The relation of deficiencies of vitamin A and of essential fatty acids to follicular hyperkeratosis in the rat.
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Animals↗
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Cholesterol and essential fatty acid deficiency.
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Cholesterol↗
Effects of essential fatty acid deficiency in young swine.
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Animals↗
Essential fatty acid uptake and metabolism in the developing rodent brain.
Studies were carried out to determine whether the brain takes up and metabolizes essential fatty acids during early postnatal development in rodents. Rats and mice were dosed with deuterium-labeled linoleic and linolenic acids either by intraperitoneal injection or by gavage. Animals were killed at different times thereafter, and organs were removed. Brains, livers, and blood were analyzed by gas chromatography--negative-ion-mass spectrometry for labeled fatty acids. To determine whether fatty acids were present in the brain apart from cerebral blood, a subset of animals was exsanguinated by perfusion with buffered saline, and the brain was then fractionated into subcellular components. Results demonstrated that the brain took up both labeled essential fatty acids within 8 h from the time of dosing. There was on average a greater uptake of linolenic acid into the cerebellum than into the cerebral cortex during the first 8 d of life in rats. The amount of linoleic acid taken into either region was similar, however. Docosahexaenoic acid intermediates, 20:5n-3 and 22:5n-3, were also found labeled in the brain. Time-course labeling experiments indicated that these intermediates may be converted to 22:6n-3 within the brain. A rise of labeled 22:6n-3 in the brain at 24 h appeared to be due to uptake of this fatty acid from the blood. The amount of labeled 22:6n-3 in the brain continued to increase beyond 24 h, and this did not appear to be correlated with its blood concentration. These results suggest that, during development in the rodent, different regions within the brain may vary in their capacity to synthesize 22:6n-3, and this may be correlated with regional growth rates.
Administration, Oral↗
Decrease in essential fatty acid content of edible fats during the frying process.
Degradation of sunflower oil, rapeseed oil, and lard during the frying operation was investigated by studying the loss of essential fatty acids compared to the accumulation of decomposition products. Linoleic and/or linolenic acid concentration was measured by GLC, and for detecting decomposition products determination of polymer content by GPC was chosen. Twelve laboratory experiments with different heating or frying conditions were run aimed at modelling practice and studying the effects of certain factors. The results indicated that loss of essential fatty acids being a parallel process to the accumulation of breakdown products is suitable both for detecting the decrease in nutritive value and for quality assessment of used frying fats. It was also found that the rate of deterioration is considerably affected by the nature of fat and the frying parameters. Study of the relationship between polymer content and the decrease in essential fatty acid concentration (using data from 110 samples) showed that high, linear correlation depending on the nature of fat can be found. Correlation coefficients and equations of regression lines were calculated.
Amino Acids, Essential↗
Essential fatty acid deficiency prevents multiple low-dose streptozotocin-induced diabetes in CD-1 mice.
Multiple i.p. injections of low-dose streptozotocin (40 mg/kg) produce insulitis, beta cell destruction, and diabetes in male CD-1 mice. Recent data also suggest that macrophages figure in the low-dose streptozotocin model. Because other recent studies have shown that essential fatty acid deficiency prevents autoimmune nephritis in mice, decreases the number of resident Ia-positive glomerular macrophages, and decreases the elicitation of macrophages into the glomerulus in inflammation, we examined the effect of essential fatty acid deficiency on the incidence and severity of insulitis and diabetes in CD-1 mice treated with low-dose streptozotocin. Streptozotocin-treated mice on the control diet uniformly developed diabetes (19/19). Essential fatty acid-deficient mice treated with streptozotocin did not develop diabetes (1/13). Mean plasma glucose levels for the control and essential fatty acid-deficient mice were 384.5 +/- 23.6 and 129.1 +/- 15.5 mg/dl, respectively, at the end of 1 month. To discern whether essential fatty acid deficiency prevented the streptozotocin-induced beta cell injury or the inflammatory response to injured beta cells, mice were repleted with daily injections of 99% pure methyl linoleate beginning 3 days after the last streptozotocin injection. These mice also quickly developed severe (3/4) or mild (1/4) diabetes. Histologic examination of the pancreata of control mice or repleted mice showed marked insulitis and beta cell destruction; in contrast, the pancreata of essential fatty acid-deficient mice showed preservation of beta cells and only focal mild peri-insulitis. Essential fatty acid deficiency thus prevents the insulitis and resultant diabetes in low-dose streptozotocin-treated CD-1 mice, suggesting a central role for macrophages and lipid mediators in this autoimmunity model.
Animals↗
Essential fatty acid metabolism in cultured rat cardiomyocytes in response to either N-6 or N-3 fatty acid supplementation.
