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PubMed1991

The incorporation of n-3 and n-6 essential fatty acids into the chick embryo from egg yolks having vastly different fatty acid compositions.

The effect of egg yolk fatty acid composition on essential fatty acid utilization by the developing chick embryo was studied by feeding laying hens a fat-free diet supplemented with oils containing widely divergent contents of the essential n-6 and n-3 fatty acids. A control hen was fed a commercial feed for laying hens. The diets contained 20 to 4370 mg/100 g n-3 fatty acids and 360 to 8020 mg/100 g n-6 fatty acids. Fertile eggs were collected in pairs: one was incubated and the other served as an unincubated control. The fatty acid content of the unincubated egg and the newly hatched chick from each pair was compared. Some 50% of the total fatty acids in the egg yolk were incorporated into the tissues of the newly hatched chick. Regardless of diet, more yolk n-6 fatty acids were incorporated into the chick compared to saturated or monounsaturated fatty acids. The percentage of incorporation especially increased from the eggs containing relatively low amounts of n-6 fatty acid. The percentage of incorporation of n-3 fatty acids was similar to that of saturated and monounsaturated fatty acids when n-3 fatty acids were plentiful in the egg yolk, but increased significantly when n-3 fatty acids were low in the eggs. There was a generally linear relationship between essential fatty acids in the egg and in the chick, although levels of docosahexaenoic acid [DHA; 22:6(n-3)] in the brain did not respond proportionally.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2006

Essential fatty acids: biochemistry, physiology and pathology.

Essential fatty acids (EFAs), linoleic acid (LA), and alpha-linolenic acid (ALA) are essential for humans, and are freely available in the diet. Hence, EFA deficiency is extremely rare in humans. To derive the full benefits of EFAs, they need to be metabolized to their respective long-chain metabolites, i.e., dihomo-gamma-linolenic acid (DGLA), and arachidonic acid (AA) from LA; and eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) from ALA. Some of these long-chain metabolites not only form precursors to respective prostaglandins (PGs), thromboxanes (TXs), and leukotrienes (LTs), but also give rise to lipoxins (LXs) and resolvins that have potent anti-inflammatory actions. Furthermore, EFAs and their metabolites may function as endogenous angiotensin-converting enzyme and 3-hdroxy-3-methylglutaryl coenzyme A reductase inhibitors, nitric oxide (NO) enhancers, anti-hypertensives, and anti-atherosclerotic molecules. Recent studies revealed that EFAs react with NO to yield respective nitroalkene derivatives that exert cell-signaling actions via ligation and activation of peroxisome proliferator-activated receptors. The metabolism of EFAs is altered in several diseases such as obesity, hypertension, diabetes mellitus, coronary heart disease, schizophrenia, Alzheimer's disease, atherosclerosis, and cancer. Thus, EFAs and their derivatives have varied biological actions and seem to be involved in several physiological and pathological processes.

Animals↗
PubMedDate not supplied

Failure of topical vegetable oils to prevent essential fatty acid deficiency in a critically ill patient receiving long-term parenteral nutrition.

This case report describes the failure of topical vegetable oils containing esters of linoleic acid to prevent essential fatty acid deficiency in a critically ill patient with trauma. A 40-year-old black man injured in a motor vehicle accident developed essential fatty acid deficiency after being maintained on long-term, fat-free parenteral nutrition plus topical vegetable oil application because of the presence of severe hypertriglyceridemia. Biochemical evidence of this deficiency included a decrease in serum linoleic, a-linolenic, and arachidonic acid levels with a corresponding increase in oleic and palmitoleic acid levels. Cutaneous manifestations consistent with this syndrome were also present. After 3 weeks of daily topical treatments with vegetable oils rich in linoleic acid, biochemical abnormalities of deficiency were still evident. Over the following 2 1/2 months, 4% to 22% of the total caloric intake was delivered as intravenous fat in addition to continued topical administration of vegetable oil. Only after supplementation with intravenous fat did the patient demonstrate clinical and biochemical signs of improvement. The results show that cutaneous administration of vegetable oils as the sole source of linoleic acid may be unable to prevent or treat essential fatty acid deficiency in a critically ill surgical patient.

Administration, Cutaneous↗
PubMed2000

Essential fatty acids in breast milk of atopic mothers: comparison with non-atopic mothers, and effect of borage oil supplementation.

