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PubMed1980

Effect of essential fatty acid deficiency on experimental allergic encephalomyelitis in rats.

Previous claims that experimental allergic encephalomyelitis (EAE) was enhanced by essential fatty acid (EFA) deficiency were reinvestigated. Deficiency was induced in Lewis rats by feeding a fat-free diet starting in late gestation, at weaning or in adult life with or without a previous period of starvation. Retardation of growth, the typical dermatitis, increased water consumption and testicular atrophy gave evidence of EFA deficiency. Control rats were fed a complete diet or a fat-free diet supplemented with corn oil. EAE was induced in EFA-deficient and control rats by conventional active sensitization with neural antigen and adjuvants or by passive transfer of living lymphoid cells from sensitized nutritionally normal donors. Contrary to previous reports, EFA deficiency did not enhance EAE in any of seven experiments, and these results were supported by histological examinations. In fact, we found inhibition of clinical signs, but not histological lesions, when EFA deficiency was moderately advanced. This was accompanied by (and probably related to) thymic atrophy, possibly due to nonspecific stress. Also we found that EFA deficiency had no effect on a non-immunological model of brain inflammation that resembles EAE in the occurrence of lymphocytic infiltrates.

Aging↗
PubMed1988

The effect of dietary essential fatty acid deficiency on the composition and properties of the liver microsomal membrane of rats.

The effect of dietary essential fatty acid (EFA) deficiency on lipid composition, fluidity and important enzyme and transport activities of liver microsomal membrane was studied in weanling rats. After 133 d of EFA deficiency, no difference was noticed in membrane phospholipid, cholesterol and protein levels, but a significant change occurred in the fatty acid composition of bilayer phospholipids. In EFA-deficient rats, linoleic (18:2(n-6] and arachidonic (20:4(n-6] acids were both severely lower while oleic (18:1(n-9], palmitoleic (16:1(n-7] and particularly 5,8,11-eicosatrienoic (20:3(n-9] acids were significantly higher than in controls. The higher level of the latter tended to compensate for the lower level of 20:4(n-6). Membrane fluidity, as estimated by the reciprocal of the order parameter S, was lower in the deficient rats than in the controls, and all the measured microsomal enzyme activities were markedly affected. NADH-Cyt b5 electron transferring system, coupled with the fatty acid desaturation system, was higher than in controls. In contrast, the cytochrome P450 complex activity was lower and some of the important liver detoxifying enzyme activities were lower due to physical-chemical changes in the microsomal membrane. Calcium uptake and Ca2+-ATPase activity were also significantly lower in EFA-deficient rats than in controls. It was concluded that fatty acid composition may be the major factor contributing to membrane fluidity and function and that EFA might play a role in regulating the intrinsic membrane protein activities.

Animals↗
PubMed2002

Reduced erythrocyte membrane essential fatty acids and increased lipid peroxides in schizophrenia at the never-medicated first-episode of psychosis and after years of treatment with antipsychotics.

Abnormal membrane phospholipid essential polyunsaturated fatty acid (EPUFA) metabolism (i.e., reduced incorporation into phospholipids and increased breakdown) has been suggested to contribute to the etiopathophysiology of schizophrenia. However, most of the published studies have reported changes in the levels of membrane EPUFA in chronic medicated patients or in drug-naive patients long after onset of illness (1-2 years). Since the EPUFA metabolism can be altered by years of untreated illness or differentially altered by various antipsychotics, the significance of EPUFA membrane status to schizophrenia psychopathophysiology is unclear. We report the erythrocyte membrane EPUFA levels in drug-naive patients within +/- 4.5 days of onset of psychosis from an Army Medical Center, and in patients treated years with antipsychotics from a Veterans Affairs Medical Center. The levels of plasma lipid peroxides (TBARS, thiobarbituric acid reactive substances), products of damaged EPUFAs, were also determined. The levels of EPUFAs, particularly arachidonic acid (AA) and docosahexaenoic acid (DHA) were significantly lower (P < 0.001) in drug-naive patients at the onset of psychosis compared to matched normal controls. These lower EPUFA levels were associated with significantly higher levels of TBARS in patients (P < 0.001). The levels of AA and DHA were also lower (P < 0.001) and TBARS higher in chronic medicated patients than normal controls. However, the EPUFA levels were higher in chronic medicated patients than drug-naive first-episode patients. These data indicate that lower membrane AA and DHA most likely predate the illness and probably contribute to the onset of illness, and furthermore treatment with some antipsychotics may increase the levels of EPUFAs. The lipid peroxidation data suggest that possible increased oxidative stress, either as a part of the illness and/or its treatment with antipsychotics, may be one of the mechanisms of reduced membrane EPUFAs. These findings may have a significant impact on improving strategies for supplementation of EPUFAs and antioxidants to improve the outcome of schizophrenia.

