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PubMed1986

Essential fatty acid and prostaglandin metabolism in Sjögren's syndrome, systemic sclerosis and rheumatoid arthritis.

Evidence from biochemical studies and from experimental animals indicates that abnormalities of essential fatty acid (EFA) and eicosanoid metabolism could lead to salivary and lacrimal gland atrophy and to immunological and cardio-vascular defects. Measurements of EFA levels in erythrocytes from patients with primary Sjögren's syndrome have shown that abnormalities are indeed present. Controlled clinical trials of supplementation with gamma-linolenic acid (GLA) as evening primrose oil (Efamol) in both primary Sjögren's syndrome and systemic sclerosis have given positive results. There are strong arguments to indicate that sophisticated manipulation of EFA metabolism may have a role to play, not only in Sjögren's syndrome but also in other rheumatological disorders.

Erythrocyte Membrane↗
PubMed1964

STRUCTURAL CHANGES IN ISOLATED LIVER MITOCHONDRIA OF RATS DURING ESSENTIAL FATTY ACID DEFICIENCY.

Liver mitochondria isolated in 0.44 M sucrose from rats deficient in essential fatty acids (EFA) oxidized citrate, succinate, alpha-ketoglutarate, glutamate, and pyruvate at a faster rate than did mitochondria isolated from normal rats; however, the oxidation of malate, caprylate, and beta-hydroxybutyrate was not significantly increased. The mitochondria from deficient rats exhibited an increased ATPase activity and extensive structural damage as revealed by electron microscope examination of thin sections. An increase in citrate oxidation and ATPase activity, together with some structural damage, could be demonstrated as early as the 4(th) week in rats on a fat-free diet. Saturated fat in the diet did not prevent the change in mitochondrial structure but accelerated its appearance. Both the biochemical and structural defects could be reversed within three weeks after feeding deficient rats a source of EFA. In the presence of a phosphate acceptor the effect of EFA deficiency on substrate oxidation was largely eliminated. A trend toward a reduced efficiency of oxidative phosphorylation was noted in mitochondria from EFA-deficient rats, but significant uncoupling was found only in the case of citrate, beta-hydroxybutyrate, and glutamate in the presence of malonate. Together with the increased ATPase activity, the uncoupling of phosphorylation could account for the poor respiratory control found with the deficient preparation. However, EFA deficiency was without effect on the respiration of liver slices, which supports the belief that the observed changes in oxidation and phosphorylation are an artifact resulting from damage sustained by the deficient mitochondria during their isolation.

Adenosine Triphosphatases↗
PubMed1979

Interaction of zinc and essential fatty acids in the rat.

Three experiments were performed to investigate the possibility of a physiological relationship between zinc and essential fatty acids (EFA). Male weanling rats were fed diets low in zinc, EFA or both and their growth rates, dermal scores and tissue fatty acid profiles determined. In experiment 1, a basal soybean protein diet containing 7 ppm of added zinc and approximately 300 ppm EFA was used in a 2 X 2 factorial design: low Zn-low EFA; adequate Zn-low EFA; low Zn-adequate EFA and adequate Zn-adequate EFA. The low zinc status accentuated signs of EFA deficiency, including dermal lesions and growth rate, but it had no significant effect on the fatty acid profile in plasma. In experiment 2, a basal casein diet containing approximately 25 ppm of EFA and less than 1 ppm of zinc, was used in a similar design. For 7 weeks two groups of weanling rats were fed ad libitum either a diet adequate in Zn and low in EFA or a diet adequate in all nutrients. From 7 to 12 weeks zinc was removed from one-half of each group and all were pair-fed to the intake of the low zinc-low EFA group. Zinc deficiency accentuated dermal lesions in the group deprived of EFA and caused enlarged joints suggestive of an arthritic-like syndrome. In experiment 3, an egg albumin based diet containing approximately 25 ppm EFA and less than 1 ppm of zinc was used in a 2 X 2 factorial design. No signs of fatty acid deficiency occurred in 5 weeks with adequate zinc. Zinc and EFA deficiency accentuated dermal scores and severely depressed growth. Zinc deficiency increased the proportion of arachidonic acid in foot skin especially in the EFA deficient group. It is concluded that there is a physiological interaction between Zn and essential fatty acids.