OBJECTIVE: To evaluate whether levels of n-6 long chain polyunsaturated fatty acids (LCPs) in human breast milk are related to the mother's atopic constitution, and whether a decreased level can be restored by gamma-linolenic acid supplementation. DESIGN: Cross-sectional study and dietary supplementation trial. SUBJECTS: 20 atopic mothers and 20 non-atopic mothers (controls), all lactating. SETTING: General population. INTERVENTIONS: The atopic mothers were randomly assigned to low (n=10) or high (n=10) dosage oral supplementation with oral borage oil for one week (230 or 460 mg gamma-linolenic acid (18:3n-6) per day). MAIN OUTCOME MEASURES: Essential fatty acid composition of the breast milk total fat fraction, determined by gas liquid chromatography. RESULTS: Arachidonic acid (20:4n-6) was lower in breast milk of atopic mothers compared with non-atopic mothers (0.39 wt% vs 0.46 wt%, difference -0.07% wt% (95% confidence limits -0.13, -0.01 wt%; P<0. 05). The ratio between linoleic acid and the sum of n-6 derivatives did not differ between these groups, indicating no difference in delta-6-desaturase (D6D) activity. Supplementation of the atopic mothers significantly increased the levels of gamma-linolenic acid and dihomo-gamma-linolenic acid in breast milk in a dose-related way, but the level of arachidonic acid was not increased. CONCLUSION: We found a decreased level of arachidonic acid in breast milk in atopic compared to non-atopic mothers, but no indication that the rate-limiting enzymatic step (D6D) is involved. Supplementation increased the precursor pool but did not restore the level of arachidonic acid. We conclude that atopy is related to a metabolic disturbance beyond the D6D enzymatic step. A low level of arachidonic acid in breast milk may be a risk factor for the development of atopy in the infant, especially when the possible underlying metabolic disturbance of EFA metabolism is inherited by the child. SPONSORSHIP: F Hoffman-La Roche (Basel, Switzerland) and Friesland Dairy Foods (Leeuwarden, The Netherlands).

Adult↗
PubMed1993

Essential fatty acids influence survival in sepsis.

Metabolites of arachidonic acid, formed from omega-6 essential fatty acids (n-6), play a pathologic role in mortality from sepsis. Metabolites of eicosapentaenoic acid, formed from omega-3 essential fatty acids (n-3), are less potent inflammatory mediators. Dietary restriction of n-6 fatty acids or supplementation with n-3 fatty acids in the form of fish oil have been shown to decrease the production of n-6 metabolites. Male Sprague-Dawley rats (350-400 g) were divided to receive either rat chow (CHOW) or essential-fatty-acid-deficient chow (EFAD) and subdivided to receive 1 mL daily of either fish oil (N3), linoleic acid (N6), or normal saline (NS), via gastric gavage. Two weeks later, half of the animals in each group underwent cecal ligation and puncture (CLP) to induce peritonitis or sham (SHAM) celiotomy. Survival was tabulated for 7 days. Survival was significantly decreased for animals undergoing CLP for both the N6 and NS groups but not for the N3 group. Omega-3 fatty acids as the sole essential fatty acids or as a supplement to a "routine" diet, when fed to rats for 2 weeks before a septic challenge, improved survival in this peritonitis model.

Animals↗
PubMed1995

Some aspects of neonatal essential fatty acid status are altered by linoleic acid supplementation of women during pregnancy.

To study the effect of maternal linoleic acid [18:2(n-6), LA] supplementation during pregnancy on neonatal essential fatty acid status, pregnant women with relatively low plasma linoleic acid concentrations before 16 wk of gestation (n = 21) were supplied with foods rich in linoleic acid, resulting in an additional intake of 10 g/d of linoleic acid from the 20th week of gestation until delivery. One of the two control groups consisted of pregnant women with comparably low plasma linoleic acid concentrations at the start of the study (LL-control group, n = 22); the other consisted of women with habitually high plasma linoleic acid concentrations (HL-control group, n = 21). The neonatal essential fatty acid status was assessed by determining the fatty acid composition of phospholipids (PL) isolated from umbilical plasma and umbilical vessel walls. The maternal linoleic acid status in the LA-supplemented group increased to a level comparable to that of the HL-control group, but the neonatal linoleic acid status did not differ from that of either control group. Linoleic acid supplementation did result in slightly, but significantly, higher total amounts of (n-6) long-chain polyenes in umbilical plasma and vein vessel wall phospholipids compared with the LL-control group. This increase was associated with significantly lower total amounts of (n-3) long-chain polyenes. In the HL-control group, the concentration of (n-3) long-chain polyenes in umbilical plasma and vessel walls was significantly lower than in the LA-supplemented and the LL-control group.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1998

The slow discovery of the importance of omega 3 essential fatty acids in human health.

