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PubMed1991

Essential fatty acid composition of human colostrum triglycerides: its relationship with adipose tissue composition.

The relationships between essential fatty acid (EFA) composition of colostrum and white adipose tissue (WAT) were examined on day 5 after delivery in 69 healthy women. Fatty acid composition was assessed by capillary gas chromatography, and 33 fatty acids were detected in colostrum and in WAT. Total polyunsaturated fatty acid (PUFA) content was similar in colostrum and in WAT (15.7 +/- 3.1% and 16.1 +/- 3.8%, respectively), but long-chain PUFA content was higher in colostrum than in WAT (2.9 +/- 0.6% and 1 +/- 0.2%, respectively; P less than 0.001). The concentrations of linoleic acid were significantly correlated between colostrum and WAT (r = 0.77, P less than 0.0001). No correlation was found for alpha-linolenic acid. The relationships between long-chain PUFA composition of colostrum and WAT suggested that individual factors along with tissue specificity of the mammary gland are involved in either the capacity of desaturating and chain-elongating pathways and/or incorporation of long-chain PUFAs into colostrum.

Adipose Tissue↗
PubMed1984

Essential fatty acids in the plasma phospholipids of patients with atopic eczema.

We have measured all the essential fatty acids (EFA) in plasma phospholipids in forty-one adults with atopic eczema and fifty normal controls. The major dietary n-6 EFA, linoleic acid, was significantly elevated, but all its metabolites, 18:3n-6, 20:3n-6, 20:4n-6, 22:4n-6, and 22:5n-6 were significantly reduced. The major dietary n-3 EFA, alpha-linolenic acid, was also elevated, though not significantly, while all its metabolites were also significantly reduced. These observations suggest that atopic eczema is associated not with any defect of EFA intake, but with abnormal metabolism, possibly involving the enzyme delta-6-desaturase. Treatment with oral evening primrose oil produced partial correction of the n-6 EFA abnormality, but had no effect on the n-3 EFAs.

Adult↗
PubMed1976

Rapid onset of essential fatty acid deficiency in the newborn.

To study the effect of fat-free alimentation on essential fatty acids (EFA), their levels in plasma phospholipids, cholesterol esters, triglycerides, and free fatty acids were measured in five sick newborns. Four patients were under 32 weeks of gestation; three were small for gestational age and one was an infant of a diabetic mother. All developed biochemical evidence of EFA deficiency during the first week of life--the smallest infant did so by the second day. Biochemical evidence of EFA deficiency included a decrease in plasma lipid arachidonic and linoleic acids, an increase in 5,8,11-eicosatrienoic acid, palmitoleic, and oleic acids and a trienoic/tetraenoic ratio of more than 0.4. Oral feeding with EFA reversed these changes. The two infants showing the most severe biochemical evidence of EFA deficiency died. Neither exchange transfusion nor multiple blood transfusions prevented or corrected the development of EFA deficiency. An alternative method for efficient and safe delivery of EFA to such infants is required.

Blood Transfusion↗
PubMed2001

Essential fatty acids as possible mediators of the actions of statins.

Statins and polyunsaturated fatty acids have similar actions: both enhance endothelial nitric oxide synthesis, inhibit the production of pro-inflammatory cytokines, lower cholesterol levels, prevent atherosclerosis and are of benefit in coronary heart disease, stroke and osteoporosis. Statins enhance the conversion of linoleic acid and eicosapentaenoic acid to their long chain derivatives. Animals with essential fatty acid deficiency show an increase in HMG-CoA reductase activity, which reverts to normalcy following topical application of linoleic acid. Similarly to statins, polyunsaturated fatty acids also inhibit HMG-CoA reductase activity. In view of the similarity in their actions and as statins influence essential fatty acid metabolism, it is suggested that essential fatty acids and their metabolites may serve as second messengers of the actions of statins.

Alzheimer Disease↗
PubMed1992

An in vitro model for essential fatty acid deficiency: HepG2 cells permanently maintained in lipid-free medium.