In this study we demonstrate that cultured rat cardiomyocytes possess the capacity to desaturate/elongate essential fatty acids (EFAs). Alpha-linolenic acid (ALA) conversion to higher metabolites was greater than linoleic acid (LA) conversion, according to the higher affinity of the delta-6-desaturase enzyme for the n-3 than for the n-6 EFAs. Gamma-linolenic acid (GLA) supplementation to the culture medium had no influence on LA conversion; but the addition of eicosapentaenoic (EPA) and docosahexaenoic (DHA) acids significantly decreased the formation of interconversion products from LA. The conversion of ALA to higher metabolites was greatly affected by GLA; EPA had no effect on ALA conversion, while DHA significantly inhibited it. Both GLA (converted mostly to dihomo-gamma-linolenic acid) and EPA can be removed from phospholipids and addressed to prostanoid biosynthesis, so avoiding their potential accumulation and the inhibition of their own production. Our data clearly indicate that supplementation of the culture medium with either n-6 or n-3 fatty acids can cause reduced levels of the other series of fatty acids. This effect may be undesirable, since both n-6 and n-3 fatty acids are important in the prevention of coronary diseases.
Animals↗
Inflammatory pleuropulmonary fibrosis in essential fatty acid deficient rats and the lack of response to methysergide.
In view of the association between essential fatty acid (EFA) deficiency and human cystic fibrosis, we have investigated the possible occurrence of pulmonary disease in rats fed an EFA deficient (EFAD) diet for 40 weeks. In contrast to a few slight spontaneous lesions consisting of pleural membrane hyperplasia, which were found in the lungs of control rats, a much greater incidence of fibrotic lesions was observed in the lungs of EFAD rats. These pleuropulmonary fibroses extended from the hyperplastic pleural membrane into the alveoli and were characterized by collagen deposition and marked macrophage infiltration to the extent that, in some cases, the alveolar septa were completely obstructed by inflammatory exudate. These findings lend indirect support to the contention that EFA deficiency plays a role in the aetiology of cystic fibrosis, at least with regard to pulmonary lesions. Administration of methysergide (10 mg/kg/day, p.o.) for a total of 11 weeks, did not alter the incidence of fibrosis in the lungs of EFAD rats, despite the finding that a man who had developed pleuropulmonary fibrosis as a result of chronic methysergide treatment exhibited a relative serum EFA deficiency. While a relative EFA deficiency may be a predisposing factor for the induction of fibrosis by chronic methysergide treatment, our data are not sufficient to make a decision upon this hypothesis.
Adult↗
A relationship between essential fatty acid and vitamin E deficiency.
To test whether vitamin E deficiency might influence the course of essential fatty acid (EFA) deficiency, Long Evans rats were fed diets containing a marginal amount (1.5% of calories) of 18:2 omega 6 or 18:3 omega 3 fatty acid with complete absence of the other and with or without vitamin E. Vitamin E contents decreased continuously in serum and liver in all rats fed the E-free diets but in the brains of only the rats fed the marginal 18:3 omega 3, E-free diet. It is considered that the vitamin E is cooxidized in the liver with 22:6 omega 3, since this fatty acid is very low in livers of the rats fed the marginal 18:2 omega 6 diet but much higher in livers of the rats fed the marginal 18:3 omega 3 diet. Brain 22:6 omega 3 values are comparable for both groups. The source of 22:6 omega 3 is evidently in the mother's milk, since following weaning there is a precipitous drop in 22:6 omega 3 in serum, liver and carcass of rats on the 18:2 omega 6--containing diet. No significant signs of EFA deficiency were seen in the E-deficient rats.
Animals↗
Short term essential fatty acid deficiency in rats. Influence of dietary carbohydrates.
The effects of long term (8-14 wk) essential fatty acid (EFA)-deprived diets in rats are well documented. In the present study, we compared, in weanling rats, the effect of a short term (two wk) hydrogenated coconut oil, EFA-deprived, diet (D) with that of a corn oil, EFA-adequate, diet (A), using either sucrose (SU) or starch (ST) as carbohydrate. After two wk, rats fed the sucrose/hydrogenated coconut oil diet developed some characteristic features of EFA deprivation: slower growth rate, decreases in linoleic and arachidonic acid of plasma phospholipids and an increase in n-9 eicosatrienoic acid of plasma phospholipids. When rats ate the starch/hydrogenated coconut oil diet, there was a similar decrease in linoleic acid of plasma phospholipids, but only a small effect on growth rate and no change in the arachidonic acid content of plasma phospholipids. EFA deprivation and sucrose had opposite effects on plasma triglyceride (TG) levels: deprivation induced a decrease, whereas the sucrose induced an increase in very low density lipoprotein (VLDL) triglycerides. The observed decrease in plasma triglyceride during EFA deprivation might result from an activation of lipoprotein lipase during the early stages of deprivation.