Adolescent↗
PubMed1995

[Essential fatty acids and prematurity: a triple experimental approach].

Previous studies in our laboratory have shown that in fetal plasma arachidonic (AA) and docosahexaenoic acid (DHA) levels are higher (about two fold) than in maternal plasma whereas the reverse situation was observed for the levels of their C18 precursors linoleic acid (AL) and alpha-linolenic acid (AAL) (13). This paradoxical situation raises the questions of the origin of the long chain polyunsaturated fatty acids (PUFAs) and of the ability of fetal liver to desaturate and elongate C18 precursors since placenta was shown not to be able to desaturate fatty acids. This question should be answered for the rationale of formula feeding supplementation either with long chain PUFAs or with their C18 precursors. Three experimental approaches can contribute to elucidate this dilemna: nutritional studies with formula supplementation, investigations on hepatic enzymes in vitro, in vivo experiments using stable isotopes. Supplementation of formulas with AAL in precise conditions (AL/AAL ratio: 6.4/1 and AL intake: 4.95% of total energetic supply) was done in a multicentric study including 88 premature newborns (32 weeks post conceptional age) for five weeks. The plasma phospholipid and red blood cell DHA status was found to be closer to human milk feeding than with standard formula feeding and most of the n-6 pathway was preserved. The data suggests that in premature newborns a significant conversion of AAL into DHA is possible provided an equilibrium is respected between AL and AAL supplies. This conversion is confirmed both by in vitro and in vivo studies: in fetal livers (obtained from therapeutic abortion) significant delta 6 and delta 5 desaturase activities were measured by a radiochemical method using reverse phase HPLC separation of [1-14C] labelled substrates and products in the n-6 and in the n-3 series. Substrate inhibition was observed especially at delta 5 desaturation and the maximum velocities were relatively limited mainly in the n-6 pathway which was slower than in the n-3 serie. These data are in agreement with recent preliminary data obtained in different laboratories with stable isotopes in vivo but in infants born in term: experiments using either 13C or deuterium labelled fatty acids concluded to the conversion of C18 essential fatty acids into AA and DHA justifying (AAL) formula supplementation for sustaining DHA status in preterm newborns.

Arachidonic Acid↗
PubMed1991

[Essential fatty acids in carcinoma].

Carcinomatous tissue consumes intensely polyenic fatty acids which are the building elements of growing biomembranes. The authors compared plasma levels of essential fatty acids (EFA) in three groups of subjects: 1. patients with carcinoma, 2. control group, 3. groups with sub-nutrition. The profile in these three groups differs significantly. In patients with carcinoma the level of derived EFA is reduced (20:4w6, 20:5w3, 22:6w3), while primary EFA (linoleic acid 18:2w6) is unaltered. The results suggest that in patients with carcinoma there is a specific reduction of EFA essential for the formation of cellular biomembranes. The reduction is probably due to the increased consumptions of derived EFA by carcinomatous tissues.

Carcinoma↗
PubMed1988

Essential fatty acid pattern of glycerolipids in rat hepatocytes in primary culture and in coculture with rat liver epithelial cells.

The linoleic acid content of phosphatidylethanolamine (PE), phosphatidylcholine (PC) and triglyceride (TG) rapidly fell in rat hepatocytes in primary culture up to four days and in coculture with liver epithelial cells up to eight days. At the same time, the level of polyunsaturated fatty acids (PUFA), especially arachidonic acid, remained constant in PE, slightly decreased in PC and dropped in TG. There was no variation of the nonessential PUFA, 20:3n-9. Linoleic acid supplementation of cultures 24 hr before the harvest induced a rise in the linoleic acid level of the three lipid classes. Arachidonic acid remained constant in TG and only slightly decreased in PE and PC at day 4 of primary culture and day 8 of coculture. The level of 20:3n-9 increased in PE and PC and much more in TG. This net increase in the arachidonic acid and 20:3n-9 levels in TG could not be explained only by a transfer from the phospholipid pools of PUFA because the phospholipid content of hepatocytes and PUFA levels of phospholipids did not vary under linoleic supplementation. The low percentage of arachidonic acid in epithelial cells rules out any participation of these cells in the increase of arachidonic acid in supplemented cocultures. Triglycerides may act as a storage pool for plasma PUFA up to four days of primary culture and eight days of coculture. Besides, coculture seems more potent than primary culture to maintain the phospholipid level, to spare the essential PUFA in PE and to increase the TG synthesis in response to linoleic acid supplementation.

