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PubMed1972

Effects of prostaglandin E 2 on rat skin: inhibition of sterol ester biosynthesis and clearing of scaly lesions in essential fatty acid deficiency.

Severe scaly lesions in the skin, especially in the feet and tail, of the rat were induced by feeding a diet deficient in essential fatty acids (EFA). Analysis of the fatty acids in skin lipids of these EFA-deficient rats showed a marked increase of monoenoic acids (16:1 and 18:1) and eicosatrienoic acid (20:3), with concomitant decreases of dienoic acid (18:2) and tetraenoic acid (20:4). Topical application of prostaglandin E(2) (PGE(2)) to the scaly lesions resulted in clearance of the lesions, but did not significantly alter the composition of fatty acids in the skin. Intraperitoneal injection of PGE(2) had no observable effect on the skin lesions. Furthermore, incubation of skin specimens from the EFA-deficient rats with (14)C-labeled glucose showed a 4-5-fold increase of incorporation of glucose carbon into lipid fractions, particularly the sterol esters, and a 3-4-fold increase in pentose cycle activity. Addition of PGE(2) to the incubation mixture resulted in approximately 70% inhibition of sterol ester biosynthesis by skin of the EFA-deficient rats. These results suggest that the effects of PGE(2) in clearing the scales may be associated with its inhibitory effect on abnormal sterol esterification in the skin of the EFA-deficient rats.

Animals↗
PubMedDate not supplied

[Substantiation studies for a method of enriching sour milk products with essential fatty acids].

Comparative investigations were conducted to produce arguments in favour of technology employed in preparing special acidified dairy products with an elevated proportion of polyunsaturated essential fatty acids for baby and dietetic nutrition. These investigations included a study into oxidative changes occurring in the vegetable oil during preparation of acidified milk by following two technological patterns that provide for introduction of the vegetable oil into the milk prior to its souring and into sour milk.

Animals↗
PubMed2004

Essential fatty acids in Huntington's disease.

Huntington's disease is an inherited neurodegenerative disorder due to a mutation in exon 1 of the Huntingtin gene that encodes a stretch of polyglutamine (polyQ) residues close to the N-terminus of the huntingtin protein. Aggregated polyQ residues are highly toxic to the neuronal cells when they enter the cell nucleus. The mechanisms by which aggregated polyQ induces neurodegeneration include the binding of abnormal huntingtin to cyclic adenosine monophosphate response element binding protein, which hampers its ability to turn on transcription of other genes; mutant huntingtin binding to the active site on the cyclic adenosine monophosphate response element binding protein, which is essential for its acetyltransferase activity and, hence, the drugs that inhibit histone deacetylase arrest polyQ-dependent neurodegeneration; and/or disrupting the ubiquitin-proteasome system. Transgenic R6/1 mice that incorporate a human genomic fragment containing promoter elements exon 1 and a portion of intron 2 of the huntingtin gene responsible for Huntington's disease develop late-onset neurologic deficits in a manner similar to the motor abnormalities of Huntington's disease and show increased survival rates and decreased neurologic deficits when supplemented with essential fatty acids throughout life. A randomized, placebo-controlled, double-blind study has shown that highly unsaturated fatty acids are beneficial to patients with Huntington's disease. These results raise the possibility that unsaturated fatty acids may prevent or arrest polyQ aggregation, inhibit histone deacetylase, and/or activate the ubiquitin-proteasome system. In view of the encouraging results with essential fatty acids in Huntington's disease, it is proposed that their possible use in other neurodegenerative conditions need to be explored.

Fatty Acids, Essential↗
PubMed2004

Effect of low-zinc status and essential fatty acids deficiency on the activities of aspartate aminotransferase and alanine aminotransferase in liver and serum of albino rats.

