PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “FATTY ACIDS, ESSENTIAL”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 379 records · Page 21Linked to original sources

[Protection of essential fatty acids by vitamin E].

The protective role of vitamin E against free-radical-mediated oxidations is discussed. In spite of the presence of vitamin E in cell membranes, as structural complex with polyunsaturated fatty acids (PUFA) of phospholipids, the question arises whether high PUFA containing diets, producing high deposition of PUFA in the tissues, can nevertheless lead to peroxidations in the body. It has been suggested that large amounts of dietary PUFA increase the requirement for vitamin E and deplete its tissue stores, particularly when PUFA are discontinued in the diet, also because of their longer half-life time than tocopherols. However, in physiological conditions, linoleic acid up to 10% of caloric intake seems to have no effects on vitamin E requirement. In contrast, in essential fatty acid (EFA) deficient animals, also the addition of small amounts of dietary EFA, by resulting in a proportional increase in PUFA content of membrane structural lipids, is associated with an increased need for vitamin E. This becomes particularly important in the case of dietary fish oils or other poorly protected fats.

Animals↗

Effects of essential fatty acid deficiency during late gestation on brain N-acetylneuraminic acid metabolism and behaviour in the progeny.

1. Rat dams given a diet containing 100 g maize oil/kg for approximately two weeks before mating and during the first 14 d of gestation, were given the same diet or one containing 100 g hydrogenated coconut oil/kg (essential fatty acid (EFA)-deficient) in place of maize oil until parturition. After parturition the dams were given the same diets and all progeny were weaned to the maize oil diet at 21 d of age. Brain N-acetylneuraminic acid (NeuNAc) content as well as neuraminidase (sialidase; (EC 3.2.1.18), and cytidine monophosphate N-acetylneuraminic acid synthetase (CMP-NeuNAc synthetase) activities were measured at days, 7, 14, 21 and 168 in the progeny. Y-maze learning was measured at 168 d. 2. Brain weight was independent of dietary fat at all ages. 3. Lack of EFA in the maternal diet during gestation and lactation depressed ganglioside and glycoprotein NeuNAc levels and the activities of sialidase and CMP-NeuNAc synthetase. 4. Maternal dietary deprivation of EFA irreversibly impaired learning behaviour of the progeny. A relationship exists between early exposure to EFA deficiency and learning potential of the progeny.

Animals↗

Essential fatty acid deficiency in well nourished young cystic fibrosis patients.

UNLABELLED: Essential fatty acid deficiency is well known in cystic fibrosis patients, but its pathogenesis remains unclear. It might be related to protein-energy malnutrition which is a common feature of cystic fibrosis or to some specific defects in fatty acid metabolism. To avoid the deleterious effects of protein-energy malnutrition, this study assesses the plasma phospholipid fatty acid pattern in well nourished young cystic fibrosis subjects. Sixteen cystic fibrosis subjects aged 6.6-20.0 years were studied and compared to 16 healthy controls matched for gender, age and nutritional status. Plasma phospholipids were separated by thin layer chromatography and phospholipid fatty acid pattern was determined by gas liquid chromatography. Anthropometry and dual-energy X-ray absorptiometry showed that lean body mass, fat-free mass and fat mass were similar in the two groups. Nutritional inquiry showed higher ingestion of macronutrients by cystic fibrosis subjects than by controls. Plasma phospholipid palmitoleic acid and eicosatrienoic acid were higher, and by contrast linoleic acid and docosahexaenoic acid were lower in cystic fibrosis subjects than in controls. The ratio linoleic acid/arachidonic acid was lower and the ratio eicosatrienoic acid/arachidonic acid was higher in cystic fibrosis subjects than in controls. CONCLUSION: Essential fatty acid deficiency is present in young cystic fibrosis subjects in the absence of protein-energy malnutrition. It means that this deficiency is probably related to specific defects in fatty acid metabolism.

Adolescent↗

Modulation of adjuvant-induced arthritis by dietary arachidonic acid in essential fatty acid-deficient rats.