Animals↗
PubMed1999

Essential fatty acids are mediators of brain biochemistry and cognitive functions.

Major advances have been made in understanding the biochemistry of essential fatty acids (FA) and their interactions with metabolic pathways leading to the production of longer and more complex fatty acids and lipids. Less understood are the roles played by FA which are known to affect neurotransmitters, peptides, releasing factors, hormones, and a variety of physiological and cognitive processes. Based on empirical findings we propose that (a) FA exert a controlling function in the modulation of neuronal membrane fluidity, and (b) the critical factor in FA action and efficacy is not absolute level but rather the ratio between various groups of FA. This approach unifies the biochemical and cognitive results obtained from many different and unrelated fields of research.

Animals↗
PubMed1994

Essential fatty acids alter the activity of manganese-superoxide dismutase in rat heart.

The effects of oil-derived dietary essential fatty acids on the activities of mitchondrial Mn-SOD (manganese-superoxide dismutase) and cytosolic cupric zinc-superoxide dismutase (Cu/Zn-SOD) were investigated in rat heart. A control group of rats was fed a stock diet for 29 d, and a second group was fed on a fat-free diet. Three other groups were fed fat-free diets that were supplemented with (i) borage oil, which is rich in linoleic (18:2n-6) and gamma-linolenic (18:3n-6) acids, (ii) fungal oil, which is rich in gamma-linolenic, but low in linoleic acid, or (iii) evening primrose oil, which is rich in linoleic acid and low in gamma-linolenic acid. An increase in the percentage composition of arachidonic acid (20:4n-6) in both the choline and ethanolamine phospholipids, together with a decrease in linoleic acid in ethanolamine phospholipids, were found in heart membranes after feeding the rats with diets containing borage oil or fungal oil as compared to those fed the stock diet. The respective activities of Mn-SOD in rats fed the borage or fungal oil diets were also significantly higher than in rats fed the stock diet alone. No change in cytosolic Cn/Zn-SOD activity was observed. Dietary supply of linoleic acid-rich evening primrose oil resulted in an increased proportion of choline phospholipid linoleic acid without any changes in arachidonic acid content or in the activity of Mn-SOD. By contrast, a reduction in the activity of Mn-SOD was detected in rats fed a fat-free diet.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Effect of dietary essential fatty acid deficiency on Ca(2+)-ATPase activity in microsomal fraction of rat submandibular gland.

1. The effect of dietary essential fatty acid (EFA) deficiency on Ca(2+)-ATPase activity of rat submandibular gland microsomal fraction was studied. 2. The specific activity of Ca(2+)-ATPase per milligram of microsomal protein was depressed about 35% in rats fed the EFA-deficient diet as compared with that in those fed the control diet. 3. Lineweaver-Burk plots for Ca(2+)-ATPase activity showed no significant differences in Km values for Ca2+ and ATP, but the Vmax was decreased in the EFA-deficient rats. 4. The above results suggest that depression of the Ca(2+)-ATPase activity in rats fed the EFA-deficient diet is probably due to the decrease in the Vmax of the enzyme.

Animals↗
PubMed1983

Essential fatty acids and maladjusted behaviour in children.

It has been suggested that hyperactivity may be produced by a deficiency in essential fatty acids (EFA) leading to a deficit in prostaglandin (PG) formation. The red blood cells EFAs levels were examined in 23 maladjusted children and in 20 normal children. Although no individual EFA showed statistically significant differences between the normal and maladjusted children, multivariate analysis showed that the levels of EFA series 2 PG precursors in maladjusted children were significantly lower than in controls as predicted (P = 0.0001).