The effects of dietary deficiencies of zinc and essential fatty acids (EFAs) or both on aspartate aminotransferase (AST) and alanine aminotransferase (ALT) were investigated in young growing rats. Four groups of albino rats were fed diets deficient in either EFA (4% hydrogenated coconut oil) or zinc (6 ppm) or both. The control diet was adequate in EFA (4% soybean oil) and zinc (100 ppm). The feeding trial lasted eight weeks and the activities of AST and ALT were determined in the liver and serum. EFA deficiency had no significant (p > 0.05) effect on liver AST. However, zinc and the double deficiencies depressed AST activity in the organ. Deficiencies of EFA, zinc and their combination depressed ALT activity in the liver significantly (p < 0.05) with a concomitant increase recorded in the serum. The data suggested alteration in endothelial permeability of the plasma membrane and thus leakage of membrane constituents in the tissue studied. It is therefore considered that these deficient diets may affect liver tissue negatively in view of the role of these enzymes in amino acid metabolism.

Alanine Transaminase↗
PubMed1981

Subcellular distribution of the cytochrome P-450 complex and glutathione peroxidase activity in vitamin E and essential fatty acid deficiency.

Glutathione peroxidase (EC 1.11.1.9.) (GSHPx) and P-450 activity were measured in hepatic mitochondrial and microsomal fractions from rats deficient in vitamin E and/or essential fatty acids (EFA). The data were compared to corresponding normal values. GSHPx was significantly decreased in the mitochondrial matrix from animals in all 3 deficiency states. In vitamin E deficiency, a non-significant decreased GSHPx activity was found in mitochondrial membranes. Opposite to these findings, GSHPx was significantly increased in mitochondrial membranes of EFA-deficient animals. In combined EFA and vitamin E deficiency, the mitochondrial membrane GSHPx activity was only insignificantly increased. The P-450 complex activity was not detectable in the mitochondrial matrix. In mitochondrial membranes and microsomes, the P-450 complex activity changed parallel to the GSHPx activity.

Animals↗
PubMed1979

Penicillin and essential fatty acid supplementation in schizophrenia.

There is evidence of a prostaglandin deficiency in schizophrenia, possibly particularly of the 1 series. Treatment of neuroleptic-resistant schizophrenics with essential fatty acids and penicillin in an attempt to increase synthesis of 1 series prostaglandins had a therapeutic effect in six severely ill patients. Two detailed case histories are described.

Adult↗
PubMed1998

Is the risk of urinary tract tumorigenesis enhanced by a marginal chronic essential fatty acid deficiency (EFAD)?

A considerable amount of experimental, clinical and epidemiological data indicate that dietary fats play a role in urinary tract tumorigenesis. In rodents, chronic essential fatty acid (EFA) deficiency seems to induce both urolithiasis and transitional hyperplasias, followed by a tendency for tumorigenesis of the urinary passages. High intake of saturated fats or non-EFAs, conditions that may induce EFA deficiency (EFAD) increase the risk of bladder cancer in case-control studies. In other cell populations, EFAs are beneficial as preventive and therapeutic nutrients for the treatment of cancer. Thus, it is reasonable to assume that abnormal metabolism and/or nutritional deprivation of EFA, by inducing a chronic or a subclinical EFA deficiency, may enhance the risk of urothelial tumorigenesis.

Epithelium↗
PubMed1998

Anxiety and adipose essential fatty acid precursors for prostaglandin E1 and E2.

OBJECTIVE: The purpose of the present study was to investigate the relation state and trait anxiety and adipose tissue essential fatty acid precursors for prostaglandins E1 and E2. METHODS: The sample consisted of 144 male and female Cretan adults, 23 to 69 years of age. Anthropometric and arterial blood pressure measurements were taken, and adipose tissue samples as well as data concerning general health habits were collected. Dietary data were collected using the weekly food frequency questionnaire and the 24-hour dietary recall method, while state and trait anxiety was assessed through the use of the Spielberger State-Trait Anxiety Inventory (STAI) and the Zung anxiety scale. RESULTS: State anxiety (STAI) related positively with sex (p < 0.0003) and negatively with adipose fat myristic acid (C14:0) (p < 0.004). Similarly, Zung trait anxiety related positively with sex (p < 0.0001) and negatively with adipose tissue myristic acid (C14:0) (p < 0.04). Spielberger trait anxiety related positively with adipose (LA + ALA)/(AA + EPA) ratio (p < 0.0002) and negatively with (C14:0) (p < 0.02) and dietary monounsaturated fat (p < 0.03). CONCLUSION: It appears that the positive relation between trait anxiety and adipose (LA + ALA)/(AA + EPA) ratio may stem from the inhibiting role of catecholamines on delta 6 and delta 5 desaturases.