A stable essential fatty acid-deficient cell type, known as HepG2-EFD, was derived from the lipoprotein-producing human hepatoma cell line HepG2. These cells are particularly useful for quantitative studies involving essential fatty acids (n-6 and n-3 fatty acids) in secreted lipoproteins. Radiolabeled essential fatty acids can be delivered to these cells without altering the specific activity of the fatty acids, since the deficient cells contain no endogenous essential fatty acids. Using these cells, radioactivity data (dpm) from metabolic studies can be converted directly to mass, and masses as low as a few pmoles can be accurately measured. HepG2-EFD cell cultures were established by growing HepG2 cells in medium containing delipidated serum. After 10 days of growth in delipidated medium, HepG2 cells were completely depleted of all essential fatty acids. Compensatory increases in nonessential fatty acids (n-9 and n-7 fatty acids) including 20:3n-9 (the Mead acid), which is the hallmark fatty acid of essential fatty acid deficiency, were also observed in HepG2-EFD cells. Despite the lack of exogenous fatty acids in the medium and the lack of essential fatty acids in the cells, export of very low density lipoprotein (VLDL)-associated apolipoprotein B by HepG2-EFD was the same as observed for parent HepG2 cells. However, the activity of beta-oxidation of fatty acids in HepG2-EFD cells was much lower than in the parent cell line.(ABSTRACT TRUNCATED AT 250 WORDS)

Apolipoproteins B↗
PubMed1977

Essential fatty acid metabolism in cultured astroblasts.

The fetal calf serum on which two astroblast cell lines were grown was shown to be deficient in essential fatty acids. The fatty acid profiles of lipids of these two cell lines showed very low amounts of polyunsaturated fatty acids. In order to know if this low level of unsaturation was due to the lack of essential fatty acids in serum, or to a lack of desaturase activities in the cells, we have investigated the modifications of the cell lipid fatty acid patterns when serum was enriched in essential fatty acids. Linoleic acid was incorporated in rather high amounts in the cell lipids, while linolenic acid was very poorly incorporated. These two essential fatty acids were converted into polyunsaturated fatty acids only when they were added alone to the serum. Both cell clones exhibited a lack in the delta 4 desaturase activity. No morphological changes of the cells occured after nine days of culture with modified serum.

Astrocytes↗
PubMed1987

The importance of essential fatty acid evaluation and supplementation in feline diets.

The importance of essential fatty acids and their supplementation in the diets of obligate carnivores should be an area of concern amongst veterinarians. Certain species of the Felinae have been shown to be obligate carnivores as a result of fatty acid desaturase enzyme deficiencies. Modern dietary practices of processing and pelleting foods can destroy the essential fatty acid (EFA) potency of these foods. Supplementation of the diet with oils high in EFA should be considered, and the possibility of EFA deficiency amongst domestic carnivores should not be overlooked.

Animal Feed↗
PubMed1984

Effect of essential fatty acid deficiency on myelin proteins.

The effect of essential fatty acid (EFA) deficiency on rat-brain myelin proteins was studied. Rats were maintained on a lipid-free diet and compared with control rats fed the same diet supplemented with 3% corn oil. At 17 days of age, each pup was injected with [3H]leucine and rats from each group were killed over a period of 163 days. Although a large decrease occurred in the total amount of myelin protein per brain, the proportions of constituent myelin proteins remained relatively unchanged. Metabolic studies showed a decrease in the net turnover of myelin proteins analogous to that previously demonstrated for myelin phospholipid (PL).

Animals↗
PubMed2004

Modulation of neonatal immunological tolerance to ovalbumin by maternal essential fatty acid intake.