Animals↗
PubMed1982

[Polyunsaturated (essential) fatty acids and their importance in pathogenesis, diagnosis and therapy of multiple sclerosis].

Various aspects concerning the pathogenetic involvement of poly-unsaturated (essential) fatty acids as biochemical co-factors in developing multiple sclerosis (MS) are reported in great detail. Our own studies have also confirmed that differences in the intake or utilization of essential fatty acids do not biochemically induce significant changes in myelin, serum or blood cells. This has long been suspected. The concept of nutritionally or metabolically induced generalized defects in all membranes, especially in the myelin sheath, as a predisposing factor to an increased susceptibility for the development of MS, provoked a gamut of pertinent studies frequently producing controversial results. Hence, these conceptions concerning the pathogenetic involvement of essential fatty acids in MS have been put to rest--even more so after the role of prostaglandins in immunoregulation had become more apparent whose biological precursors are essential fatty acids. Thus, the immunosuppressive effect of high dosage of essential fatty acids under experimental conditions could be explained, disclosing new assessments concerning therapy, new pathogenetic models and further biochemical research.

Blood Cells↗
PubMed1981

Essential fatty acid deficient rats: a new model for evaluating arachidonate metabolism in shock.

Essential fatty acid deficient (EFAD) rats are significantly more resistant to the lethal effects of S. enteritidis endotoxin (20 mg/kg, IV) than normal control rats. Compared to endotoxin-treated normal rats, EFAD rats also manifested less severe alterations of hepatic and lysosomal integrity and became less hypoglycemic. Administration of the ethyl ester of the essential fatty acid, arachidonic acid (100 mp, IP) two days prior to challenge with S. enteritidis endotoxin (20 mg/kg) in EFAD rats restored their sensitivity to endotoxin, as denoted by a 100% mortality compared to a 24% mortality (P less than 0.01) in EFAD rats. Treatment of EFAD rats with the fatty acid docosahexaenoic acid, a non-prostaglandin and thromboxane precursor, (100 mg, IP) produced significantly less (less than 0.01) mortality than ethyl-arachidonate-treated groups (ie, 40% vs 100%). The arachidonate metabolite, thromboxane B2 (TxB2), increased from nondetectable plasma levels (less than 200 pg/ml) to 2285 +/- 449 pg/ml (N = 10) at 30 min and remained elevated for 180 minutes after endotoxin administration in nondeficient rats. However, plasma TxB2 was not detectable in endotoxin-treated EFAD rats and was only slightly elevated in groups supplemented with docosahexaenoic acid (273 +/- 104 pg/ml, N = 6) after 30 minutes. In ethyl arachidonate (100 mg, IP) supplemented EFAD rats, plasma TxB2 rose to 873 +/- 204 pg/ml (N = 8), 30 min after endotoxin. Pretreatment of the ethyl-arachidonate-supplemented EFAD group with a specific thromboxane synthetase inhibitor, 7-(1-imidazolyl)-heptanoic acid (30 mg/kg, IV), significantly reduced mortality 100% to 50% (P less than 0.05) from endotoxic shock. These observations suggest a deleterious role for arachidonic acid and its conversion to TxA2 in the pathogenesis of endotoxic shock.

Acid Phosphatase↗
PubMed1978

Trace metal and essential fatty acid deficiency during total parenteral nutrition.

While deficiences of trace metals and essential fatty acids are rare in humans fed orally, the widespread use of total parenteral nutrition (TPN) has increased the likelihood of encountering these deficiences. A 14-year-old boy, with total villous atrophy of the small intestine, suffered from severe malnutrition and was placed on a conventional TPN regimen. Although not immediately recognized, he rapidly developed deficiencies of zinc, copper and essential fatty acids. Careful monitoring of the course of the illness and the responses to sequential treatments with zinc, lipid, and copper given intravenously allowed examination of the effects of the deficiencies on skin, intestine, liver, and hemopoietic systems and helped to establish normal requirements for the metals. The progress of the illness suggested that patients with intestinal malabsorption may be especially at risk of developing some of these lesser known complications of TPN.