Adipose Tissue↗
PubMed1989

Relationship of decreased hepatic lipase activity and lipoprotein abnormalities to essential fatty acid deficiency in cystic fibrosis patients.

Polyunsaturated fatty acids are known to affect plasma lipids and lipoproteins but there is no information on the effect of essential fatty acid (EFA) deficiency on lipoprotein composition. The purpose of this study was to characterize lipoproteins from 17 cystic fibrosis (CF) patients in relationship to their EFA status (eicosatrienoic/arachidonic acid ratio) and compare them with those of 10 healthy siblings (SIB) and of 10 unrelated controls. In 7 EFA-deficient (EFAD) and 10 EFA-sufficient (EFAS) patients, hypocholesterolemia was associated with a decrease of HDL-cholesterol and of LDL-cholesterol which was more marked in the EFAD group. Similarly, although triglyceride enrichment of VLDL, LDL, HDL2, and HDL3 with a concomitant reduction of cholesteryl esters from all particles except HDL2 was observed in both CF groups, it was more sizable in the EFAD patients. These changes led to an increase in the particle size of VLDL, LDL, and HDL2 whereas the distribution of HDL3 was skewed to smaller particles. Alterations in the apoprotein composition of particles were greater in EFAD than in EFAS. A decrease of total postheparin lipolytic activity was observed in the two groups of CF patients as well as in siblings. It was entirely accounted for by hepatic lipase (mumol FFA/ml per h) which was more severely diminished in EFAD (2.8 +/- 0.6) than in EFAS (4.4 +/- 0.7) and SIB (5.1 +/- 0.5). Although the two groups of CF children differed in terms of growth, severity of malabsorption, and vitamin E status, these data suggest that disturbance of lipoprotein concentration, composition, size, and metabolism (hepatic lipase) may be in part related to EFA deficiency. Further studies are necessary to explore the effect of EFA deficiency on hepatic lipase activity.

Adolescent↗
PubMed1990

Release of essential fatty acids from the rat mesenteric vascular bed perfused in vitro: modulation by zinc.

The rat mesenteric vascular bed releases prostaglandins when perfused in vitro. The present study evaluated the effect of perfusion of the rat mesenteric vascular bed in vitro with a buffer containing 0, 3, 6, or 9 nM of added zinc on the release of essential fatty acids over a 150-min period. Long chain fatty acids in the mesenteric lipids and in total lipid of the perfusion effluent were assayed by gas liquid chromatography. The presence of 6 nM zinc in the perfusing buffer almost completely prevented the change in 16-22 carbon long chain fatty acids in the mesenteric phospholipids and decreased the release of free fatty acids in comparison to that occurring in the absence of additional zinc. The results suggest that physiological amounts of zinc in the perfusion medium reduce the release of essential fatty acid from rat mesenteric lipids.

Animals↗
PubMed1989

Essential fatty acid treatment--effects on nerve conduction, polyol pathway and axonal transport in streptozotocin diabetic rats.

This study was designed to examine the effect of dietary supplementation with essential fatty acids (evening primrose oil--5% weight:weight added to the diet) on acute neurophysiological and neurochemical defects in streptozotocin-diabetic rats. Diabetic rats, which were not given evening primrose oil, showed highly significant elevations of nerve sorbitol and fructose combined with a depletion of nerve myo-inositol. In those animals there was also a 40% reduction (p less than 0.02) in the accumulation of axonally transported substance P-like immunoreactivity proximal to a 12 h sciatic nerve ligature together with reduced motor nerve conduction velocity (13% [p less than 0.001] and 20% [p less than 0.001] in two separate experiments). Treatment of other diabetic rats with evening primrose oil prevented completely the development of the motor nerve conduction velocity deficit without affecting sorbitol, fructose or myo-inositol levels or the deficit in axonal transport of substance P. In a second experiment, treatment of diabetic rats with evening primrose oil was associated with significant attenuation of the conduction velocity deficit, but not complete prevention.