Adolescent↗
PubMed1996

Impact of essential fatty acid deficiency on hepatic sterol metabolism in rats.

The major aim of the current investigation was to define whether essential fatty acid (EFA) deficiency modifies the intrahepatic metabolism and biliary output of sterols in rats. EFA-deficient diet caused an impoverishment in linoleic, arachidonic, and docosahexaenoic acids, and a marked enrichment in the eicosatrienoic acid of the plasma, liver, and hepatic microsomes. During a short term of biliary drainage, a significant decline of the pool size of biliary sterols was noted in EFA-deficient rats compared with control rats. To assess the biosynthesis of biliary components, the common bile duct was cannulated and the pool size depleted (24 hours). Subsequently, a 6-hour bile collection disclosed a significant decrease (nmoles/min/g liver) in bile acids (4.8 +/- 0.3 vs. 8.4 +/- 0.7, P < .005), cholesterol (0.26 +/- 0.01 vs. 0.34 +/- 0.02, P < .05), and phospholipids (1.49 +/- 0.11 vs. 2.82 +/- 0.32, P < .005) in EFA-deficient rats compared with controls (n = 6/group). When cholesterogenesis was measured by the incorporation of [14C]acetate and 3H20 into cholesterol, using liver slices, it was also found to be significantly (P < .001) reduced in EFA-deficient rats. The activity of hepatic 3-hydroxy-3-methylglutaryl coenzyme A reductase, the rate-limiting enzyme in cholesterol biosynthesis, was consistently lower (80 percent, P < .001) in EFA-deficient rats. In parallel experiments, the direct measurement of microsomal acyl-CoA:cholesterol acyl-transferase (ACAT) showed a decrease averaging 52 percent (P < .001). This is in striking contrast to the elevated activity (157 percent, P < .005) of cholesterol 7 alpha-hydroxylase, the rate-limiting enzyme in bile acid biosynthesis. Current experiments also suggest that the enzyme regulation involving phosphorylation and dephosphorylation is modified by EFA deficiency. Among the structural alterations observed in the morphology of hepatocytes in EFA-deficient rats, the lumen of bile canaliculi was reduced in size. These results underline the importance of EFA in the major mechanisms involved in the maintenance of hepatocyte sterol balance.

Acetates↗
PubMed2001

Changes in the maternal essential fatty acid profile during early pregnancy and the relation of the profile to diet.

BACKGROUND: Although the pattern of the essential fatty acids (EFAs) changes considerably from week 10 of pregnancy to term, no information is available on changes in EFA concentrations in the early stages of pregnancy. OBJECTIVE: The main objectives were to assess the EFA status, particularly that of 22:6n-3, in women during the first 10 wk of pregnancy and to investigate the relation of EFA status to dietary EFA intake during this period. DESIGN: Healthy women (n = 24) planning to become pregnant were recruited. The fatty acid composition of plasma and erythrocyte phospholipids was determined before and at weeks 4, 6, 8, and 10 of pregnancy. Food intake was assessed at entry into the study and at week 10 of pregnancy by using food-frequency questionnaires. RESULTS: A small but nonsignificant increase in dietary intake of 22:6n-3 was found. The plasma phospholipid content of 22:6n-3 (% by wt) increased continuously during the first 10 wk of pregnancy. At week 10 of pregnancy, the plasma percentages of 16:0, 20:3n-6, and 20:4n-6 had increased significantly, whereas the percentages of the 18-24-carbon saturated fatty acids, 18:2n-6, and the ratio of n-6 to n-3 fatty acids had dropped significantly. The composition of erythrocyte phospholipids showed changes similar to those observed in plasma. CONCLUSIONS: Maternal plasma and erythrocyte phospholipid 22:6n-3 concentrations start to increase in very early pregnancy, which cannot be explained by changes in dietary intake alone. This rise probably represents early maternal adaptations to meet the requirements of highly proliferating and differentiating tissues at this stage of fetal development.

Adult↗
PubMed1987

Influence of an essential fatty acid deficient diet on absorption of topical hydrocortisone in the rat.

Using a rat dermatosis model, produced by dietary essential fatty acid deficiency (EFAD), which is characterized by histological changes and elevated transepidermal water loss, changes in skin permeability were studied using [14C]-hydrocortisone (HC). Skin, serum and urinary levels of HC were measured, and absorption and excretion of HC in EFAD rats compared with that in control rats on a normal diet. This animal model has demonstrated the importance of the functional integrity of the horny layer in skin penetration.