Adolescent↗
PubMed1999

Neonatal dietary zinc deficiency in artificially reared rat pups retards behavioral development and interacts with essential fatty acid deficiency to alter liver and brain fatty acid composition.

The objective of this study was to investigate whether short-term zinc deficiency in the early neonatal period would exacerbate the effects of essential fatty acid (EFA) deficiency on liver and brain long-chain polyunsaturated fatty acid (LCPUFA) composition, as well as on behavioral development in artificially reared rat pups. Using a 2 x 2 factorial design, male Long-Evans rat pups were reared artificially from postnatal d 5 to 16; pups were fed through gastrostomy tubes with rat formula deficient in zinc and/or EFA. As expected, EFA deficiency significantly reduced levels of arachidonic acid [AA, 20:4(n-6)] and docosahexanoic acid [DHA, 22:6(n-3)] in liver phosphatidylcholine (PC) and brain phosphaditylethanolamine (PE), and increased 22:5(n-6) levels in liver and brain PC and PE. There were significant interactions between zinc and EFA in liver such that zinc deficiency reduced AA and DHA in the EFA-adequate groups, but significantly increased AA in the EFA-deficient groups. Contrary to the hypothesis, short-term zinc deficiency did not exacerbate the effects of EFA deficiency in liver phospholipids. In brain PE, a significant interaction between EFA and zinc was observed such that zinc deficiency increased 22:5(n-6) concentrations in EFA-adequate but not in EFA-deficient groups. Regardless of their EFA status, zinc-deficient rats were growth retarded and demonstrated deficits in locomotor skills. Possible effects of long-term zinc and EFA deficiency on brain function should be investigated in future studies.

Analysis of Variance↗
PubMedDate not supplied

Effects of essential fatty acid deficiency on the induction of liver microsomal membranes by phenobarbital: an ultrastructural and biochemical investigation.

The essential fatty acids, particularly arachidonic, are important components of intracellular membrane systems. Their absence during dietary manipulation has been postulated to cause alterations in both composition and function of membranes and associated enzyme systems. In the current investigation, the effect of essential fatty acid deficiency on the induction of hepatic microsomal membranes my phenobarbital was studied. Control rats were fed a standard chow diet and either injected daily for 4 days with phenobarbital or with a placebo. Experimental animals were given an essential fatty acid-deficient (EFAD) diet and similarly injected with either phenobarbital or placebo. Following the above regimens, liver tissue was obtained for electron microscopy and biochemical membrane analysis. Control animals given phenobarbital displayed a marked proliferation of smooth endoplasmic reticulum in comparison to placebo controls. In contrast, EFAD rats did not exhibit an endoplasmic reticulum response to phenobarbital injection and appeared to recover from the drug administration injection more slowly than control animals. The alterations in fatty acid composition characteristic of an EFAD diet were observed in the microsomal membranes of the deficient animals. The concentrations of palmitic, palmitoleic, oleic, and 5,8,11-eicosatrienoic acids were significantly increased above that found in control animals. Concentrations of linoleic and arachidonic acids were reduced. Phenobarbital administration significantly increased the concentrations of palmitic, linoleic, and arachidonic acids in microsomal fractions of chow-fed animals but not in EFAD animals. Conversely, eicosatrienoic acid concentrations increased in phenobarbital-treated EFAD animals but not in chow-fed, drug-injected rats. The triene/tetraene ratio reflected these alterations. Essential fatty acid deficiency causes biochemical alterations of the hepatic microsomal membranes which are exaggerated by the administration of phenobarbital. These compositional changes appear to alter the functional ability of the membranes to proliferate in response to phenobarbital and, thereby, inhibit the efficaceous metabolism of this drug.

Animals↗
PubMed1981

Essential fatty acid deficiency in critically ill surgical patients.