Animals↗
PubMed1988

Reversal of epidermal hyperproliferation in essential fatty acid deficient guinea pigs is accompanied by rapid generation of inositol triphosphate.

This study probes the extent of coupling between the reversal of epidermal hyperproliferation induced by essential fatty acid (EFA) deficiency in guinea pigs, the hydrolysis of epidermal phosphatidylinositol 4,5-bisphosphate (PtdIns4,5P2), and the rapid formation of inositol triphosphate (InsP3). Our data revealed that the incorporation of free [3H]-inositol into phosphatidylinositol 4P and PtdIns4,5P2 of microsomal preparations from hyperproliferative epidermis was markedly elevated when compared with epidermis from normal-fed animals. The reversal of the hyperproliferating epidermis by dietary cross-over supplementations with safflower oil and primrose oil resulted in striking morphological normalization, cellular decrease in epidermal DNA synthesis, decrease in the biosynthesis of 14C-PtdIn4,5P2 from precursor 14C-inositol, and a significant increase in the rapid generation of transient InsP3 by epidermis from the cross-over-fed animals. These findings taken together indicate that the reversal of epidermal hyperproliferation to normal in guinea pig skin and the increased capability of the tissue microsomal preparation to generate InsP3 are linked in this tissue, and raise the possibility that epidermal inositol-phospholipid metabolism may play a role in the pathogenesis of cutaneous hyperproliferative disorders.

Animals↗
PubMed1995

Essential fatty acid deficiency prevents multiple low-dose streptozotocin-induced diabetes in naive and cyclosporin-treated low-responder murine strains.

We have previously shown that essential fatty acid (EFA) deficiency prevents diabetes and ameliorates insulitis in low-dose streptozotocin (LDS)-treated male CD-1 mice. The effects of EFA deficiency on the incidence of diabetes after LDS treatment has not been examined in other strains. In contrast to highly susceptible CD-1 mice, several other strains of mice are only partially susceptible to LDS treatment and do not develop appreciable insulitis; however, the susceptibility of these strains can be markedly increased by cyclosporin A (CsA) pretreatment to reduce suppressor cell function. Weanling male BALB/cByJ, DBA/2J, and C57BL/6J mice were placed on EFA-deficient (EFAD) or control diets for 2 months and then divided into experimental and control groups. Ten EFAD and 10 control mice from each strain received LDS treatment (40 mg/kg/d 5 d); an additional 10 EFAD BALB/cByJ and another 10 control BALB/cByJ mice received subcutaneous CsA injections (20 mg/kg/d) for 14 days prior to and for 5 days simultaneous with LDS treatment (40 mg/kg/d 5 d). Plasma glucose levels for all mice were determined 3 times per week for 3 weeks after LDS treatment. Mean plasma glucose levels (+/- SEM) at the end of the experiment were significantly lower in the EFAD groups vs control groups in BALB/cByJ (P < 0.001), DBA/2J (P < 0.00001), and C57BL/6J (P = 0.012) mice. CsA supplementation increased the severity of diabetes in LDS-treated BALB/cByJ mice (P < 0.0005); however, EFA deficiency also prevented diabetes in CsA-supplemented BALB/cByJ mice.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Racially determined abnormal essential fatty acid and prostaglandin metabolism and food allergies linked to autoimmune, inflammatory, and psychiatric disorders among Coastal British Columbia Indians.

British Columbia Coastal Indians possess abnormal patterns of essential fatty acid (EFA) and prostaglandin (PGE) metabolism as racially determined genetic traits, probably a consequence of evolving for tens of thousands of years on a diet extremely rich in EFA's. EFA metabolism abnormalities and unusual epidemiological patterns suggest fundamental pathologies so subtle as to be obscured in other groups, yet readily observable among these Indians. It is hypothesized that eicosapentaenoic acid and prostaglandin El deficiencies predispose Coastal Indians to food allergies which in turn predispose them to autoimmune, inflammatory, and psychiatric disorders.

