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PubMed1978

Linoleic acid effects on epidermal DNA synthesis and cutaneous prostaglandin levels in essential fatty acid deficiency.

An essential fatty acid (EFA) deficient state has been induced in hairless mice. The epidermal changes included hyperkeratosis, hypergranulosis and acanthosis. Epidermal DNA synthesis was increased 3-fold compared with normal diet mice. Prostaglandin E (PGE) and prostaglandin F (PGF) levels, measured by radioimmunoassay, were much reduced in the EFA deficient mice skin. 10% Linoleic acid applied topically for 2 weeks corrected the gross and histological skin abnormalities and reduced epidermal DNA synthesis to normal values. The levels of PGE and PGF were only partially corrected. Linoleic acid applied to normal diet mice increased skin levels of PGE and PGF compared with the control vehicle treated normal diet mice. These results provide further evidence for the importance of essential fatty acids in the control of epidermal proliferation and differentiation. The importance of PGE and PGF in controlling epidermal DNA synthesis in EFA deficiency is less clear.

Animals↗
PubMed1980

[Essential fatty acids and animal development].

With the exception of some cell strains in culture, the animal cells need w6 linoleic acid and its superior polyinsaturated derivatives for their structural growth and their multiplication. Deficiency of linoleic acid leads to growth failure, organic fraility and death of the animal. Involvement of the prostaglandins is not demonstrated. w3 linolenic acid and its superior derivatives are essential for the development of the sea animals. Linolenic acid appears also essential for the mammal nervous cells at the step of cell division anterior to myelinisation. Disponibility of the essential fatty acids for the mammal fetus is principaly assumed by the mother liver of which the metabolic activity in conversion of the precursors to superior derivatives and synthesis of transport lipoproteins is increased. Involvement of the polyunsatured acids in satisfying the structural and energetic needs of the developing animal concerns predominantly--but not exclusively--the cell membranes structure and fluidity and activity of the functional proteins (enzymes, mitochondrial oxydophosphorylation).

Animals↗
PubMed1998

Essential fatty acids and sleep: mini-review and hypothesis.

The neurochemical basis of sleep mechanisms (onset and maintenance) is still controversial although the phenomenon itself is known to be mediated by more than a single molecule. The list of suggested endogenous sleep substances is rather long, and there is no single 'sleep center' identified in the brain. The role of fatty acids, and essential fatty acids in particular, has been ignored in sleep research. This review proposes an integration of the current knowledge about the effects of fatty acids in sleep neurochemistry, wherein fatty acids are seen to exert a direct effect on neuronal membrane structure or indirectly on the dynamics of biochemical compounds (complex lipids, prostaglandins, neurotransmitters, amino acids, interleukins) necessary for the initiation and maintenance of sleep.

Alzheimer Disease↗
PubMed1989

Direct transesterification of plasma fatty acids for the diagnosis of essential fatty acid deficiency in cystic fibrosis.

This study was aimed at redefining criteria for essential fatty acid (EFA) deficiency with the use of the direct transesterification procedure (1986. J. Lipid Res. 27: 114-120) and at determining whether a simple assay of total fatty acids (FA) is as predictive of EFA deficiency as the FA pattern from plasma, red cell, and platelet phospholipids. Fasting blood samples were taken from 163 cystic fibrosis (CF) patients who were encouraged to consume 35-40% of their calories as fat. Their mean (+/- SD) age was 9.6 +/- 4.8 yr. The control group consisted of 44 unaffected siblings aged 13.1 +/- 3.1 yr. The 20:3(n-9)/20:4(n-6) ratio in 77 (47%) CF children was more than 2 SD above the values (mean +/- SD) of 0.021 +/- 0.007 obtained in the 44 controls. Groups of EFA-sufficient (n = 10) and EFA-deficient (n = 7) subjects were selected for further studies. The plasma total FA 20:3(n-9)/20:4(n-6) ratios of 0.029 +/- 0.003 in EFA-sufficient and of 0.216 +/- 0.103 in EFA-deficient was as good a discriminant as FA in phospholipids from plasma, red cell PC, and platelets. Among the 21 individual fatty acids, 20:3(n-9), which was also found in controls, and 16:1(n-7) (palmitoleic) proved to be the most sensitive indices of EFA deficiency. They are equally reliable in plasma, red cells, and platelets, but the inverse linear relationship (r = -0.91) between the n-7 family and 18:2(n-6) proved to be more closely associated with EFA deficiency than the one (r = 0.66) between 20:3(n-9) and 20:4(n-6).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1997

Calcium metabolism, osteoporosis and essential fatty acids: a review.