Controlled feeding of linoleic acid (LA) or arachidonic acid (AA) to essential fatty acid-deficient (EFAD) rats was used to define the relationship between dietary AA and the inflammatory response evoked during adjuvant-induced arthritis. Based on energy percentage, EFAD rats were fed AA at the human daily equivalent (1x; 5.5 mg/day) or 10 times that amount (10x; 55 mg/day) or, alternatively 0.5x of LA (273 mg/day). Feeding of 0.5x LA restored the plasma level of AA to that in chow-fed controls. In contrast, feeding of 1x AA only partially restored the plasma level of AA; 10x AA was required to fully replete AA. In parallel to the degree of repletion of AA in plasma, there were accompanying decreases in the levels of palmitoleic acid, oleic acid, and Mead acid. Compared to rats fed the standard laboratory chow diet (Control), edema in the primary hind footpads was decreased by 87% in EFAD, 71% in EFAD + 1x AA, 45% in EFAD + 10x AA, and 30% in EFAD + 0.5x LA. The decrease in edema in the footpads of EFAD rats was nearly identical to the decrease in edema in the footpads of Control rats dosed with indomethacin. Hind footpad edema correlated with the final AA plasma level and eicosanoid levels extracted from hind footpad tissue, but not with neutrophil infiltration. The data showed that 0.5x LA and 10x AA, but not 1x AA, could quickly replete AA, accompanied by the synthesis of AA-derived eicosanoids and restoration of edema. These results suggest that in humans consumption of the average daily amount of AA without concurrent ingestion of LA would not alleviate an EFAD state.

Animals↗

Deficiencies of essential fatty acids and vitamin E in cystic fibrosis.

In 25 children (13 male; 12 female) with cystic fibrosis aged 6 months to 16 years and 24 matched controls total serum vitamin E levels and fatty acid patterns of serum cholesterol esters, phospholipids and triglycerides are demonstrated. Compared to controls (1.02 +/- 0.24 mg/dl) the total serum vitamin E levels are significantly decreased in patients with cystic fibrosis (0.30 +/- 0.26 mg/dl) (p less than 0.01). There is no significant difference comparing the fatty acid patterns of the serum ester fractions of both groups. Differences can be seen best in the cholesterol ester fraction. In this fraction linoleic acid shows a trend to be decreased in the cystic fibrosis patients compared to the control group. A possible influence of height velocity on the levels of essential fatty acids is discussed.

Adolescent↗

Structural and metabolic alterations of lung phosphatidylcholines by essential fatty acid deficiency.

The influences of early changes in essential fatty acid deficiency on the structure and metabolism of lung phosphatidylcholine were studied. In addition to general characteristics observed due to essential fatty acid deficiency such as significant decreases in linoleate and arachidonate, and concomitant increases in oleate and eicosatrienoate, a pronounced decrease in palmitate was noted in lung phosphatidylcholine, particularly in the 2-position. The decrease of palmitate in lung phosphatidylcholine was due to a similar decrease in disaturated classes, particularly in the dipalmitoyl species. These structural changes in phosphatidylcholine were found to be more significant in alveolar wash than in lung parenchyma and lamellar body fractions. The specific activities of phosphatidylcholine and its disaturated classes in lung parenchyma and alveolar wash were significantly lower in the deficient state than in the controls at 2, 6, and 12 hr after the injection of [9,10(-3)H]palmitate. However, relatively more of the phosphatidylcholine in the deficient state appeared in the alveolar space, disappearing more rapidly from the alveolar space than did the phosphatidylcholine in the controls. These results suggest that dietary linoleate may be a factor in regulating the amount of disaturated phosphatidylcholine in the lung, a principal component of lung surfactant, and also a factor in controlling the metabolism of alveolar phosphatidylcholine.

Animals↗

Incorporation of 14C into tissue lipids after oral administration of [1-14C]linoleic acid in rats fed different levels of essential fatty acids.