Animals↗
A double-blind trial of essential fatty acid supplementation in patients with tardive dyskinesia.
This study reports the results of a trial of essential fatty acid (EFA) supplementation in psychiatric patients (predominantly schizophrenics) with movement disorders. Evidence of EFA deficiency in these patients was observed. The antidyskinetic effect of EFA supplementation was marginally significant but not clinically important. However, active treatment produced highly significant improvements in total psychopathology scores and schizophrenia subscale scores, and a significant improvement in memory.
Antipsychotic Agents↗
An imbalance of dietary essential fatty acids retards behavioral development in mice.
This study investigated the effects of an imbalance of dietary essential fatty acids on behavioral development. Pregnant and lactating mice were fed a diet with a very low (n-6):(n-3) ratio, in which the (n-6) and (n-3) fatty acids were provided solely as linoleic acid [LA, 18:2 (n-6)] and very high levels of docosahexaenoic acid [DHA, 22:6 (n-3)], respectively. The development of the pups was compared with that of pups of similar age and body weight that had been undernourished by rearing in large litters. On the day of conception (Day 0), pregnant B6D2F1 mice were assigned randomly to one of four dietary groups. Two of these groups were fed lab chow, and after birth varied in terms of the number of pups per litter, large (LgLIT) = 12, and normal (NmLIT) = 6. The remaining two groups both had six pups per litter, but varied in dietary (n-6):(n-3) ratio, low (LoRAT = 0.32) and normal (NmRAT = 4.0). On Day 32 postconception both the LgLIT and the LoRAT groups had lower body weights and were behaviorally retarded relative to their respective NmLIT and NmRAT controls. Nonetheless, there was some sparing of function in both these groups, as they were behaviorally advanced relative to younger animals of a similar body weight. These findings show that the growth retardation seen in the offspring of dams fed a diet with a low (n-6):(n-3) ratio and very high levels of DHA is accompanied by behavioral retardation of a similar degree to that seen in malnourished pups.
Animals↗
Essential fatty acid status in plasma phospholipids of mother and neonate after multiple pregnancy.
During singleton pregnancy, maternal essential fatty acid (EFA) status decreases progressively. After multiple pregnancy it can be expected that the neonatal and maternal EFA status is even lower. To study whether the maternal EFA supply to the fetus is a limiting factor to the neonatal EFA status, we compared the plasma phospholipid EFA status of newborn multiplets (30 pairs of twins and 7 sets of triplets) with that of singletons (n = 89) at birth and that of their mothers at delivery. After correction for gestational age, a slightly lower EFA status was found in maternal and umbilical plasma from multiplets compared to singletons. No relation was found between the difference in birthweight of the smallest and the largest neonate of a set of multiplets and the difference in cord plasma EFA levels. Correlations between maternal and umbilical plasma EFA levels were comparable for multiple and singleton pregnancies. Therefore, adequate dietary intake is required to guarantee an optimal neonatal EFA status, especially during multiple pregnancy.
Birth Weight↗
Effect of essential fatty acid deficiency on maternal, placental, and fetal rat tissues.
Prolonged dietary deprivation is needed to produce essential fatty acid (EFA) deficiency. But lack of EFA also impairs reproductive function. Inclusion of small amounts of linoleic acid in the diet can overcome this difficulty; further, if large amounts of oleic acid are included in the diet, this competes with the utilization of 18:2 producing EFA deficiency. Using this approach, female rats were fed a fat-free diet containing 5% oleic acid w/w (with 2-3% 18:2) as the only source of fat for 4 months. They were mated and on the 21st day of gestation, the fatty acids of fetal tissues, placenta, maternal liver and plasma were analyzed and compared to controls on a stock diet. Fetuses from the experimental group were smaller and contained higher amounts of 18:1 and 20:3 omega 9 indicating EFA deficiency. The omega 6 fatty acids in the polar lipids of placenta of the EFA-deficient group were not significantly lower than the controls, in spite of lower concentrations in the maternal plasma, suggesting a unique capacity of the placenta to concentrate omega 6 fatty acids, which in turn may be utilized for prostaglandin synthesis needed for inducing labor and other vascular changes in the fetus.
Animals↗
Essential fatty acid deficiency depletes rat glomeruli of resident macrophages and inhibits angiotensin II-induced eicosanoid synthesis.
