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PubMed1981

Essential fatty acid status in premature newborns fed by nasoduodenal technique.

The fatty acid composition of plasma phospholipids and the triene (20:3, n=9) to tetraene (20:4, n=6) ratio in the same lipid fraction have been determined, as indices of the essential fatty acid status, in a group of 22 healthy premature newborns fed by the nasoduodenal technique. Determinations have been carried out on the first and fifth day of life for all 22 newborns, and also on the tenth and 30th day of life for 12 of them. The normal plasma levels of essential fatty acids obtained indicate a satisfactory utilization of dietary essential fatty acids under these unusual nutritional conditions.

Duodenum↗
PubMed1981

Essential fatty acid deficiency in malnourished children.

Fatty acid patterns of major classes of lipids of serum were measured in forty Argentine children ages 2 to 24 months admitted to the hospital with chronic malnutrition. A normal control group of 48 children from the same population was also examined. Serum lipids were extracted and separated into phospholipids, cholesteryl esters, triglycerides, and free fatty acids. These were converted to methyl esters which were analyzed by gas chromatography. In chronic malnutrition, the fatty acid patterns of phospholipids and cholesteryl esters indicated changes characteristic of essential fatty acid deficiency of moderate degree. The total omega 6 acids were found to be highly significantly diminished from normal, and the ratio of 20:3 omega 9/20:4 omega 6 was highly significantly increased. Decreased proportions of omega 6 metabolites suggested impaired desaturase activity, and elevated ratios of 22:4 omega 6/20:4 omega 6 and 20:2 omega 6/18:2 omega 6 suggested increased chain elongation in chronic malnutrition.

Argentina↗
PubMed1990

Diet-induced alterations of lipids during cell differentiation in the small intestine of growing rats: effect of an essential fatty acid deficiency.

The lipid components of columnar cells harvested from rat small intestine were analyzed at each step of cell maturation. The effect of dietary lipids on the evolution of lipids in differentiating cells was studied using two diets representative either of a control or of an essential polyunsaturated fatty acid deficient lipid supply. Two groups of weanling rats were fed a semisynthetic diet composed of corn oil (control diet) or hydrogenated coconut oil (deficient diet) for 11 weeks. Intestinal cells were extracted according to their position along the villus column. Linoleic and arachidonic acids constitutive of cell phospholipids increased as cells migrated from the lower to the mid-part of the crypt-villus axis only with the control diet. This gradient disappeared after a 3-week feeding period with hydrogenated coconut oil diet so that columnar cells of essential fatty acid deficient rats exhibited the same overall fatty acid composition all along the crypt-villus axis. Essential fatty acid deficiency resulted in an increase of both the triene to tetraene and arachidonic acid to linoleic acid weight ratios regardless of the maturational step of cells. As compared to the control diet, the essential fatty acid deficient diet induced a decrease of both the cholesterol and free fatty acid to phospholipid molar ratios only in lower villus cells. We conclude that (a) progressive compositional modifications of lipids occur while ascending the crypt-villus axis and (b) essential fatty acid deficiency induces substantial alterations of the lipid evolution normally linked to cell differentiation.

Animals↗
PubMed2000

Effect of L-arginine-nitric oxide system on the metabolism of essential fatty acids in chemical-induced diabetes mellitus.

Several studies have shown that the activities of delta-6-desaturase and delta-5-desaturase are depressed in experimental diabetes and in humans with insulin- and non-insulin-dependent diabetes mellitus (type I and type II diabetes mellitus respectively). Furthermore, treatment with insulin is known to correct the defects in desaturases in rats and humans with diabetes, especially in type I. In a recent study, we demonstrated that L-arginine and nitric oxide can prevent alloxan-induced beta cell damage, and the severity of diabetes, and restore the antioxidant status to near normal levels. But, no information is available as to the relationship between L-arginine-nitric oxide system and the metabolism of essential fatty acids in diabetes mellitus. In the present study, it was noted that the plasma levels of saturated fatty acids: stearic and palmitic were increased where as unsaturated fatty acids such as oleic, linoleic, gamma-linolenic and eicosapentaenoic acids (OA, LA, GLA and EPA respectively) were decreased in alloxan-induced diabetic rats. In the liver phospholipid (PL) fraction, GLA, DGLA (dihomo-GLA) and alpha-linolenic acid (ALA) were decreased in the alloxan-treated group; in the muscle PL fraction, LA, GLA and DGLA were low, whereas an increase in the saturated fatty acid content was noted. L-arginine (the precursor of nitric oxide) and sodium nitroprusside (a nitric oxide donor) treatment of alloxan-induced diabetic rats enhanced the levels of LA, GLA and DGLA. Further, nitric oxide synthase inhibitor, L-NMMA, prevented this beneficial action of L-arginine-nitric oxide system on essential fatty acid metabolism. The abnormalities in the essential fatty acid metabolism observed also reverted to normalcy following control of diabetes with insulin. These results indicate that nitric oxide can enhance the activities of delta-6- and delta-5 desaturases, which are depressed in diabetes, and suggests that there is a close interaction between L-arginine-nitric oxide system and the metabolism of essential fatty acids.

