 and the omega-3 series (0.5% LCP). LCP values in plasma lipids remained stable during the observation period in infants fed human milk. In contrast, LCP decreased markedly in plasma lipids of infants fed the conventional formula. Since the precursor fatty acids linoleic and alpha-linolenic acids were high in their diet and plasma, this finding indicates that premature infants have a limited capacity for LCP biosynthesis and may require their dietary supplementation. Infants fed the LCP enriched formula had significantly higher LCP proportions in plasma lipids than infants given the conventional formula, but less than infants fed human milk. Our results demonstrate that small concentrations of dietary LCP have marked effects on plasma lipid composition, particularly on phospholipids, suggesting that dietary LCP are preferentially channelled into structural lipids. We conclude that the essential fatty acid status of formula-fed premature infants can be improved by a supplementation of omega-6- and omega-3-LCP.

Dietary Fats, Unsaturated↗
PubMed1987

Metabolic and functional alterations in macrophages induced by essential fatty acid deficiency.

Essential fatty acid (EFA) deficiency has been shown to protect against the glomerulonephritis in a murine model of systemic lupus erythematosus. Since macrophages are an important cellular constituent of the inflammatory lesion, the effects of EFA deficiency on the eicosanoid metabolism and function of these cells were determined. EFA-deficient macrophages exhibited a depletion of phospholipid arachidonate and an accumulation of 20:3(n-9); phosphatidylinositol was the phospholipid most affected. When these macrophages were stimulated with unopsonized zymosan, they produced markedly less leukotriene C4 and B4 than control macrophages. EFA-deficient macrophages also synthesized leukotriene C3 from endogenous 20:3(n-9). No leukotriene B3 was detected. In contrast to the effects on leukotriene production, prostaglandin and thromboxane production were only minimally affected by EFA deficiency. When challenged with zymosan, EFA-deficient macrophages released less arachidonate relative to control macrophages and released half again as much 20:3(n-9) as arachidonate. Release of arachidonate from phosphatidylcholine in the EFA-deficient cells was highly selective for arachidonate; however, release of arachidonate from phosphatidylinositol was depressed relative to control and was not selective. Incubation of macrophages with exogenous arachidonate and 20:3(n-9) established that 20:3(n-9) decreased leukotriene C4 and B4 synthesis from arachidonate but did not affect prostaglandin production. To determine the functional effects of the deficiency state, receptor-mediated pinocytosis and phagocytosis were also examined in EFA-deficient cells. EFA-deficient macrophages exhibited a marked reduction in receptor-mediated pinocytosis. Phagocytosis, however, was unaffected by the deficiency state. These effects on macrophage eicosanoid metabolism and function may comprise a significant component of the anti-inflammatory effect of EFA deficiency.

Animals↗
PubMed1977

Human essential fatty acid deficiency: treatment by topical application of linoleic acid.

An essential fatty acid (EFA) deficiency developed in a 19-year-old man who was being maintained on a long-term regimen of fat-free, intravenous hyperalimentation fluids. The EFA deficiency was reversed after 21 days by daily, topical application of linoleic acid to the patient's skin. The ratio of eicosatrienoic acid (20:3, n-9) to eicosatetraenoic acid (20:4, n-6) decreased to normal levels in the skin and serum with clinical improvement of the EFA deficiency syndrome. The cutaneous manifestations (scalp dermatitis, alopecia, and depigmentation of hair) were reversed with continued, topical application of safflower oil, which contains 60% to 70% linoleic acid.

Administration, Topical↗
PubMed1988

Effect of dietary linoleic acid and essential fatty acid deficiency on resting metabolism, nonshivering thermogenesis and brown adipose tissue in the rat.

Rats were fed a diet either deficient (0.05%) in essential fatty acids (EFA), or providing 4% (control) and 10% (surplus) of the total energy intake in the form of linoleic acid. All diets were isoenergetic and provided 13.9% of the energy as fat. The rats were kept at 29 or 5 degrees C. Growth and food intake of rats fed linoleic acid surplus at either temperature for 10 wk were not different from that of controls; basal metabolism, norepinephrine-induced nonshivering thermogenesis (NST) and thermogenic variables in the brown adipose tissue (amount of mitochondria and mitochondrial uncoupling protein) also were not different. The effects of EFA deficiency were drastically enhanced in the cold: After 10 wk of consuming a diet low in EFA at 5 degrees C, the body weight of rats was 75% of that of controls (87% at 29 degrees C); the food intake was 135% of controls at 5 degrees C (120% at 29 degrees C). The resting respiration in deficient rats was 125% of controls at 5 degrees C (110% at 29 degrees C); body temperatures as low as 35.1 degrees C were measured in deficient rats after 3 wk at 5 degrees C; the cold tolerance of the rats was significantly diminished (30% died within 3 wk at 5 degrees C), thus emphasizing the essential role of dietary EFA during cold stress. Norepinephrine-induced NST and the thermogenic parameters in brown fat were not influenced by EFA deficiency.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue, Brown↗
PubMed1979

Intensification of essential fatty acid deficiency in the rat by dietary trans fatty acids.