Although linoleic and linolenic acids have been known to be necessary for normal growth and dermal function since 1930, the omega 3 essential fatty acids (EFA) have not received much attention until recently. The two families of acids are metabolized by the same enzymes, making them competitive. Gross deficiencies of omega 6 plus omega 3 EFA have been observed in humans, induced by attempts at total parenteral nutrition (TPN) with preparations devoid of lipids. Deficiency of omega 3 acids has been induced by TPN containing high omega 6 and low omega 3 fatty acids. In natural human populations, a wide range of omega 3 and omega 6 proportions have been found, ranging from high omega 3 and low omega 6 content to low omega 3 and high omega 6 content, showing inverse correlation between sigma omega 6 and sigma omega 3. In humans with neuropathy or impairment of the immune system, significant deficits of omega 3 EFA have been measured.

Aged↗
PubMed2006

Essential fatty acid deficiency profile in patients with nephrotic-range proteinuria.

Plasma free fatty acids are bound to albumin, filtered through the glomeruli, and reabsorbed at the proximal nephron. The aim of the present investigation was to determine if urinary loss of fatty acids results in essential fatty acid (EFA) deficiency in patients with nephrotic-range proteinuria. We studied 12 patients aged 9 months to 23 years (eight male, four female) four suffering from congenital nephrotic syndrome (NS) and eight from different renal diseases. Six patients were studied postrenal transplantation. Proteinuria ranged between 41 and 829 mg/m2/h. Results were compared with data obtained in 83 healthy children. The patients had significantly lower values for plasma arachidonic acid content and EFA index (omega3 + omega6/omega7 + omega9). Deficiency in polyunsaturated fatty acids (PUFA) was especially manifest in infants with congenital NS. Plasma content of arachidonic and docosahexaenoic acids related negatively with the degree of proteinuria. In the lineal regression model, the degree of proteinuria explained 60% of the variability of plasma values of those fatty acids. We conclude that plasma fatty acid status should be regularly monitored in patients with nephrotic-range proteinuria, especially in young infants with congenital NS, who represent a population at special risk with regard to neurological development.

Adolescent↗
PubMed1999

Lipid peroxides, nitric oxide and essential fatty acids in patients with Plasmodium falciparum malaria.

Long chain polyunsaturated fatty acids derived from essential fatty acids have been shown to be toxic to Plasmodium falciparum both in vitro and in vivo. Here, we present evidence to suggest that in patients with Plasmodium falciparum malaria the levels of lipid peroxides (a marker of free radical generation) nitric oxide (a potent free radical with immunomodulatory actions), and concentrations of linoleic acid (LA) and alpha-linolenic acid (ALA) are low, whereas those of eicosapentaenoic acid (EPA) are high. The ability of the fatty acids to kill P. falciparum is dependent on their capacity to stimulate free radical generation in neutrophils and macrophages. EPA is more potent than LA in killing the parasite. In view of this, the results of the present study suggest that in patients with P. falciparum malaria the decreased levels of lipid peroxides and nitric oxide may contribute to the persistence of the infection, whereas elevated levels of EPA may be a feeble attempt to overcome this defect.

Animals↗
PubMed1985

Essential fatty acids in the liver and adipose tissue of genetically obese mice: effect of supplemental linoleic and gamma-linolenic acids.

Genetically obese mice (ob/ob) and their lean litter-mates were given diets iso-energetically supplemented with sucrose, hydrogenated coconut oil, safflower oil or evening primrose (Oenothera biennis) oil. Weight gain over 15 weeks was significantly greater in the evening primrose oil-supplemented obese mice than in the other groups. In all the groups of obese mice, liver total phospholipids contained proportionally less linoleic acid and more dihomo-gamma-linolenic acid and arachidonic acid than did the lean controls. As a percentage of total fatty acids, n-3 essential fatty acids (EFA) in liver and adipose tissue lipids were significantly lower in the obese mice than in the lean controls. Supplementation with EFA-rich oils (safflower and evening primrose oil) increased the proportional composition of n-6 EFA and decreased the n-3 EFA more in the liver total phospholipids of the lean than the obese mice.