8,11,14-Eicosatrienoic Acid↗
PubMed1994

Effect of essential fatty acid deficiency on the fatty acid composition and arachidonic acid levels in rat maxillae and mandibles.

The fatty acid composition of total lipids and total phospholipids of maxillae and mandibles of rats fed an essential fatty acid-deficient (EFAD), marginally FAD (MEFAD), and a control diet was determined. Patterns typical of an EFA deficiency such as a decrease in the levels of linoleic acid and archidonic acid along with concomitant increase in the levels of palmitoleic acid, oleic acid, and 5,8,11-eicosatrienoic acid were observed in the EFAD groups. Concentrations of arachidonic acid were significantly lower in total lipids of mandibles and maxillae of rats in the EFAD, but not in the MEFAD rats, than those of the controls.

Animals↗
PubMed1978

Changes in essential fatty acids in plasma lipid fractions of polytraumatized patients with different parenteral nutrition.

We investigated changes in the fatty acid pattern of plasma lipids during the phase of total parenteral nutrition in two groups of polytraumatized patients. For parenteral nutrition we gave L-amino acid solutions in a dose of 0.24 g N day-1kg-1 body weight. In addition, we administered in the first group glucose and fructose, and in the second group glucose, fructose and fat emulsions in a total dose of 30 kcal day-1kg-1 body weight. In the latter group, the proportion of the fat emulsions was 30-40% of the calories administered. The most striking findings were the decrease of the essential fatty acids with regard to the phospholipid fraction from about 60% to 30% in the early post-traumatic phase. In the first group of patients we observed a further reduction of the essential fatty acids in the period of observation. This could be avoided by administering fat emulsions of the same type as we gave in the second group of patients. The functions of essential fatty acids in membranes and in the intermediary metabolism are discussed.

Dietary Fats↗
PubMed1988

Senna still causes laxation in rats maintained on a diet deficient in essential fatty acids.

The laxative effect of senna has been investigated in normal and essential fatty acid deficient (EFAD) rats. Oral administration of senna pod extract (7-5-90 mg kg-1) produced a dose-dependent increase in the number of soft faeces excreted by normal rats. Senna 30 mg kg-1 also reversed net absorption of water and increased the prostaglandin (PG) production in the colonic lumen of normal rats by about four times. Oral administration of senna pod extract to rats, maintained on a fat-free diet for 30-90 days, produced diarrhoea and reversed net absorption of water as in normal rats. However, a fat-free diet reduced the PG production drastically in the colonic lumen both in senna-free rats and in senna-treated rats. In EFAD rats carrageenan oedema, but not dextran oedema, was also drastically reduced. Since PG mediation is not present in EFAD rats we conclude that the PG are not essential for laxation induced by senna and that water secretion and PG production in the rat intestinal lumen are unrelated.

Animals↗
PubMed1993

Essential fatty acid deficiency increases interstitial IA-positive cells in rat kidney and accelerates renal allograft rejection.

Essential fatty acid deficiency has been reported to result in depletion of interstitial macrophages from rat kidneys and to permit transplantation of these kidneys across a fully allogeneic barrier without need for immunosuppression. In view of the potential for application of this phenomenon to xenografts, this study attempted to confirm the observation. Kidneys from rats fed normal or essential fatty-acid-deficient diets were transplanted to DA recipients. The donors' livers and contralateral kidneys were analyzed for their fatty acid profile in liver phospholipids, and the kidneys were examined by immunohistology for interstitial Ia(+) cells. EFAD resulted in an increase in renal interstitial Ia(+) cells detected by MRC-OX6 (anti-RT1Bpublic) from 13.5 +/- 2.9 (control diet fed rats) to 22.8 +/- 3.6 in rats on a stringent EFAD diet. Graft survival of kidneys from these EFAD rats was significantly shorter than that of kidneys from control diet fed rats. In direct contrast to the original report, this study found that EFAD caused a marked increase in renal interstitial Ia(+) cells and a reduction in allograft survival of EFAD donor kidneys.