Essential fatty acid (EFA) deficiency exerts a beneficial effect on immune-mediated glomerulonephritis, preventing both the tissue injury and consequent mortality. Because both macrophages and eicosanoids are thought to play pathogenic roles in glomerulonephritis, and because macrophages play an important role in modulating arachidonate metabolism at sites of renal injury, the effects of EFA deficiency on the population of resident glomerular macrophages and on glomerular eicosanoid generation were examined. EFA deficiency led to a striking reduction in the number of resident glomerular macrophages and a corresponding reduction in the number of resident glomerular Ia+ cells. This phenomenon was not strain-specific, was not due to a decrease in circulating monocytes, was not a function of changes in cell surface labeling characteristics, and was not restricted to a specific subset of glomeruli. In addition, EFA deficiency affected other areas of the renal cortex: a comparable depletion of interstitial macrophages and Ia+ cells was also observed. In conjunction with the decrease in glomerular macrophages seen with the deficiency state, a marked decrease in both basal and angiotensin II-stimulated glomerular eicosanoid production was noted. In contrast to angiotensin II, platelet-activating factor-induced eicosanoid production was not significantly affected by the deficiency state. These changes in glomerular eicosanoid production could not be attributed to changes in glomerular cyclooxygenase or reacylation capacity. Dietary (n-6) fatty acid supplementation, but not (n-3) fatty acid supplementation, reversed both the decrease in glomerular macrophages and the diminished eicosanoid metabolism seen with the deficiency state. Understanding the mechanisms behind the changes in the glomerular microenvironment induced by EFA deficiency may provide a basis for elucidating the protective effect of dietary fatty acid manipulation on immune-mediated glomerulonephritis.
Angiotensin II↗
Oral correction of essential fatty acid deficiency in cystic fibrosis.
A combination of pancreatic insufficiency and inadequate caloric intake may produce essential fatty acids (EFA) deficiency in patients with cystic fibrosis. Seventy-five percent of the adolescents and young adults with poor weight gain in our clinic were EFA-deficient by total plasma linoleic acid criteria. Twenty of these patients were placed on an oral hyperalimentation regimen containing 230% of calories required for basal energy expenditure, 40% as fat. Forty percent of these (8/20) achieved normal EFA levels on this diet. Eight of the nonresponding patients were given an additional 5% of their caloric intake as linoleic acid monoglyceride. All who maintained caloric intake achieved normal EFA levels. Normalization of EFA levels was associated with a number of clinical benefits including increase in weight and activity and, in five teenage girls, regulation of menses. The 16 control patients who received standard pancrelipase therapy and nutritional supplements remained fatty acid deficient. We conclude that oral hyperalimentation can restore EFA levels in cystic fibrosis patients if adequate calories are available to provide energy needs.
Cystic Fibrosis↗
Plasma and erythrocyte essential fatty acids during total parenteral nutrition in infants: effects of a cutaneous supply.
In order to prevent essential fatty acid (EFA) deficiency induced by fat-free total parenteral nutrition (TPN), 10 infants on TPN were rubbed three times daily for 20 days using oenethera oil (80% EFA). Total EFA amount provided cutaneously was 1900 mg/kg/d. Plasma and red blood cells phospholipids were determined on days 1 and 20 in these 10 treated and six untreated infants on TPN and compared with those of normal control infants. On day 1, plasma nonessential FA including 20:3 n-9(p less than 0.01) were increased in both TPN groups while 18:2 n-6 and 18:3 n-3 (p less than 0.001 and p less than 0.01) were decreased. On the 20th day, EFA deficiency had worsened with a decrease in plasma level of 20:4 n-6 (p less than 0.02) and a higher than normal triene/tetraene ratio : 3.4 +/- 1.1 and 2.3 +/- 0.6 vs 0.1 +/- 0.1 (p less than 0.02). As for red blood cells phospholipids, 16:0 was increased and 18:2 n-6 and 20:3 n-6 were decreased (p less than 0.05) on day 1. On day 20, these FA were more abnormal while 20:3 n-9 became significantly increased (p less than 0.05). No difference was observed between the TPN groups at any time. These results show that cutaneous application of large amounts of EFA-rich oil is unable to prevent or cure TPN induced EFA deficiency.
Absorption↗
Diet-induced essential fatty acid deficiency in ambulatory patient with type I diabetes mellitus.
We report a case of symptomatic essential fatty acid deficiency (EFAD) occurring in a free-living individual with type I diabetes mellitus who was voluntarily following a high-carbohydrate, fat-restricted diet. The patient was 43 yr old with type I diabetes for 18 yr and no chronic complications. His self-imposed diet excluded all red meats, fats, and oils. After several months of this diet, the patient developed lethargy and a pruritic, diffuse, scaly, and erythematous rash. Biochemical studies revealed a mildly elevated SGOT and abnormally low levels of linoleic, linolenic, and arachidonic fatty acids. Treatment with linoleic acid supplementation in his diet improved the rash, normalized SGOT, and corrected the fatty acid profile. We conclude that EFAD may occur in a free-living individual after consuming a very-low-fat diet.
Adult↗