Essential fatty acid (EFA)-deficient animals develop severe osteoporosis coupled with increased renal and arterial calcification. This picture is similar to that seen in osteoporosis in the elderly, where the loss of bone calcium is associated with ectopic calcification of other tissues, particularly the arteries and the kidneys. Recent mortality studies indicate that the ectopic calcification may be considerably more dangerous than the osteoporosis itself, since the great majority of excess deaths in women with osteoporosis are vascular and unrelated to fractures or other bone abnormalities. EFAs have now been shown to increase calcium absorption from the gut, in part by enhancing the effects of vitamin D, to reduce urinary excretion of calcium, to increase calcium deposition in bone and improve bone strength and to enhance the synthesis of bone collagen. These desirable actions are associated with reduced ectopic calcification. The interaction between EFA and calcium metabolism deserves further investigation since it may offer novel approaches to osteoporosis and also to the ectopic calcification associated with osteoporosis which seems to be responsible for so many deaths.

Animals↗
PubMed1991

The anti-diabetogenic effect of essential fatty acid deficiency in multiple low-dose streptozotocin-treated mice persists if essential fatty acid repletion occurs outside of a brief window of susceptibility.

We have previously shown that essential fatty acid deficiency prevents diabetes mellitus and ameliorates insulitis in multiple low-dose streptozotocin-treated male CD-1 mice and that repletion with 99% pure methyl linoleate 3 days after the last injection causes diabetes. In the present study, we examined whether repletion of low-dose streptozotocin-treated deficient mice will cause diabetes whenever repletion occurs. Essential fatty acid deficiency was induced by dietary manipulation and was confirmed biochemically. Groups of deficient mice were repleted 6 h, 1 week, 2 weeks, 4 weeks and 8 weeks after the last low-dose streptozotocin treatment; the incidence of diabetes (i.e., non-fasting plasma glucose levels greater than 11.2 mmol/l) and group mean plasma glucose levels were 93% (19.4 mmol/l), 37% (14.8 mmol/l), 40% (13.7 mmol/l), 20% (9.0 mmol/l), and 8% (7.8 mmol/l) respectively. The incidence and mean glucose levels for low-dose streptozotocin-induced control chow-fed and non-repleted essential fatty acid deficient CD-1 mice were 100% (30.2 mmol/l) and 0% (4.2 mmol/l). The incidence and severity of insulitis also decreased with increasing repletion intervals. These results demonstrate a brief window of susceptibility of less than 8 weeks duration during which repletion will initiate an autoimmune response directed at low-dose streptozotocin-induced Beta-cell neoantigens in low-dose streptozotocin-treated essential fatty acid deficient mice.

Animals↗
PubMed2001

Dietary trans fatty acids combined with a marginal essential fatty acid status during the pre- and postnatal periods do not affect growth or brain fatty acids but may alter behavioral development in B6D2F(2) mice.

The objective of this study was to investigate whether dietary trans fatty acids (TFA) during the pre- and postnatal periods would exacerbate the effects of marginal essential fatty acid (EFA) status on growth, brain long-chain polyunsaturated fatty acids (LC-PUFA) and behavioral development in B6D2F(2) mice. Pregnant B6D2F(1) females were randomly assigned to one of the following three diets: marginal EFA plus 22% trans 18:1 (mEFA + TFA); marginal EFA (mEFA); and control (CON). The total 18:1 content in all diets was similar. The offspring were weaned and maintained on the same diets. Both the mEFA and mEFA + TFA groups had reduced growth and brain weight compared with CON, but did not differ from one another. As expected, the mEFA and mEFA + TFA groups had reduced docosahexaenoic acid [DHA; 22:6(n-3)]) and increased 22:5(n-6) concentrations in brain phosphatidylcholine (PC) and phosphatidylethanolamine (PE) compared with the CON group, but again did not differ from one another. Reversal learning in the T-water maze was significantly slower in the mEFA + TFA groups compared with the mEFA group and both were slower than the CON group. These findings illustrate that TFA combined with a marginal EFA status do not exacerbate the effects of marginal EFA status on growth or brain LC-PUFA. However, long-term effects of dietary TFA during the pre- and postnatal period on behavioral development and neural function should be investigated in future studies.