Two studies were conducted using male rats to assess the effect of trans fatty acids upon essential fatty acid (EFA) deficiency. In the first study 5% corn oil (CO), hydrogenated coconut oil (HCNO) or margarine stock (MS, partially hydrogenated soybean oil) were fed, and the levels of trans fatty acids in tissue lipids were measured. The trans fatty acids present in MS were found to intensify EFA deficiency and to be retained in tissue lipids to a high degree, especially in heart phospholipids (PL). In the second study, as the level of trans fatty acids increased in the diet, increasingly higher levels of trans fatty acids were deposited in the heart PL. As dietary trans acid increased, a decrease in total omega 6 fatty acids, and a decrease in the sum of 18:2 omega 6 + 20:4 omega 6 - 20:3 omega 9 fatty acids in heart PL occurred, both criteria indicating a shift toward an increasing EFA deficiency state. Studies of delta 5 desaturase activity of liver microsomes in selected groups showed an increase in the conversion of 20:3 omega 6 to 20:4 omega 6 as the trans fatty acid level in the diet increased.

Animals↗
PubMed1978

Linoleic acid effects on epidermal DNA synthesis and cutaneous prostaglandin levels in essential fatty acid deficiency.

An essential fatty acid (EFA) deficient state has been induced in hairless mice. The epidermal changes included hyperkeratosis, hypergranulosis and acanthosis. Epidermal DNA synthesis was increased 3-fold compared with normal diet mice. Prostaglandin E (PGE) and prostaglandin F (PGF) levels, measured by radioimmunoassay, were much reduced in the EFA deficient mice skin. 10% Linoleic acid applied topically for 2 weeks corrected the gross and histological skin abnormalities and reduced epidermal DNA synthesis to normal values. The levels of PGE and PGF were only partially corrected. Linoleic acid applied to normal diet mice increased skin levels of PGE and PGF compared with the control vehicle treated normal diet mice. These results provide further evidence for the importance of essential fatty acids in the control of epidermal proliferation and differentiation. The importance of PGE and PGF in controlling epidermal DNA synthesis in EFA deficiency is less clear.

Animals↗
PubMed1989

Direct transesterification of plasma fatty acids for the diagnosis of essential fatty acid deficiency in cystic fibrosis.

This study was aimed at redefining criteria for essential fatty acid (EFA) deficiency with the use of the direct transesterification procedure (1986. J. Lipid Res. 27: 114-120) and at determining whether a simple assay of total fatty acids (FA) is as predictive of EFA deficiency as the FA pattern from plasma, red cell, and platelet phospholipids. Fasting blood samples were taken from 163 cystic fibrosis (CF) patients who were encouraged to consume 35-40% of their calories as fat. Their mean (+/- SD) age was 9.6 +/- 4.8 yr. The control group consisted of 44 unaffected siblings aged 13.1 +/- 3.1 yr. The 20:3(n-9)/20:4(n-6) ratio in 77 (47%) CF children was more than 2 SD above the values (mean +/- SD) of 0.021 +/- 0.007 obtained in the 44 controls. Groups of EFA-sufficient (n = 10) and EFA-deficient (n = 7) subjects were selected for further studies. The plasma total FA 20:3(n-9)/20:4(n-6) ratios of 0.029 +/- 0.003 in EFA-sufficient and of 0.216 +/- 0.103 in EFA-deficient was as good a discriminant as FA in phospholipids from plasma, red cell PC, and platelets. Among the 21 individual fatty acids, 20:3(n-9), which was also found in controls, and 16:1(n-7) (palmitoleic) proved to be the most sensitive indices of EFA deficiency. They are equally reliable in plasma, red cells, and platelets, but the inverse linear relationship (r = -0.91) between the n-7 family and 18:2(n-6) proved to be more closely associated with EFA deficiency than the one (r = 0.66) between 20:3(n-9) and 20:4(n-6).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1991

The anti-diabetogenic effect of essential fatty acid deficiency in multiple low-dose streptozotocin-treated mice persists if essential fatty acid repletion occurs outside of a brief window of susceptibility.