Autoimmune Diseases↗
PubMed1980

Requirement of essential fatty acids in the diet for development of the mouse mammary gland.

The ductal system of mammary glands in C3H mice that were started on diets deficient in essential fatty acid(s) (EFA) 1--2 weeks after weaning developed at a normal rate. The alveolar structures, however, began to disappear in the mice after 17 weeks on the EFA-deficient regimen. Injection sc of linoleic acid prevented the atrophic process. Alveoli were also absent in the glands of multiparous mice that were maintained for 32 weeks on the EFA-deficient diet. When the EFA-deficient regimen was started in females during midpregnancy and maintained continuously thereafter, both ductal and alveolar structures failed to develop in the mammary glands of the offspring. Linoleic acid appears to be required for development of ductal and alveolar structures during growth of the mammary gland and also for maintenance of the alveolar structures in the adult mammary gland.

Animals↗
PubMed1996

Interactions between essential fatty acid, prostanoid, polyol pathway and nitric oxide mechanisms in the neurovascular deficit of diabetic rats.

Impaired omega-6 essential fatty acid metabolism and exaggerated polyol pathway flux contribute to the neurovascular abnormalities in streptozotocin-diabetic rats. The potential interactions between these mechanisms were examined by comparing the effects of threshold doses of aldose reductase inhibitors and evening primrose oil, alone and in combination, on neurovascular deficits. In addition, high-dose aldose reductase inhibitor and evening primrose oil treatment effects were challenged by co-treatment with the cyclo-oxygenase inhibitor, flurbiprofen, or the nitric oxide synthase inhibitor, NG-nitro-L-arginine. Eight weeks of diabetes caused an 18.9% reduction in sciatic motor conduction velocity (p < 0.001). This was only modestly ameliorated by a 0.1% dietary supplement of evening primrose oil or the aldose reductase inhibitors ZD5522 (0.25 mg.kg-1.day-1 and WAY121 509 (0.2 mg.kg-1.day-1 for the final 2 weeks. However, joint treatment with primrose oil and ZD5522 or WAY121 509 caused marked 71.5 and 82.4% corrections, respectively, of the conduction deficit. Sciatic nutritive blood flow was 43.1% reduced by diabetes (p < 0.001) and this was corrected by 67.8% with joint ZD5522 and primrose oil treatment (p < 0.001). High-dose WAY121 509 (10 mg. kg-1.day-1 and primrose oil (10% dietary supplement) prevented sciatic conduction velocity and nutritive blood flow deficits in 1-month diabetic rats (p < 0.001). However, these effects were abolished by flurbiprofen (5 mg.kg(-1).day-1 and NG-nitro-L-arginine (10 mg.kg-1.day-1) co-treatment (p < 0.001). Thus, the data provide evidence for synergistic interactions between polyol pathway/nitric oxide and essential fatty acid/cyclo-oxygenase systems in the control of neurovascular function in diabetic rats, from which a potential therapeutic advantage could be derived.

Acetanilides↗
PubMed2005

Influence of subcutaneous injection of essential fatty acids on the stress-induced modifications of rat platelet aggregation and membrane lipid composition.

Membrane lipids play an important role in the function of blood platelets but the mechanisms by which the lipid composition of the platelet membrane is adjusted remain unclear. It has been shown that stress and poly-unsaturated fatty acids modified the lipid composition of blood plasma and platelet lipids, but very little is known about the effect of stress and fatty acids on membrane platelet lipid composition. The purpose of the present investigation was to study the influence of the essential fatty acids: linoleic, linolenic and arachidonic acids on the composition of the platelet membrane lipids of rats assigned to heat and restraint stress. It was shown that injections of polyunsaturated fatty acids decrease or suppress the stress-induced increase in platelet aggregation, suppress the stress-induced modification of the composition of the platelet membrane lipids and modify the fatty acid composition of the platelet membrane phospholipids.

Animals↗