Animals↗
PubMed1986

Increased requirements for essential fatty acids in atopic individuals: a review with clinical descriptions.

Patients with atopic eczema and a mixture of allergic illnesses show biochemical evidence suggesting impairment in the desaturation of linoleic acid and linolenic acid by the enzyme delta-6 dehydrogenase. Consequences of this enzyme defect are 1) diminished synthesis of the 20-carbon polyunsaturated fatty acids, which are prostaglandin precursors and 2) a reduction in the concentration of double bonds in the cell membrane. A distortion in the production of prostaglandins and leukotrienes, which might result from this block, can account for the immunological defects of atopy and a variety of clinical symptoms experienced by atopic individuals. Dietary supplementation with essential fatty acids relieves the signs and symptoms of atopic eczema, may improve other types of allergic inflammation, and may also correct coexisting symptoms as diverse as excessive thirst and dysmenorrhea. Further research is suggested to test the hypothesis that some atopic states represent a condition of essential fatty acid dependency owing to defective desaturation of dietary fatty acids.

Adult↗
PubMed1992

Triacylglycerol: an important pool of essential fatty acids during early postnatal development in rats.

Developmental changes in the content and composition of major organ lipid pools are not well known. Our objective was to assess quantitatively the changes in lipids, particularly those containing long-chain fatty acids, in the placenta and the brain, liver, and carcass of the fetal and suckling rat. Pregnant dams were killed at days 15, 18, and 21 (term) of pregnancy and the placentas and fetuses removed and analyzed; suckling rats were killed at days +3, +6, and +9 of lactation. Whereas the long-chain fatty acid content of the phospholipids (mg/g) of the fetal or suckling rat remained relatively constant from day 18 of pregnancy to day +9 of lactation, long-chain fatty acids in triacylglycerols increased from prenatal values by 10- to 12-fold during the first 9 postnatal days. Prenatally, triacylglycerol accounted for no more than 32% of total whole body essential fatty acids (day 21), but postnatally this increased to 81-88%. From day 21 to day +9, the proportion of n-6 and n-3 essential fatty acids within the total triacylglycerol pool of the suckling rat increased 71 and 317%, respectively. We conclude that in the suckling rat, triacylglycerol is quantitatively the most important source of essential fatty acids during at least the first 9 days of life.

Animals↗
PubMed1979

Essential fatty acid deficiency and adrenal cortical function in vitro.

Adrenocortical cells were prepared from rats maintained on essential fatty acid-deficient diets and control litter mates. Cells from control rats had high concentrations of essential fatty acids in the cholesteryl ester fraction of which approximately 22% was arachidonate. In contrast, cells from EFA-deficient rats had only 2.5% arachidonate in the cholesteryl esters, even though the total esterified cholesterol level was comparable to that of controls. In place of the essential fatty acids, the cholesteryl esters of these cells were rich in 20:3(n--9) and 22:3(n--9). When cells from EFA-deficient rats were incubated with ACTH or dibutyryl cyclic AMP, the output of corticosterone was the same as in controls. Also sterol esters were hydrolyzed to the same extent as in controls despite the unusual composition of the fatty acid esters. The phospholipids in both control and EFA-deficient cells contained high levels of arachidonate but were not hydrolyzed in either type of cell during incubation with ACTH or dibutyryl cyclic AMP. The results indicate that high levels of the prostaglandin precursors, namely linoleate and arachidonate, are not a sine qua non for the steroidogenic action of ACTH or cyclic AMP.

Adrenal Cortex↗
PubMed1980

A new concept of lifestyle-related cardiovascular disease: the importance of interactions between cholesterol, essential fatty acids, prostaglandin E1 and thromboxane A2.

