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At least 1,423 records · Page 79Linked to original sources
PubMed1996

Utilization of precursor essential fatty acids in culture by skin fibroblasts from schizophrenic patients and normal controls.

Based on the lower levels of long-chain polyunsaturated analogs of essential fatty acids (EPUFAs) in plasma membrane phospholipids of red blood cells, brain and cultured skin fibroblasts from schizophrenic patients, a defective utilization (uptake, conversion to EPUFAs and incorporation into membrane phospholipids) of precursor EFAs has been suggested. Utilization of radiolabeled linoleic (LA, 18:2(n-6)) and alpha-linolenic (ALA, 18:3(n-3)) acids was studied in cultured skin fibroblasts from patients with established schizophrenia and at the first episode of psychosis, and normal controls. Uptake and incorporation of both the EFAs were similar in fibroblasts from both groups of patients studied compared with normal controls. However, although the utilization of LA into arachidonic acid (AA, 20:4n-6) was similar in patients and controls, the utilization of eicosapentaenoic acid (EPA, 20:5(n-3)) into docosahexaenoic acid (DHA, 22:6(n-3)) was significantly lower in first-episode psychotic patients (patients, 96.33 +/- 27.16 versus normals, 161.66 +/- 26.33 nmoles per mg total protein; P = < 0.001). This data indicates that the level of delta 6- as well as delta 5-desaturase may be normal. However, the levels of delta 4-desaturase may be lower in fibroblasts from schizophrenic patients even at the first episode of psychosis.

Adult↗
PubMed1995

Essential fatty acid deficiency prevents autoimmune diabetes in nonobese diabetic mice through a positive impact on antigen-presenting cells and Th2 lymphocytes.

Protective effects of essential fatty acid deficiency (EFAD) on autoimmunity were shown in rodents. Our goal was to investigate the mechanisms of EFAD effects on autoimmune diabetes in nonobese diabetic (NOD) mice. Weanling female mice were randomized between a control diet group and an EFAD diet group, and the development of diabetes and immune response was determined over a 6-month period. The cumulative incidence of diabetes was significantly reduced in the EFAD group (20 vs 68.75% in the control group; p < 0.01), without affecting the insulitis process. Splenocyte reactivity to phytohemagglutinin and anti-CD3 antibody was significantly increased in EFAD-fed mice (p < 0.01). The EFAD group also exhibited a dramatic increase in baseline (29-fold) and antigen-presenting cell (APC)-stimulated (10-fold) T cell responses in syngeneic mixed leukocyte reaction. These responses were associated with a marked increase in splenocyte interleukin-4 (IL-4) production, a reduction in interferon-gamma production, and a down-regulation of CD45RB isoform expression. Macrophages in the EFAD group exerted a reduced suppressive effect on concanavalin A-induced splenocyte proliferation and were found to release increased amounts of tumor necrosis factor-alpha and IL-1 and reduced amounts of prostaglandin E2. These results clearly demonstrate that EFAD prevents diabetes in NOD mice. The data suggest an enhanced activity of Th2-like cells, as well as an effect on APC activity linked to alteration in eicosanoid metabolism.

Animals↗
PubMed2004

A randomized, controlled study to evaluate the steroid sparing effect of essential fatty acid supplementation in the treatment of canine atopic dermatitis.

A randomized, double blind, placebo-controlled multicentre clinical trial of 12 weeks' duration was undertaken in 60 dogs with atopic dermatitis to evaluate the steroid sparing effect of essential fatty acid supplementation. The dogs were randomly assigned to receive either a combination of borage seed oil and fish oil or a placebo, in addition to prednisolone tablets. All dogs received a standardized basal diet. Owners of the dogs recorded pruritus daily using a 10 cm visual analog scale and the dosage of prednisolone was established based on the pruritus score, according to written instructions. The dosage of prednisolone and the use of any concurrent treatment (shampoo and/or ear-cleanser) were recorded by the owner on a daily basis. The investigators graded the skin lesions at days 0, 42 and 84. The use of prednisolone during the test period was lower in the active group, but the difference was not statistically significant (P = 0.32). The test period was sequentially divided into 43-84, 50-84, 57-84, 64-84, 71-84 and 78-84 days. On day 64, the difference between the active group and the placebo group reached statistical significance (P = 0.04) with an increasing difference towards the end of the study. A statistically significant reduction in the pruritus scores and the total clinical scores from day 0 to day 84 was apparent in both groups (P < 0.0001). At the end of the study, both the pruritus score and the total clinical score were lower in the active group. Our findings indicate a steroid sparing effect of essential fatty acid supplementation in canine atopic dermatitis and, furthermore, that there is a time lag before the effect is attained.