The present study examines whether dietary essential fatty acid (EFA) intake influences the induction of oral tolerance to ovalbumin (OA) in neonatal and adult rats. During late gestation and throughout lactation Sprague-Dawley rats were fed a diet supplemented (S) with EFA (7% soybean oil), or a diet deficient (D) in EFA (7% hydrogenated lard). The rat offspring were subsequently exposed to OA either via the milk at 10-16 days (neonatal rats), or as adults via the drinking water at 7-9 wk of age. Oral administration of OA to the adult rats lead to suppression of the delayed-type hypersensitivity (DTH) reactivity and IgG antibody response against OA, which was not influenced by their diets. In the offspring of the dams fed the D diet antigen exposure via the milk resulted in suppression of the serum antibody levels and DTH reaction against OA indicating induction of oral tolerance. Higher transforming growth factor beta (TGF-beta) mRNA levels in the draining lymph nodes suggested this to be mediated by regulatory T cells. In contrast, OA exposure of the dams fed the S diet did not result in a suppressed OA response of their offspring. Thus, the quality of FA ingested by the mother may have effects on the development of immunological tolerance to dietary antigens in the offspring. Our results might have importance for the understanding of the increase in allergy related to the Western type of diet.

Age Factors↗
PubMed1990

Prevention of diabetes in the BB rat by essential fatty acid deficiency. Relationship between physiological and biochemical changes.

Essential fatty acid (EFA) deficiency exerts a striking protective effect in several animal models of autoimmune disease. We now report that EFA deprivation prevents diabetes in the BB rat, an animal model of human insulin-dependent diabetes mellitus. In diabetes-prone (DP)-BB rats, the incidences of spontaneous diabetes and insulitis (the pathological substrate of autoimmune diabetes) were greatly reduced by EFA deficiency. This beneficial effect of the deficiency state was also seen in diabetes-resistant (DR)-BB rats that, after treatment with antibody to eliminate RT6+ T cells, would otherwise have become diabetic. The susceptibility of EFA-deprived DP-BB rats to spontaneous diabetes was restored when they were given dietary supplements of linoleate at 70 d of age (during the usual period of susceptibility), but not when they were repleted beginning at 120 d (after the peak incidence of diabetes). EFA deficiency did lead to growth retardation, but calorically restricted control rats demonstrated that the protective effect of the deficiency state was not a function of decreased weight. To examine the relationship between the biochemical changes of EFA deficiency and its physiological effects in this system, we compared the fatty acid changes that occurred in EFA-deficient animals that did and did not develop diabetes. Nondiabetic animals had significantly lower levels of (n-6) fatty acids (i.e., linoleate and arachidonate) and higher levels of oleate, an (n-9) fatty acid, than did diabetic animals. Levels of 20:3(n-9), the fatty acid that uniquely characterizes EFA deficiency, were similar in both groups, however. Among diabetic EFA-deficient rats, the age at onset of diabetes was found to correlate inversely with the level of (n-6) fatty acids, the least depleted animals becoming diabetic earliest, whereas there was no correlation with levels of 20:3(n-9). Among animals repleted with linoleate beginning at 70 d, restoration of susceptibility to diabetes correlated with normalization of the level of arachidonate. In summary, EFA deprivation reduced the frequency of diabetes in both DP and RT6-depleted DR-BB rats. This protective effect was strongly associated with depletion of (n-6) fatty acids, particularly arachidonate, but not with accumulation of the abnormal 20:3(n-9). Conjecturally, arachidonate and/or a metabolite may play a key role in mediating inflammatory injury in this animal model of autoimmune diabetes.

Animals↗
PubMed1987

Cutaneous application of safflower oil in preventing essential fatty acid deficiency in patients on home parenteral nutrition.

Essential fatty acid deficiency (EFAD) is observed in patients with massive bowel resection who are placed on home parenteral nutrition (HPN). We investigated the use of cutaneously applied safflower oil to prevent EFAD. Five subjects on HPN supplemented with intravenous (IV) fat emulsions underwent a three-phase study: 1) no IV fat emulsions for 4 wk; 2) cutaneous safflower oil for 4-6 wk; 3) oral safflower oil for 4 wk. Fatty acid profiles (FAP) of plasma were obtained during each phase. Significant decreases in linoleic and arachidonic acid occurred by the end of phase 1 and the triene:tetraene ratio rose from a baseline value of 0.1 to 0.5. This ratio returned to 0.2 by the end of phase 2 and significant increases in linoleic and arachidonic acid occurred. Only one of five subjects completed the oral phase (3). Cutaneous safflower oil may improve plasma FAP but adequacy of tissue stores remains unanswered. Liver function tests need to be monitored if this treatment modality is utilized.