A proposal to account for the inter-relationships between established risk factors and cardiovascular disease is presented. In this concept, the critical substance is prostaglandin (PG) E1 which is a vasodilator, an inhibitor of platelet aggregation, an inhibitor of cholesterol and collagen biosynthesis and an inhibitor of smooth muscle proliferation. PGE1 biosynthesis is enhanced by the essential fatty acid, linoleic acid, by the platelet aggregating agent thromboxane (TX) A2, by cholesterol and by melatonin. These factors may participate in a negative feedback control loop. As a result of the operation of this loop, any tendency for PGE1 levels to fall is followed by increased cholesterol and TXA2 biosynthesis, and enhanced platelet aggregation, vasoconstriction, smooth muscle proliferation and collagen biosynthesis. Enhancement of PGE1 biosynthesis will have the opposite effects. Factors known to increase PGE1 biosynthesis include essential fatty acids, vitamin C, ethanol, pyridoxine, zinc and probably niacin, all of which are known to have some protective effects against cardiovascular disease. The hypothesis predicts that lowering of cholesterol biosynthesis by any method other than enhanced PGE1 formation, while reducing the risk of cardiovascular disease, will increase the risk of other disorders. The hypothesis suggest new approaches to treatment and new ways of combining existing treatments. Colchicine, which at low concentrations may imitate and action of melatonin, has particularly interesting possibilities. Colchicine and related compounds have already been shown to have potent cholesterol-lowering and anti-atherogenic actions in both humans and animals.

Cardiovascular Diseases↗
PubMed1998

Distal procto-colitis, natural cytotoxicity, and essential fatty acids.

OBJECTIVES: Recently, it has been postulated that patients with ulcerative colitis have altered natural cytotoxicity, in particular natural killer (NK) and lymphokine-activated killer (LAK) cell activities. These cellular mechanisms have been postulated to play an etiological role in the pathogenesis of the disease process. We have shown previously that the essential fatty acids (EFA) eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) specifically inhibit natural cytotoxicity. Our aim was to evaluate the role of omega-3 EFA in the modulation of natural cytotoxicity and disease activity in patients with distal procto-colitis. METHODS: In this pilot study patients were randomized into two groups. Each patient received either fish oil extract (EPA, 3.2 g, and DHA, 2.4 g) (n = 9) or sunflower oil (placebo) (n = 9) daily in a double-blind manner for 6 months. Monthly assessments of disease activity (clinical and sigmoidoscopic scores) and histological evaluation of mucosal biopsies were carried out. Also, the circulating levels and activities of NK and LAK cells, using flow cytometric analysis (CD16+ CD56+) and in vitro 51 chromium release assays (K562), respectively, were monitored. RESULTS: After 6 months' supplementation with EFA, there was improvement in the clinical activity compared with pretreatment evaluation. There was significant reduction in the sigmoidoscopic and histological scores in the EFA group compared with the placebo group. Essential fatty acid supplementation for 6 months also induced significant reduction in the circulating numbers of CD16+ and CD56+ cells and the cytotoxic activity of NK cells, compared with the placebo group. CONCLUSIONS: This pilot study has demonstrated that omega-3 fatty acids can suppress natural cytotoxicity and reduce disease activity in patients with distal procto-colitis. These findings suggest a therapeutic strategy for managing patients with inflammatory bowel disease.

Adult↗
PubMed1987

Effects of essential fatty acid deficiency on epidermal O-acylsphingolipids and transepidermal water loss in young pigs.

Linoleate-rich O-acylglucosylceramides and acylceramides are thought to be of major significance for the physical structure and function of the epidermal permeability barrier. In the present investigation, the effects of a linoleate-free diet on O-acylsphingolipids and their associated functions were investigated. Starting at 5 days of age, male pigs were fed diets containing 12% of either lard or hydrogenated coconut oil. Transepidermal water loss was measured with an electrolytic water analyzer at weekly intervals. Pigs were killed at intervals, and epidermal lipids were isolated and analyzed. Fatty acid compositions were determined by gas-liquid chromatography (GLC). Within 2-3 weeks, pigs on the diet containing coconut oil began to display biochemical and physiological symptoms of essential fatty acid deficiency. Within 2 months, this group had extremely scaly skin and transepidermal water loss was elevated to five times that of controls. The progressive increase in transepidermal water loss correlated with replacement of linoleate by oleate in both acylceramide and acylglucosylceramide. The formation of lamellar granules and intercellular lipid sheets in the stratum corneum was not impaired in essential fatty acid deficiency as judged by electron microscopy. These results suggest that the linoleic acid normally found in the O-acylsphingolipids is not essential for formation of the epidermal membrane system. Rather, it appears that the nature of the ester-linked fatty acid in the O-acylsphingolipids regulates the permeability of this membrane system.

