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Results for “FATTY ACIDS, ESSENTIAL”

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At least 1,009 records · Page 56Linked to original sources
PubMed1982

Treatment of Sjogren's syndrome with essential fatty acids, pyridoxine and vitamin C.

Sjogren's Syndrome (S.S.) is characterized clinically by oral and ocular dryness and immunologically by its frequent association with autoimmune diseases and the presence of various circulating autoantibodies. Evidence has been presented suggesting that S.S. may be due to a relative deficiency of PGE1 and that elevating PGE1 levels may reduce oral and ocular dryness. In an attempt to increase PGE1 levels, precursors of PGE1 including di-homo-gamma linolenic acid, ascorbic acid and pyridoxine in the form of dietary supplements were administered to 10 patients with S.S. for 10 weeks. There was no significant improvement in any of the patients during the treatment period compared to assessments done pre and post treatment. Measurements of oral and ocular dryness of 6 patients on prostaglandin synthetase inhibiting anti-inflammatory medications were similar to the 4 patients on no medication.

Ascorbic Acid↗
PubMed1986

Comparative studies of the responses of two strains of rats to an essential fatty acid deficient diet.

A comparative study of two strains of rats to an EFA deficient diet was conducted. Parameters of insulin status in BHE and Sprague-Dawley rats were measured. No differences in growth were observed. The strains differed in their hepatic and adipose tissue response to insulin stimulation of glucose oxidation and conversion to fatty acids. Hepatic tissue from EFA deficient BHE rats converted more glucose to fatty acid under the influence of insulin than their controls while diet had no effect on glucose oxidation. Hepatic tissue from EFA deficient Sprague-Dawley rats oxidized more glucose than their controls but diet did not affect fatty acid synthesis. A reverse of these strain and diet differences was observed in adipose tissue. These results suggest that the genetic heritage of the rat may determine the type of response to EFA deficiency.

Adipose Tissue↗
PubMed1988

Interactive effects of live weight, basal diet and fat supply on essential fatty acid status and blood concentrations of glucose, insulin and thyroxine measured postprandially in pigs.

1. The composition of the basal diet (purified vs complete feed ingredients provided as a cassava and a barley based diet, respectively), type of dietary fat [saturated fatty acids (18:0) supplied as fully hydrogenated soya bean oil vs unsaturated fatty acids (18:2) supplied in the form of soya bean oil] and the live wt of the animals (40 vs 80 kg) highly influenced the EFA status of the body and postprandial blood concentrations of glucose, insulin and thyroxine. 2. Interactive effects of live wt, type of basal diet and fat supply on EFA status and postprandial blood levels are discussed.

Animals↗
PubMed1987

The transfer of radiolabelled n-6 essential fatty acids by the mammary system of the tree-shrew (Tupia tana).

The fatty acid content of tree-shrew milk has been determined from analysis of the stomach content of infants immediately after suckling. Comparison of the n-6 fatty acid composition of the stomach contents, liver and brain demonstrate a striking increment in the ratio of arachidonic to linoleic acid. Feeding radioactively labelled linoleic acid to the mother 24 hr prior to suckling showed that 12-20% was transferred to the milk. Evidence from the appearance of the radioactivity administered as linoleic acid into arachidonic acid indicates that this species is able to desaturate linoleic acid.

Animals↗
PubMed1991

Disturbances of essential fatty acid- and prostaglandin E-mediated immunoregulation in atopy.

Impaired suppressor T lymphocyte maturation and function in atopic individuals are explained by an insufficient transmission of prostaglandin E (PGE) signals during thymic lymphocyte differentiation as well as an impaired ability of the atopic immune system to activate suppressor T-cells by PGE-mediated feed back mechanisms. We demonstrate that spontaneous in vitro immunoglobulin E synthesis of atopic peripheral blood mononuclear cells could be suppressed by the addition of 10(-6) M to 10(-5) M PGE1 or PGE2. Decreased plasma and breast milk levels of PGE-precursor fatty acids and reduced numbers of PGE2-receptors on atopic lymphocytes have been observed in atopic individuals. These insights might offer a novel approach for the prevention of atopic disease by substitution of the atopic pregnant and nursing woman and her newborn infant with long chain omega-6-fatty acids.

Adult↗
PubMed2005

Essential fatty acid transfer and fetal development.

Docosahexaenoic acid (22:6n-3) and arachidonic acid (20:4n-6) are important structural components of the central nervous system. These fatty acids are transferred across the placenta, and are accumulated in the brain and other organs during fetal development. Depletion of 22:6n-3 from the retina and brain results in reduced visual function and learning deficits: these may involve critical roles of 22:6n-3 in membrane-dependent signaling pathways and neurotransmitter metabolism. Transfer of 22:6n-3 across the placenta involves specific binding and transfer proteins that facilitate higher concentrations of 22:6n-3 and 20:4n-6, but lower linoleic acid (18:2n-6) in fetal compared with maternal plasma, or in the breast-fed or formula-fed infant. However, human and animal studies both demonstrate that maternal diet impacts fetal 22:6n-3 and 20:4n-6 accretion. After birth, parenteral lipid, human milk and infant formula feeding all result in a marked decrease in plasma 22:6n-3 and 20:4n-6 and an increase in 18:2n-6. Estimation of fetal tissue fatty acid accretion suggests that current preterm infant feeds are unlikely to meet in utero rates of 22:6n-3 accretion. Consideration needs to be given to whether fetal plasma 22:6n-3 and 20:4n-6 enrichment and the low 18:2n-6 facilitates accretion of 22:6n-3 and 20:4n-6 in developing tissues.