Animals↗
PubMed1988

[Skin changes, pathophysiology and therapy in deficiency of essential fatty acids].

Linoleic acid (C18: 2n-6) is a free fatty acid considered as essential in man; this is mainly based on the fact that man is incapable of its synthesis and that its deficiency accounts for a defined clinical picture. Linoleic acid (LA) is an essential component of cellular membranes and plays, therefore, an important role in cells; moreover, it plays a functional part on account of its precursory position of eicosanoids. For these reasons, the skin is a preferential target in case of LA deficiency, which alters the barrier function of the skin as well as the immunoregulation of the epidermic homeostasis. Man's requirement of LA has been estimated 4% of the total energy supply, i.e. 7-10 g daily. Deficiency of LA may arise from various factors: insufficient supply; metabolic anomalies (mostly due to advanced age and hepatopathies which may particularly alter the metabolic process of desaturation). Symptoms due to LA deficiency are xerosis and erythematosquamous dermatitis. The clinical picture being non-specific may be confused with other vitamin deficiencies, all the more because of metabolic interactions between these vitamins and various trace elements. Thus--in order to make the diagnosis--plasmatic fatty acid fractioning by means of gaseous phase chromatography is indicated in case of therapy-resistant eczematous dermatitis associated with malnutrition. These findings may be confirmed by measuring either the ratio of eicosatrienoic acid vs. arachidonic acid or the ratio of LA vs. arachidonic acid (in case of a disturbed metabolism of fatty acids). The treatment consists of regular oral, parenteral or topical application of essential fatty acids. Topical administration is especially indicated, because these patients, although often suffering from impaired intestinal absorption, reveal a tenfold percutaneous absorption rate of fatty acids.

Aged↗
PubMed1993

Hormonal and biochemical profiles of premenstrual syndrome. Treatment with essential fatty acids.

Women diagnosed as suffering from premenstrual syndrome and symptom free controls were compared on hormonal parameters, glucose tolerance, mineralocorticoids, cholesterols, triglycerides, apolipoprotein (a), magnesium and calcium in the follicular and luteal phases of the menstrual cycle. The effect of treatment with essential fatty acids on the biochemical variables was also evaluated in a randomized, double-blind crossover design. The results showed that the hormonal and biochemical profiles of women with PMS and symptom free controls were markedly similar, except for aldosterone which was lower in the follicular and luteal phases and cholesterol which was higher in the follicular phase in women with PMS. No effects of treatment with essential fatty acids were found for any of the biochemical variables studied.

Adult↗
PubMed1993

Contrasting effects of treatment with omega-3 and omega-6 essential fatty acids on peripheral nerve function and capillarization in streptozotocin-diabetic rats.

Essential fatty acid metabolism is impaired by diabetes mellitus and this may be important in the aetiology of peripheral nerve dysfunction. The effects of gamma-linolenic acid (omega-6) and fish oil (omega-3) alone, and in combination, on nerve function and capillarization were examined in 2-month streptozotocin-diabetic rats. Diabetes resulted in approximately 15% and 23% decreases in saphenous sensory and sciatic motor nerve conduction velocities, respectively (p < 0.001). Motor and sensory conduction velocities were in the non-diabetic range after both preventive and reversal omega-6 treatment of diabetic rats (p < 0.001). No significant changes occurred in omega-6 treated non-diabetic rats. Preventive omega-3 treatment was largely ineffective. Reversal treatment with a combination of omega-6 and omega-3 fatty acids was marginally effective and improved motor (p < 0.05), but not sensory conduction velocity. In vitro measurement of sciatic nerve resistance to hypoxic conduction failure in diabetic rats revealed a 56% increase in the time taken for the compound action potential amplitude to be reduced by 80% (p < 0.01) compared to non-diabetic rats. This was partially prevented by omega-6 treatment (29% increase, p < 0.01). Reversal omega-6 treatment had a lesser effect (37% increase, p < 0.05 compared to untreated diabetic rats). omega-3 treatment had no significant effect on conduction failure time. Sciatic endoneurial capillary density increased by 11% with preventive omega-6 treatment (p < 0.05), but was unaffected by reversal omega-6 and by omega-3 treatments.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Essential fatty acid requirements in human nutrition.