Plasma fatty acid profiles of 33 critically ill surgical patients receiving fat-free parenteral nutrition were examined at weekly intervals up to 28 days. While plasma total fatty acid concentration remained relatively constant and within the normal range, marked compositional alterations were apparent. Levels of linoleate (18:2 omega 6), the major essential fatty acid in man, fell below normal values (754 +/- 259 micrograms/ml) in 67 percent of patients within 1 week after cessation of oral intake. Decreases in other omega 6 unsaturated fatty acids, derived from linoleate, were also apparent. In contrast, gradual increases were observed in levels of endogenously synthesized fatty acids, palmitate (16:0), palmitoleate (16:1) and oleate (18:1 omega 9). A fatty acid unique to essential fatty acid deficiency, 5,8,11 eicosatrienoate (20:3 omega 9), appeared in 25 percent of the patients during the first week and in all patients by the third week of study. Considering the rapid appearance and progression of these biochemical changes, early initiation of linoleate supplementation appears justified to forestall the development of related clinical sequelae.

Adolescent↗
PubMed2004

Essential fatty acids and their role in the treatment of impulsivity disorders.

Essential fatty acids (EFAs) have been shown to benefit patients with depression, schizophrenia and dementia. More recently, their role in disorders characterised by impulsivity has attracted some attention. The psychiatric conditions of attention-deficit hyperactivity disorder and borderline personality disorder as well as the phenomena of deliberate self-harm and violence have been ameliorated by the supplementation of EFAs in a number of recent clinical trials. This paper summarises the burgeoning clinical and basic research indicating the existence of significant deficits of EFAs in impulsivity disorders and the supplementation studies of EFAs in these diverse conditions, all of which remain a major therapeutic challenge.

Aggression↗
PubMed1983

Essential fatty acid deficiency, prostaglandin synthesis and humoral immunity in Lewis rats.

Essential fatty acid (EFA) deficiency is known to alter the immune response in several experimental systems. To further evaluate the effects of EFAs on immunity Lewis rats were fed diets either adequate or deficient in EFAs for 70-80 days. EFA-adequate rats responded to an i.v. injection of 5 X 10(8) sheep erythrocytes with a sharp, short-lived rise in splenic levels of PGE and PGF within 2 minutes after injection. EFA deficiency resulted in a diminution of this PG response. PG production in liver homogenates was also depressed in EFA-deficient liver. An i.v. injection of sheep erythrocytes resulted in a humoral response against this antigen, measured as hemolytic plaque-forming cells in the spleen. EFA deficiency, as well as pretreatment of EFA-adequate rats with indomethacin, an inhibitor of PG synthesis, resulted in a stimulation of the plaque-forming cell response over that observed in control, EFA-adequate rats. The alterations in immune response resulting from changes in PG synthetic capacity may be important in the etiology of certain immunodeficiency syndromes such as the lupus-erythematosus-like autoimmune disease in NZB/W mice.

Animals↗
PubMedDate not supplied

Essential fatty acid status in adult patients receiving soybean-base formula.

Essential fatty acid (EFA) status was assessed in 48 normal Thai adults and 6 patients who required tube feeding ro 2-4 wk with commercial soybean-base formula (Sobel, Mead Johnson). Each 1000 kcal of this formula provided 40.2 g protein, 32.8 g fat, 136 g carbohydrate, 13.9 g linoleic acid, 2.9 g linolenic acid, and 0 g arachidonic acid. The linoleic acid status in these patients before receiving soybean-base formula was inadequate, as evidenced by the significantly lower serum 18:2-W6 percentage but higher serum 16:1-W7 and 18:1-W9 percentages than those in normal adults. These changes were reversed while receiving soybean-base formula. A significant positive correlation between linoleic acid intake and its serum level was demonstrated. There was a significant decrease in serum 20:4-W6 percentage while receiving soybean-base formula. This could be related to the absence of this EFA in the formula and suppression of biotransformation of 18:2-W6 to 20:4-W6 in the presence of a significant amount of 18:3-W3. None of the patients had 20:3-W9 in the serum or developed scaly dermatitis throughout the study.

Adult↗
PubMed1979

[Studies on the modification of wound healing by a lack of essential fatty acids].

A fat-free diet produces a deficiency of essential fatty acids in Wistar rats. This is associated with disturbances of wound healing in the colon and skin due to an impaired collagen metabolism, since hydroxyproline content in the wound area is decreased. The results are of clinical significance with regard to total parenteral nutrition in surgical patients.

Animals↗