We have previously shown that essential fatty acid deficiency prevents diabetes mellitus and ameliorates insulitis in multiple low-dose streptozotocin-treated male CD-1 mice and that repletion with 99% pure methyl linoleate 3 days after the last injection causes diabetes. In the present study, we examined whether repletion of low-dose streptozotocin-treated deficient mice will cause diabetes whenever repletion occurs. Essential fatty acid deficiency was induced by dietary manipulation and was confirmed biochemically. Groups of deficient mice were repleted 6 h, 1 week, 2 weeks, 4 weeks and 8 weeks after the last low-dose streptozotocin treatment; the incidence of diabetes (i.e., non-fasting plasma glucose levels greater than 11.2 mmol/l) and group mean plasma glucose levels were 93% (19.4 mmol/l), 37% (14.8 mmol/l), 40% (13.7 mmol/l), 20% (9.0 mmol/l), and 8% (7.8 mmol/l) respectively. The incidence and mean glucose levels for low-dose streptozotocin-induced control chow-fed and non-repleted essential fatty acid deficient CD-1 mice were 100% (30.2 mmol/l) and 0% (4.2 mmol/l). The incidence and severity of insulitis also decreased with increasing repletion intervals. These results demonstrate a brief window of susceptibility of less than 8 weeks duration during which repletion will initiate an autoimmune response directed at low-dose streptozotocin-induced Beta-cell neoantigens in low-dose streptozotocin-treated essential fatty acid deficient mice.

Animals↗
PubMed1988

Rat neutrophil function, and leukotriene generation in essential fatty acid deficiency.

Since the essential fatty acid linoleic acid is the precursor of arachidonic acid and thus of leukotrine B4 (LTB4), essential fatty acid deficiency (EFAD) may result in decreased synthesis of this stimulator of neutrophil granulocyte functions. Peritoneal and blood neutrophils from rats fed a diet with only 0.3% of energy requirements as linoleic acid and exhibiting biochemical evidence of EFAD showed substantial functional impairments compared to neutrophils from rats maintained on a diet with 3% of the energy requirement as linoleic acid. Oxidative burst activation (assessed by chemiluminescence), chemotaxis and aggregation were impaired upon stimulation with formylpeptides or the ionophore A23187. In contrast, these functions were intact on stimulation with exogenous LTB4. Chemiluminescence was slightly but not significantly enhanced in EFAD rat neutrophils compared to controls when stimulated with phorbol myristate acetate (PMA). There were no differences between EFAD and control peritoneal neutrophils in the number of f-met-leu-phe (fMLP) receptors, or in their affinity for the ligand, assessed with fML(3H)P. The fraction of responding cells also were similar, assessed with dichlorofluorescein diacetate fluorescence. Moreover, the endogeneous LTB4 production in response to A23187 or fMLP was decreased by 57.7% and 63.5%, respectively, in EFAD peritoneal neutrophils. Thus, EFAD was associated with reductions of LTB4 production and neutrophil responsiveness to A23187 and formylpeptides but not to LTB4 or PMA, which supports the hypothesis that endogeneous LTB4 may contribute to the activation of neutrophil functions involved in inflammation and host defense.

Animals↗
PubMedDate not supplied

Effects of hypocaloric diet low in essential fatty acids on in vitro human adipose tissue prostaglandin production and essential fatty acid status.

Very-low-calorie, fat-free defined-formula diets have been routinely used to treat obese patients. However, the effect of feeding a defined-formula diet low or devoid of essential fatty acids (EFAs) on EFA metabolism has not been determined. The aim of this investigation was to determine the effect of 400 kcal/day of Optifast 70 on EFA metabolism as determined by serum and adipose tissue levels of omega-6 fatty acids and measurements of in vitro human adipose tissue prostaglandin production. Five obese subjects entered the study after 1 wk of weight maintenance and then were placed on 12 wk of weight reduction. Blood and tissue samples were obtained before and after 4, 8, and 12 wk of weight reduction. Subjects tolerated 12 wk of dieting without any adverse reactions and lost an average of 21.7 +/- 7.0 kg. There was no significant effect of weight reduction on the levels of linoleic or arachidonic acid found in adipose tissue. There was a significant decrease in adipose tissue prostaglandin production of prostacyclin I2, measured as 6-keto-PGF1 alpha, after 12 wk of weight reduction. There was no significant change in the levels of thromboxane A2, measured as TXB2. There was a significant increase in serum arachidonic acid levels with no change in linoleic acid levels. The results demonstrated that the use of a diet devoid of EFA had no significant effect on omega-6 EFA metabolism as measured by serum and tissue levels and the ability of adipose tissue to produce prostaglandins in vitro.

Adipose Tissue↗