Administration, Topical↗
PubMed1993

Transcutaneous application of oil and prevention of essential fatty acid deficiency in preterm infants.

The topical application of vegetable oil was assessed as an alternative means of providing essential fatty acids (EFA) to parentally fed preterm infants who were not receiving lipid. Three infant pairs ranging in gestational age from 26-32 weeks were studied. Safflower oil or safflower oil esters (1 g linoleic acid/kg/day) were applied to available areas daily. All infants rapidly developed biochemical EFA deficiency. The plasma fatty acid profiles were similar in infants with or without topical oil, and all returned to normal once parenteral lipid was introduced. We found no evidence to suggest that the transdermal route is of use in the nutritional management of preterm infants.

8,11,14-Eicosatrienoic Acid↗
PubMed1975

The development of essential fatty acid deficiency in healthy men fed fat-free diets intravenously and orally.

The hypothesis that clinical and biochemical essential fatty acid deficiency (EFA) might occur from the feeding of eucaloric, fat-free diets was tested in two experiments in healthy men. In Study I, eight men were given fat-free, eucaloric diets containing 80% of calories as glucose and 20% as amino acid hydrolysates by a constant drip over a 24-h period. The diets were fed in succession for periods of 2 wk each, either through a superior vena cava catheter or via a nasogastric tube. EFA deficiency was detected by decreases in linoleic acid and by the appearance of 5, 8, 11-eicosatrienoic acid in lipid fractions of plasma. Linoleic acid decreased significantly during 2 wk of the fat-free diet given intravenously from 48.8 to 9.8% (percent of total fatty acids) in cholesterol esters, from 21.2 to 3.2% in phospholipids, from 9.6 to 2.0% in free fatty acids, and from 14.1 to 2.6% in triglycerides. Eicosatrienoic acid, normally undetectable, appeared 0.6% in cholesterol esters, 2.5% in phospholipids, 0.2% in free fatty acids, and 2.3% in triglycerides. EFA deficiency occurred similarly during the nasogastric feeding. In Study II a subject received the same diet continuously by the nasogastric route for 10 days followed by a 24-h fast. He was then given the fat-free diet intermittently in three meals per day for 3 days. Finally, he was repleted with a diet containing 2.6% linoleic acid. By the 3rd day of the continuous nasogastric feeding, linoleic acid had fallen significantly and eicosatrienoic acid had appeared in plasma lipid fractions as in Study I. These findings were accentuated by day 10. Adipose tissue fatty acid composition did not change. Free fatty acid outflow from adipose tissue was presumably suppressed during the 10 days of continuous feeding. With increased free fatty acid outflow during fasting and intermittent feeding, linoleic acid rose and eicosatrienoic acid decreased. After 13 days of repletion with dietary linoleic acid, the EFA deficiency readily develops when fat-free diets containing glucose are given intravenously or orally as constant 24-h infusions. These diets are similar to the hyperalimentation formulas now being used clinically.

Adipose Tissue↗
PubMed1987

Criteria for essential fatty acid deficiency in plasma as assessed by capillary column gas-liquid chromatography.

To develop criteria for deficiency of essential fatty acids (EFA), we used capillary-column gas-liquid chromatography to determine fatty acids (percentage of total fatty acids) in plasma obtained in the fasting state from 56 reference subjects and from 10 patients with intestinal fat malabsorption and suspected EFA deficiency. Fatty acid evaluations (percentage of total fatty acids) that allowed for a clear distinction (P less than 0.01) between reference subjects and patients, based on values two standard deviations below or above the reference mean, included values for linoleic acid (18:2w6) below 27%, and values for palmitic acid (16:0), palmitoleic acid (16:1w7), oleic acid (18:1w9), vaccenic acid (18:1w7), and Mead acid (20:3w9) exceeding 21%, 2.6%, 23.3%, 2.1%, and 0.21%, respectively. Ratios of total EFA to total non-EFA of less than 0.60 and of Mead acid to arachidonic acid of greater than 0.025 also served to identify patients, and were not found in reference subjects. Significant inverse correlations between percentages of plasma EFA and plasma mono-unsaturated fatty acids were noted. Our reference-interval data can be used to assess normality of plasma EFA status.

Adult↗