Administration, Cutaneous↗
PubMed1988

Essential fatty acid deficiency in premature infants.

To better characterize essential fatty acid (EFA) deficiency in neonates, we assessed 63 premature infants by serial determinations of plasma fatty acids for the level of linoleic acid, the presence of an abnormal trienoic acid (5,8,11-eicosatrienoic acid [20:3 omega 9]), and the ratio of this compound to arachidonic acid, ie, the triene-tetraene ratio. The data indicated that at age 7 d, 67% of these infants had low plasma linoleic acid levels, 62% showed readily detectable 20:3 omega 9, and 44% had a high triene-tetraene ratio. Infants fed by age 2 d had a normal mean linoleate level at 7 d and none showed detectable 20:3 omega 9 by 10 d. In contrast, infants who were not fed until 7 d showed a very high incidence of abnormal fatty acid status. By maintaining a daily record of linoleate intake, we calculated from regression models that the average amount required to achieve normal fatty acid nutrition was 1.19 g.kg-1.d-1.

8,11,14-Eicosatrienoic Acid↗
PubMed1984

Essential fatty acids in perspective.

There are two families of essential fatty acids, the linoleic and linolenic. Linoleic acid (C18:2n-6), found mainly in vegetable seed oils, is desaturated and elongated in the body, forming arachidonic acid (C20:4n-6). Linolenic acid (C18:3n-3), the main dietary source of which is leaves, is desaturated and elongated, forming two fatty acids that are prevalent in fish oils: timnodonic (C20:5n-3) and clupanodonic (C22:6n-3). EFA are very easily peroxidized in air, but vitamin E protects against this. There are three functions of EFA. The most important is as part of phospholipids in all animal cellular membranes: in deficiency of EFA faulty membranes are formed. A second is in the transport and oxidation of cholesterol: EFA tend to lower plasma cholesterol. A third function is as precursors of prostanoids which are only formed from EFA. Deficiency of EFA in experimental animals causes lesions mainly attributable to faulty cellular membranes: sudden failure of growth, lesions of skin and kidney and connective tissue, erythrocyte fragility, impaired fertility, uncoupling of oxidation and phosphorylation. In man pure deficiency of EFA has been studied particularly in persons fed intravenously. A relative deficiency (that is, a low ratio in the body of EFA to long-chain saturated fatty acids and isomers of EFA) is common on Western diets and plays an important part in the causation of atherosclerosis, coronary thrombosis, multiple sclerosis, the triopathy of diabetes mellitus, hypertension and certain forms of malignant disease. Various factors affect the dietary requirement of EFA.

Arteriosclerosis↗
PubMed1993

[Essential fatty acids in neonates at risk and in the mother's milk].

The participation of essential fatty acids and their derivatives in the blood (serum) of physiological healthy neonates (physiological pregnancy, physiological delivery) is compared with the spectrum of essential fatty acids of risk newborns (prematurity, prematurity with the tocolytic therapy and hypotrophic newborns). In the following part the presence and participation of essential fatty acids in the human maternal milk were measured. The milk of healthy mothers, of mothers with preterm delivery (37 week of gestation), of diabetic mothers were mutually compared and finally the values of mentioned essential fatty acids in formula Feminar and in the milk from the bank were established. As a consequence of our observations, they point out the absence or serious deficit of some essential fatty acids in certain groups of risk newborns as well as in the milk of diabetic mothers, of mothers with preterm delivery and in Feminar and Milk-bank. The presented facts--after their opinion--could be well judged as a rational basis for adequate nutritional therapy in risk newborns.

Animals↗
PubMed1990

[Significance and motivation of the clinical use of essential fatty acid derivatives, especially gamma-linolenic acid].