Arachidonic acid (20:4 omega-6) and docosahexaenoic acid (22:6 omega-3) are major acyl components of cell membrane phospholipids, and are particularly enriched in the nonmyelin membranes of the central nervous system. Dietary deficiency of linoleic acid (18:2 omega-6) and linolenic acid (18:3 omega-3) during development has been shown to result in reduced levels of 20:4 omega-6 and 22:6 omega-3 in the developing central nervous system, and this has been associated with altered learning behaviour and visual function. Synthesis of 20:4 omega-6 and 22:6 omega-3 depends on the dietary intake of 18:2 omega-6 and 18:3 omega-3, respectively, and the activity of the fatty acid desaturase-elongase enzymes. Oxidation of 18:2 omega-6 and 18:3 omega-3 for energy, or direct acylation of 18:2 omega-6 into triglycerides, cholesteryl esters, and phospholipids, could also influence the amount of 20:4 omega-6 and 22:6 omega-3 formed. The tissue levels of 20:4 omega-6 and 22:6 omega-3, or other (omega-6) and (omega-3) fatty acids, compatible with optimum growth and development or health are not known. The amount of preformed 22:6 omega-3 in the diet of adults, infants fed various milks or formulae, or animals is reflected in the circulating lipid levels of 22:6 omega-3. Human milk levels of (omega-6) and (omega-3) fatty acids vary, depending in part on the mother's diet. A valid, scientific approach to extrapolate dietary essential fatty acid requirements from the composition of human milk or the circulating lipids of infants fed different diets has not been agreed on.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1978

Incidence and severity of experimental allergic encephalomyelitis and cerebral prostaglandin synthesis in essential fatty acid deficient and aspirin-treated rats.

Experimental allergic encephalomyelitis (EAE) was induced in rats of the Lewis strain fed diets adequate or deficient in essential fatty acids (EFA). After induction of the disease, the diets were supplemented with aspirin (3.75 g/kg diet), and the effects of the drug on the course of EAE and on the synthesis of prostaglandin F (PGF) by brain slices from diseased animals and their Freund controls were examined. Aspirin supplementation delayed the onset of EAE in both dietary groups. EFA-deficient rats experienced an incidence and severity of the disease similar to that of aspirin-free, EFA-deficiet rats, while the EFA-adequate group showed a greater severity but not an increased incidence, compared to aspirin-free controls. Aspirin treatment led to an increased PGF production by brain slices from rats on either diet and not subjected to an immunochallenge. When the diet was deficient in EFA, challenge with antigen plus adjuvant or adjuvant alone tended to decrease PGF synthesis by brain slices, and when the diet was adequate in EFA, immunochallenge caused a marked depression on PGF synthesis. It was concluded that the PG synthetase inhibitor aspirin can alter the course of EAE in the rat, providing further evidence that PGs or related metabolites may be involved in the immune response in this disease.

Animals↗
PubMed1975

The influence of essential fatty acids and food restriction on the specific activities of hepatic lipogenic and glutamate-metabolizing enzymes in the laying hen.

1. Extended feeding of an essential fatty acid (EFA)-deficient diet to laying hens increased liver size and liver lipid concentration. 2. The specific activities of hepatic lipogenic and glutamate-metabolizing enzymes were increased by feeding the EFA-deficient diet. 3. Restriction of daily food intake to 75% of ad lib. intake did not affect the response to dietary fat concentration. 4. Hepatic enzyme activities in hens fed on restricted amounts of food and killed just before, or after, the normal daily feeding time indicated no reduced capacity for lipogenesis at the earlier time.

ATP Citrate (pro-S)-Lyase↗
PubMed1992

The effects of dietary treatment with essential fatty acids on sciatic nerve conduction and activity of the Na+/K+ pump in streptozotocin-diabetic rats.

1. This study examined the effects of dietary essential fatty acid supplementation (5% (w/w) evening primrose oil) upon sciatic motor nerve conduction velocity and 86Rb+ pumping in sciatic nerve endoneurial preparations in rats with 4 to 5 weeks of streptozotocin-induced diabetes. 2. Control diabetic rats (dietary supplementation with 5% (w/w) hydrogenated coconut oil) exhibited a reduction in motor nerve conduction velocity (16%; P less than 0.05) compared to similarly-fed non-diabetic controls, but there was no significant alteration in ouabain-sensitive 86Rb+ pumping, a parameter reflecting activity of the Na+/K+ pump. 3. Treatment of diabetic rats with evening primrose oil prevented completely the development of the motor nerve conduction velocity deficit without affecting the severity of diabetes. Evening primrose oil treatment did not significantly affect motor nerve conduction velocity of non-diabetic animals. 4. Evening primrose oil treatment caused a significant reduction in activity of the Na+/K+ pump in sciatic nerves of diabetic animals (45%; P less than 0.05). 5. These results suggest that the acute conduction velocity defect arising in streptozotocin-diabetic rats, and the actions of evening primrose oil upon this, are independent of any effect on activity of the Na+/K+ pump. Other putative mechanisms are discussed.

Animals↗