Animals↗
PubMed1986

Influence of different dietary concentrations of linoleic acid on the essential fatty acid (EFA) status and functional characteristics of porcine hepatic and cardiac mitochondria.

The effect of different dietary concentrations of linoleic acid (0.2, 1.1 and 2.1% of gross energy in experiment 1 and 0.7, 1.6 and 2.3% of gross energy in experiment 2) on the EFA status and the functional characteristics of hepatic and cardiac mitochondria was investigated in pigs raised for 140 days from 10 to 105 kg live wt on their respective diets. As judged from the ratios of 20:3n9 to 20:4n6 of hepatic and cardiac mitochondrial total lipids the pigs receiving 0.2% of dietary gross energy as linoleic acid were EFA-deficient, while the pigs receiving 0.7% of dietary gross energy as linoleic acid were on the borderline of EFA deficiency. Mitochondrial protein yield and the functional parameters (endogenous respiration, respiration of exogenous NADH, state 2, 3 and 4 respiration, RCI-values, ADP/O ratios and synthetic rates of ATP) as measured in both hepatic and cardiac mitochondria with two substrates pyruvate plus malate and succinate in the presence of rotenone were not significantly (P greater than 0.05) affected by the different dietary concentrations of linoleic acid. The findings indicate a slow turnover of EFA and a low desaturation/elongation activity of the associated enzymes in the pig.

Animals↗
PubMed1988

Rat neutrophil function, and leukotriene generation in essential fatty acid deficiency.

Since the essential fatty acid linoleic acid is the precursor of arachidonic acid and thus of leukotrine B4 (LTB4), essential fatty acid deficiency (EFAD) may result in decreased synthesis of this stimulator of neutrophil granulocyte functions. Peritoneal and blood neutrophils from rats fed a diet with only 0.3% of energy requirements as linoleic acid and exhibiting biochemical evidence of EFAD showed substantial functional impairments compared to neutrophils from rats maintained on a diet with 3% of the energy requirement as linoleic acid. Oxidative burst activation (assessed by chemiluminescence), chemotaxis and aggregation were impaired upon stimulation with formylpeptides or the ionophore A23187. In contrast, these functions were intact on stimulation with exogenous LTB4. Chemiluminescence was slightly but not significantly enhanced in EFAD rat neutrophils compared to controls when stimulated with phorbol myristate acetate (PMA). There were no differences between EFAD and control peritoneal neutrophils in the number of f-met-leu-phe (fMLP) receptors, or in their affinity for the ligand, assessed with fML(3H)P. The fraction of responding cells also were similar, assessed with dichlorofluorescein diacetate fluorescence. Moreover, the endogeneous LTB4 production in response to A23187 or fMLP was decreased by 57.7% and 63.5%, respectively, in EFAD peritoneal neutrophils. Thus, EFAD was associated with reductions of LTB4 production and neutrophil responsiveness to A23187 and formylpeptides but not to LTB4 or PMA, which supports the hypothesis that endogeneous LTB4 may contribute to the activation of neutrophil functions involved in inflammation and host defense.

Animals↗
PubMed1981

[Essential fatty acid deficiency in childhood].