Animals↗
PubMed2004

Essential fatty acids and phospholipase A2 in autistic spectrum disorders.

A health questionnaire based on parental observations of clinical signs of fatty acid deficiency (FAD) showed that patients with autism and Asperger's syndrome (ASP) had significantly higher FAD scores (6.34+/-4.37 and 7.64+/-6.20, respectively) compared to controls (1.78+/-1.68). Patients with regressive autism had significantly higher percentages of 18:0,18:2n-6 and total saturates in their RBC membranes compared to controls, while 24:0, 22:5n-6, 24:1 and the 20:4n-6/20:5n-3 ratio were significantly higher in both regressive autism and ASP groups compared to controls. By comparison, the 18:1n-9 and 20:4n-6 values were significantly lower in patients with regressive autism compared to controls while 22:5n-3, total n-3 and total dimethyl acetals were significantly lower in both regressive autism and ASP groups compared to controls. Storage of RBC at -20 degrees C for 6 weeks resulted in significant reductions in highly unsaturated fatty acid levels in polar lipids of patients with regressive autism, compared to patients with classical autism or ASP, or controls. Patients diagnosed with both autism and ASP showed significantly increased levels of EPA ( approximately 200%) and DHA ( approximately 40%), and significantly reduced levels of ARA ( approximately 20%), 20:3n-6 and ARA/EPA ratio in their RBC polar lipids, when supplemented with EPA-rich fish oils, compared to controls and non-supplemented patients with autism. Patients with both regressive autism and classical autism/Asperger's syndrome had significantly higher concentrations of RBC type IV phospholipase A2 compared to controls. However, patients with autism/ASP, who had taken EPA supplements, had significantly reduced PLA2 concentrations compared to unsupplemented patients with classical autism or ASP.

Asperger Syndrome↗
PubMed1997

Essential fatty acid deficiency in renal failure: can supplements really help?

Abnormal fatty acid metabolism may contribute to clinical problems such as itching, abnormal perspiration, susceptibility to infection, delayed wound healing, anemia, and increased hemolysis, as seen in patients with chronic renal failure. A double-blind study of patients on hemodialysis who received either fish oil, olive oil, or safflower oil documented that patients may have increased levels of the proinflammatory prostaglandin PGE2 and that fish oil intervention may decrease these levels, change the fatty acid profile, improve hematocrit levels, and improve patient perception of symptoms of pruritus.

Diet Records↗
PubMed1997

Essential fatty acid preparation improves biochemical and cognitive functions in experimental allergic encephalomyelitis rats.

This study examined the possible effects of a novel mixture of fatty acids, SR-3 (a specific ratio of alpha-linolenic acids), on brain biochemistry and on learning deficits induced by injection of an agent that induces experimental allergic encephalomyelitis. Treatment with SR-3 caused a decrease in myelin and changes in the fatty acid profile of brain synaptosomes, and a learning deficit. Eighteen days of treatment with SR-3 reversed the biochemical and learning deficit significantly, but did not restore them to normal levels. We propose that, most probably, the main action of SR-3 is the modulation of the cholesterol level, which in turn causes the modulation of the fatty acid profile and enhances learning by allowing improved neuronal communication.

Analysis of Variance↗
PubMed1977

Platelet dysfunction in the neonate with essential fatty acid deficiency.

Platelet aggregation in response to ADP was studied in five EFA-deficient sick premature newborn infants who were receiving fat-free parenteral nutrition. EFA deficiency was diagnosed by analysis of plasma lipid fatty acid values. The deficient infants had impaired platelet aggregation when compared to other low-birth-weight infants fed orally who served as control subjects (maximum 18.1% versus 43.4% at 2.5 muM ADP; 34.5% versus 52.2% at 5.0 muM ADP). In addition, the platelets from EFA-deficient infants demonstrated clearly evident disaggregation. On recovery from their deficient state, the low-birth-weight infants had platelet functions similar to those of apparently healthy premature infants. Clinical hemorrhage occurred in four of the EFA-deficient infants. Thus a deficiency of arachidonic acid, the precursor of thromboxane A2, is correlated with an impairment of the aggregation of platelets, a phenomenon mediated by thromboxane A2. This correlation provides the basis for a hypothesis that the observed EFA deficiency is causally related to the platelet dysfunction.

Adenosine Diphosphate↗