Adipose Tissue↗
PubMed1987

Essential fatty acids, prostaglandins, and alcoholism: an overview.

Essential fatty acids (EFAs) are major structural components of the brain and through their effects on membrane properties can influence nerve conduction, transmitter release, and transmitter action. Prostaglandins (PGs) derived from EFAs have profound behavioral effects and are also able to modify conduction and transmitter function. Effects of alcohol on EFAs and PGs are therefore good candidates for explaining at least some of the actions of alcohol on brain function. Ethanol has three main known actions on EFA and PG metabolism: it reduces blood linoleic acid levels and induces or exaggerates EFA deficiency states; it blocks metabolism of linoleic acid to EFA metabolites which are known to be important in brain structure; and it enhances conversion of the linoleic acid metabolite, dihomo-gamma-linolenic acid, to PGE1. This review demonstrates that some of the short-term behavioral effects of ethanol and some of its long-term adverse effects on brain, liver, and other tissues may be partly explicable in terms of ethanol actions on EFA and PG metabolism. Modification of such metabolism by dietary and other means has already been shown to influence the effects of alcohol and alcohol withdrawal in both humans and animals. This promises to be a fruitful source of investigation with substantial implications for the understanding and treatment of alcoholism.

Alcoholism↗
PubMed1979

Forebrain fatty acid composition during development in protein-calorie and essential fatty acid deficiencies in the rat.

Rats were fed three different dietary levels of essential fatty acids (EFA), 3.0, 0.75 and 0.1 cal%, representing normal, subnormal and severely deficient dietary intakes. From the animals kept on these diets, with a protein content of 16 cal%, 3-month-old females were randomly selected to be fed diets with only 6 cal% protein but with unchanged amounts of EFA. The rats were then mated, and the effects of the diets were studied in the forebrains of their offspring. The growth and the fatty acid patterns of the ethanolamine phosphoglyceride and total phosphoglyceride fractions were studied during the first 60 days of life. Addition of protein-calorie deficiency to rats severely undernourished in EFA mitigated the biochemical signs of EFA deficiency. In EPG the developmental pattern with a decrease of 20:4 (n-6) and an increase of 22:6 (n-3) was retarded between 11 and 21 days of age in the protein-calorie deficient groups suggesting a delay in the maturation of the forebrain.

Aging↗
PubMed1994

Essential fatty acid metabolism in south Indians.

Coronary artery disease (CAD), hypertension and diabetes mellitus are more common in Indians compared to their incidence in the Western population. The exact reason for this is not known. One of the risk factors for the development of and complications due to CAD, hypertension and diabetes mellitus could be hyperinsulinemia and insulin resistance and low plasma levels of arachidonic acid and eicosapentaenoic acid, metabolites of dietary essential fatty acids (EFAs), cis-linoleic and alpha-linolenic acids. Fatty acid analysis of the plasma phospholipid (PL) fraction of normal Indians showed that they have low concentrations of arachidonic acid, eicosapentaenoic acid and docosahexaenoic acid in comparison to those seen in Canadian and Minnesota (USA) normals. Since insulin can activate EFA metabolism, this alteration in the EFA metabolism may, at least, in part explain the high incidence of CAD, hypertension and diabetes mellitus and insulin resistance and hyperinsulinemia that are common in Indians.

Adult↗
PubMed1997

The effects of essential fatty acids preparation in the treatment of intrauterine growth retardation.

A treatment of intravenous infusion of glucose, amino acids, and emulsion enriched in essential fatty acids (EFAs), linoleic, and linolenic acids were given to 30 pregnant women with intrauterine growth retardation (IUGR) and 28 non-EFAs treated cases as controls. There was a marked gain in fetal biparietal diameter (BPD) and in the estimated weight of the treated group over the control group. The mean birth weight was significantly different in the two groups. Fetal BPD increased much more in patients treated with EFAs at 28-34 gestational weeks than those at 34 1/7-37 weeks, which indicates that early initiate complement of n-3 and n-6 fatty acids to IUGR mothers may correct pregnancy-induced EFAs deficiency and maternal-fetal malnutrition, which demonstrates a fetal catch-up of growth in the brain and the whole body.

Adult↗