Essential fatty acid deficiency can develop in man as the consequence of an inadequate diet or fatty acid malabsorption. Daily requirements in childhood vary from 1 to 4 caloric percent. Many abnormalities are described following essential fatty acid deficiency, such as cessation of growth, dermatitis, loss of hair, increased susceptibility to bacterial infections, histological abnormalities and disturbances of biochemical and physiological processes. These disorders can be explained as the result of a disturbed membrane structure and function, due to an abnormal serum fatty acid composition. This is also important in diagnosis of essential fatty acid deficiency. Supplementation of essential fatty acids can be realised by oral and parenteral route or by cutaneous application. A patient is described with an essential fatty acid deficiency. Cutaneous application of a linoleic acid rich mixture resulted in an enhanced growth velocity.

Administration, Topical↗
PubMed1996

Role of essential fatty acids in the function of the developing nervous system.

The basis for n-3 fatty acid essentially in humans includes not only biochemical evidence but functional measures associated with n-3 deficiency in human and nonhuman primates. Functional development of the retina and the occipital cortex are affected by alpha-linolenic acid deficiency and by a lack of docosahexaenoic acid (DHA) in preterm infant formulas and, as reported more recently, in term diets. Functional effects of n-3 supply on sleep-wake cycles and heart rate rhythms support the need for dietary n-3 fatty acids during early development. Our results indicate that n-3 long-chain polyunsaturated fatty acids should be considered provisionally essential for infant nutrition. DHA may also be required by individuals with inherited metabolic defects in elongation and desaturation activity, such as patients with peroxisomal disorders and some forms of retinitis pigmentosa.

Animals↗
PubMedDate not supplied

Effects of hypocaloric diet low in essential fatty acids on in vitro human adipose tissue prostaglandin production and essential fatty acid status.

Very-low-calorie, fat-free defined-formula diets have been routinely used to treat obese patients. However, the effect of feeding a defined-formula diet low or devoid of essential fatty acids (EFAs) on EFA metabolism has not been determined. The aim of this investigation was to determine the effect of 400 kcal/day of Optifast 70 on EFA metabolism as determined by serum and adipose tissue levels of omega-6 fatty acids and measurements of in vitro human adipose tissue prostaglandin production. Five obese subjects entered the study after 1 wk of weight maintenance and then were placed on 12 wk of weight reduction. Blood and tissue samples were obtained before and after 4, 8, and 12 wk of weight reduction. Subjects tolerated 12 wk of dieting without any adverse reactions and lost an average of 21.7 +/- 7.0 kg. There was no significant effect of weight reduction on the levels of linoleic or arachidonic acid found in adipose tissue. There was a significant decrease in adipose tissue prostaglandin production of prostacyclin I2, measured as 6-keto-PGF1 alpha, after 12 wk of weight reduction. There was no significant change in the levels of thromboxane A2, measured as TXB2. There was a significant increase in serum arachidonic acid levels with no change in linoleic acid levels. The results demonstrated that the use of a diet devoid of EFA had no significant effect on omega-6 EFA metabolism as measured by serum and tissue levels and the ability of adipose tissue to produce prostaglandins in vitro.

Adipose Tissue↗
PubMed1981

Essential fatty acid supplemented diet increases renal excretion of prostaglandin E2 and water in essential fatty acid deficient rats.

Weanling male rats were fed an essential fatty acid (EFA)-deficient diet for 25 weeks and then switched to an EFA-supplemented diet for 3 weeks. Control rats received the EFA-supplemented diet for 25 weeks and then the EFA-deficient diet for 3 weeks. Throughout the last 19 weeks, the rats were housed in metabolic cages once a week for a 24-hr period. urinary excretion of prostaglandin E2 (PGE2) was estimated by radioimmunoassay. Throughout a period of 12 weeks (weeks 13-24) water consumption increased ca. 60%, and urine output and PGE2 excretion decreased ca. 45% and 70%, respectively, in the EFA-deficient rats, Feeding EFA-supplemented diet to the EFA-deficient rats for 3 weeks decreased the water consumption and raised the urine output to that observed in the controls. However, the urine output was corrected within 1 day whereas the water consumption was not corrected until the second measurement 8 days after the dietary change. The PGE2 excretion increased more than 9-fold (from 18 +/- 8 ng/24 hr to 165 +/- 51 ng/24 hr) 1 day after EFA-supplementation, followed by a decrease to 86 +/- 29 ng/24 hr over the following 24 weeks. On the basis of the present data, it is suggested that EFA deficiency in rats causes diminished PGE2 excretion, which can be normalized by EFA supplementation. The normalization of the urine flow may, in part, be caused by the concomitant considerable increase in endogenous PGE2 synthesis.