Acylation↗
PubMed1987

Studies of the modulation of essential fatty acid metabolism by fatty acids in cultured neuroblastoma and glioma cells.

In cultured neuroblastoma cells (N1E-115), the metabolism of the essential fatty acid, linoleic acid (18:2 (n-6)), to arachidonic acid (20:4(n-6)) can be altered by other fatty acids in a manner supporting a concerted action of the modulating fatty acid on the desaturation and chain elongation enzymes. In further examination of mechanisms involved, cultured glioma (C-6) or neuroblastoma-glioma hybrids (NG-108-15) cells showed similar patterns of activation by some fatty acids (e.g., 20:3(n-6) and 20:4(n-6)), and inhibition (e.g., 18:3(n-3) or 22:6(n-3)) or no effect (e.g., 18:1(n-9), 20:3(n-3)) by others. In contrast, only inhibition by 20:4(n-6) was seen in cultured HeLa cells, suggesting that the intracellular interactions may not be universal in all cell lines. For fatty acids that activate 20:4(n-6) formation, the lag observed when substrate and activator were administered simultaneously was eliminated by preincubation with activator. Maximal activation occurred within 4 h for neuroblastoma and 2 h for glioma; in each cell line activation declined steadily for 10 h after removal of the activator. Inhibition of protein synthesis did not alter activation. As 98% of the fatty acid incorporated was esterified to triacylglycerol or phospholipid and only the triacylglycerol mass expanded, several manipulations to potentially alter the flow of acyl chains between these lipid pools were evaluated using dual-label and pulse-chase experiments. Results suggested that competition between 18:2(n-6) utilization for esterification to phospholipid and the desaturation-chain elongation sequence as well as a more direct and specific interaction of certain fatty acids with the enzymes may influence 20:4(n-6) formation. A model to explain these observations is discussed.

Arachidonic Acid↗
PubMed1983

Tolerance to ethanol in rats bred on essential fatty acid deficient diets.

We bred three generations of Sprague-Dawley rats on a diet deficient in essential fatty acids, low-EFA (0.3 energy %), whereas age matched controls received normal-EFA (3.0 energy %). Subgroups (N = 6) of female rats were given daily IP injections of ethanol (3.0 g/kg) or isocaloric glucose for 23 consecutive days. On days 1 and 22 blood-ethanol profiles, rates of ethanol metabolism and ethanol-induced impairment of motor coordination were measured after the challenge dose of 3.0 g/kg. Rats exposed to ethanol ate and drank more than controls and gained more body weight over the 23 days. Low-EFA rats were slightly more impaired than normal EFA rats after an acute dose of ethanol even though the peak blood ethanol concentrations reached were about the same at 2.9 mg/ml (63 mmol/l). After chronic ethanol treatment a functional tolerance developed in both dietary groups but the degree of tolerance was less clearcut in low EFA rats. Metabolic tolerance was confirmed after chronic treatment in both dietary groups as shown by steeper slopes (19-27%) of the ethanol elimination curves. But no significant differences in the development of metabolic tolerance were apparent in rats on low EFA and normal EFA diets.

Animals↗
PubMed1989

The effects of essential fatty acid deficiency on brown adipose tissue activity in rats maintained at thermal neutrality.

1. The consequences of essential fatty acid (EFA) deficiency on the resting metabolism, food efficiency and brown adipose tissue (BAT) thermogenic activity were examined in rats maintained at thermal neutrality (28 C). 2. Weanling male Long-Evans rats were fed a hypolipidic semi-purified diet (control diet: 2% sunflower oil; EFA-deficient diet: 2% hydrogenated coconut oil) for 9 weeks. 3. They were kept at 28 C for the last 5 weeks. Compared to controls, in EFA-deficient rats the growth shortfall reached 21% at killing. 4. As food intake was the same in EFA-deficient and control rats, food efficiency was thus decreased by 40%. 5. Resting metabolism expressed per surface unit was 15% increased. 6. Non-renal water loss was increased by 88%. 7. BAT weight was 28% decreased but total and mitochondrial proteins were not modified. 8. Heat production capacity, tested by GDP binding per BAT was 69% increased in BAT of deficient rats. 9. The stimulation of BAT was established by two other tests: GDP inhibition of mitochondrial O2 consumption and swelling of mitochondria. 10. It is suggested that the observed enhancement of resting metabolism in EFA-deficient rats is, in part, due to an activation of heat production in BAT.

Adipose Tissue, Brown↗