Although they were discovered in the first half of our century, essential fatty acids have started commanding clinical interest only during the last few years. Their vast possibilities for therapeutic use make basic knowledge of their chemical nature and physiologic significance a necessity. Essential fatty acids (linoleic and alpha-linolenic acid) are important not only in themselves but also as precursors of other polyunsaturated fatty acids. Besides, from some of these compounds an important series of substances is derived, such as prostaglandins, thromboxanes, prostacyclins, and leukotrienes. The sequence of enzymatic reactions on which the biosynthesis of these substances depends is altered in certain human pathologies. The key to the mechanism of action of some oils, such as evening primrose oil, is the fact that it contains as active principle the product of the blocked enzymatic reaction.

Animals↗
PubMed1990

Accelerated essential fatty acid deficiency by delta 9 desaturase induction: dissociation between the effects on liver and other tissues.

Essential fatty acid (EFA) deficiency is an important tool in probing the role of arachidonic acid (20:4(n-6] in pathophysiologic processes, but requires stringent and prolonged deprivation of (n-6) fatty acids. The present study investigated whether induction of the delta 9 desaturase, which is responsible for the synthesis of oleate, the precursor of 20:3(n-9) which uniquely accumulates in the deficiency state, might serve to accelerate the biochemical and biological effects of EFA deficiency. By alternately fasting and feeding animals a fat-free diet, it was possible to induce markedly the delta 9 desaturase selectively in liver. This dietary manipulation in consequence led to dramatic and rapid changes in hepatic phospholipid fatty acid composition. Within 2 weeks, 20:3(n-9) to 20:4(n-6) ratios in liver phospholipids were several fold greater than those seen in animals fed a fat-free diet alone. These changes, however, contrasted with those seen in the serum and other tissues. The mol% of 20:3(n-9) in serum was not increased by delta 9 desaturase induction and the 20:3(n-9) to 20:4(n-6) ratio was only modestly increased. The effects of delta 9 desaturase induction were even more attenuated in tissues other than the liver. Desaturase induction led to a doubling in the 20:3(n-9) to 20:4(n-6) ratio in phosphatidylcholine in renal cortex and heart, although the ratio in the other phospholipids was unaffected. The 20:3(n-9) to 20:4(n-6) ratio in peritoneal macrophage phospholipids was unaffected by desaturase induction. Thus, delta 9 desaturase induction greatly augments the synthesis of (n-9) fatty acids within the liver and leads to the rapid and substantial accumulation of the abnormal fatty acid, 20:3(n-9). This markedly augmented synthesis of hepatic 20:3(n-9), however, is not reflected in increased plasma levels of 20:3(n-9), and thus the effects of delta 9 desaturase induction are attenuated in tissues other than the liver. These data underscore the notable ability of the liver to maintain polyunsaturated fatty acid homeostasis.

Animals↗
PubMed2006

Relationship between umbilical cord essential fatty acid content and the quality of general movements of healthy term infants at 3 months.

Prenatal essential fatty acid (EFA) status might be an important factor in the development of the central nervous system (CNS). The aim of the present study was to evaluate the relationship between the fatty acid compositions of the umbilical blood vessels at birth, used as a proxy of prenatal EFA status, and quality of general movements (GMs) at 3 mo. Umbilical artery and vein fatty acid compositions were investigated in a mixed group of breastfed infants and infants fed with formula with or without long-chain polyunsaturated fatty acid (LCPUFA) supplementation. At the age of 3 mo, video assessment of the quality of GMs was performed to evaluate neurologic condition. The quality of GMs was scored by assessing the degree of variation, complexity, and fluency. Outcomes were classified as normal-optimal, normal suboptimal, mildly abnormal, and definitely abnormal movements. Information on potential confounders, including the type of postnatal feeding, was collected prospectively. Associations between fatty acid status at birth and quality of GMs were investigated, and multinomial logistic regression analyses were carried out. None of the infants showed definitely abnormal movements. Infants with mildly abnormal GMs had a lower EFA index, lower arachidonic acid (AA) content, higher total n-9 fatty acid, and higher total monounsaturated fatty acid (MUFA) content in the umbilical artery compared with infants with normal GMs. Multivariate analyses confirmed these findings. We conclude that mildly abnormal GMs are associated with a less favorable EFA status in the umbilical artery.

Central Nervous System↗