Animals↗
PubMed1992

Plasma and red blood cell fatty acid values as indexes of essential fatty acids in the developing organs of infants fed with milk or formulas.

The dietary requirement of n-6 and n-3 fatty acids for normal biochemical and functional development of the central nervous system (CNS) is an important, unresolved issue in infant nutrition. High levels of arachidonic acid (AA; 20:4n-6) and docosahexaenoic acid (DHA; 22:6n-3) are found in the CNS and are important to normal learning and visual function. Dietary fatty acids may be desaturated and elongated to AA and DHA, respectively, but may also be oxidized for energy. Synthesis of AA and DHA in the young infant, therefore, depends on adequate desaturase enzyme activity, as well as an adequate supply of dietary 18:2n-6, 18:3n-3, and energy. Levels of AA and DHA are lower in the plasma and red blood cell (RBC) lipids of infants fed formula rather than human milk and are not increased with increased formula 18:2n-6 or 18:3n-3 supply. The decline in AA and DHA in infants fed formula becomes evident in the order plasma phospholipid greater than RBC phosphatidylcholine greater than RBC phosphatidylethanolamine. As in infants, piglets fed formula rather than natural milk have lower plasma and RBC AA and DHA concentrations. Despite lower levels in the plasma and RBC, analyses of CNS lipids demonstrated adequate AA and DHA in piglets fed formula with greater than 7% kcal 18:2n-6 and greater than 0.3% kcal 18:3n-3. This finding suggests that circulating lipid fatty acids are not specific indexes of organ deficiency. The rapid decrease in circulating lipid AA and DHA concentrations experienced by premature infants during early postnatal parenteral and enteral nutrition, however, may be related to oxidation of 18:2n-6 and 18:3n-3, rather than equilibrium of circulating lipids with the dietary fatty acids. Arachidonic acid and DHA may be conditionally essential nutrients for these infants because of oxidation of 18:2n-6 and 18:3n-3 for energy during periods of negative energy balance.

Animals↗
PubMed1978

Fatty acid composition of submandibular salivary gland lipids in essential fatty acid deficient rats.

Essential fatty acid (EFA) deficiency was induced in young weanling rats by feeding a fat-free diet or a diet containing 7% Hydrogenated coconut oil (HCO). At intervals of 4, 8, and 16 weeks, rats from the deficient and the control groups were killed and their Submandibular Salivary Glands (SMSG) were dissected out and extracted for lipids. The fatty acid composition of total lipids, triglycerides (TG), free fatty acids (FFA), phosphatidyl choline (PC), and phosphatidyl ethanola-mine (PE) fractions was determined. The levels of 16:1 and 18:1 were increased whereas those of 18:2 and 20:4 were decreased in the EFA-deficient groups as compared to the controls. 5,8,11-eicosatrienoic acid (20:3 omega9) accumulated in the total lipids as well as other lipid fractions of the SMSG from the deficient rats. The levels of this fatty acid increased as the EFA-deficiency progressed. Changes in fatty acid composition of SMSG lipids of EFA-deficient rats were associated with a reduction in flow rate of whole saliva. Protein concentration and amylase activity of saliva was the same in the two groups.

Animals↗
PubMed1974

Diagnosis and treatment of essential fatty acid deficiency in man.

Essential fatty acid deficiency was found on four occasions in three adult patients with malabsorption after intestinal resection. Diagnosis was primarily based on the gas chromatographic finding of the abnormal fatty acid 5, 8, 11- (omega9) eicosatrienoic acid in plasma lecithin. None of the patients had received parenteral nutrition with a fat-free source of calories but all had been on a reduced intake of dietary fat at some stage. Treatment with intravenous Intralipid rapidly reversed the abnormal plasma fatty acid pattern and also cleared the rash in the patient wih he most severe deficiency.

Aged↗