Rats from an inbred Sprague-Dawley strain were fed purified diets with a low (0.3% of the total energy), normal (3%) or high (10%) content of essential fatty acids (EFA) for several generations. Thirty- to 34-d-old male rats of at least the sixth generation to be fed these diets were given a single intragastric dose of [1-14C]linoleic acid in olive oil, and the respiratory CO2, urine and feces were collected for 20 h. The 14C activity was determined in the respiratory CO2, urine and feces as well as in total lipids and lipid classes of the whole animal and in nine tissue groups. The content of total lipids and lipid classes was similar in all groups. The rats in the low EFA group retained significantly more radioactivity (51%) in the tissues than the rats fed the normal EFA (34%) or the high EFA (27%) diets. In all groups most of the radioactivity was found in the skeletal muscles, skin, liver and white fat, but the retention was greater in the low EFA group than in the other groups, except in the white and brown fat. In the carcass and most tissues, the proportion of the retained 14C activity recovered in the phospholipids increased with decreasing EFA level in the diet, whereas in the triglycerides the opposite was found. Expressed as percent of administered dose, the total retention of radioactivity in the phospholipids was 31, 13 and 8% in the low, normal and high EFA group, respectively, while the retention in the triglycerides was about the same in all groups (17-18%).

Animals↗

Essential fatty acids and phenolic acids from extracts and leachates of southern cattail (Typha domingensis P.).

We have been able to isolate several phytotoxic compounds from aqueous extracts and leachates of cattails (Typha domingensis) using activated charcoal as an absorbant, followed by successive extraction with organic solvents, analysis by GC/MS, and structural elucidation by NMR spectroscopy when possible. The phytotoxins were identified as essential fatty acids (linoleic acid and alpha-linolenic acid) and phenolic compounds of known phytotoxic activity (caffeic acid from the aqueous extracts; caffeic, p-coumaric, and gallic acid from the leachates). Both extracts and the phytotoxins in the extracts have the potential of inhibiting the growth and chlorophyll production of several ecologically relevant species.

Fatty Acids, Essential↗

Essential fatty acid deficiency in patients receiving simultaneous parenteral and oral nutrition.

Essential fatty acid deficiency is a common finding in patients nourished parenterally with hypertonic glucose and amino acids. In this study, we measured the linoleate concentration in the livers of 3 groups of patients. All the patients had operable upper gastrointestinal tract malignancies. Group I ate the hospital's regular diet ad libitum. Group II were given total parenteral nutrition (TPN), Group III received both enteral and parenteral nutrition and obtained about 35% of their caloric intake from food. The percentage of total liver fatty acids as linoleate were group I, 15.2 +/- 1.2%, group II, 3.7 +/- 1.4%, and group III, 2.8 +/- 1.6%. Data are expressed as the mean +/- 1 SEM. The patients who received 35% of their calories by mouth as food and the patients on TPN were found to be equally depleted in linoleate.

Aged↗

Modulation of intestinal vitamin D receptor availability and calcium ATPase activity by essential fatty acids.

The physiological mechanisms by which essential fatty acids (EFAs) affect calcium (Ca(2+)) retention is not clear, but suggestions have included changes in membrane fluidity, receptor modulation and induction of second messengers. The vitamin D receptor (VDR) is essential for the functioning of 1,25(OH)(2)D(3)which increases Ca(2+)absorption. Activity of the intestinal basolateral membrane (BLM) Ca(2+)ATPase correlates with the degree of Ca(2+)absorption. Therefore, changes in ATPase activity and VDR availability due to EFAs may influence calcium retention. We have investigated the effect of long-term dietary supplementation with EFAs on Ca(2+)ATPase activity (measured colourimetrically) and VDR availability (measured with the ELISA technique) after the loss of oestrogen induced by ovariectomy (OVX) in female Sprague Dawley rats. Control animals underwent anaesthesia and a surgical procedure but the ovaries were left intact (sham). Ca(2+)ATPase activity was significantly lower in OVX animals than in the intact animals (P<0.05) and following supplementation with EFAs, was significantly higher than in sham controls (P<0.05). A higher number of VDR was measured after OVX and declined due to EFA supplementation; these differences in activity of the ATPase and number of receptors could be ascribed to membrane changes due to EFA supplementation, feedback control by serum calcium or the direct influence of the EFAs.

Animals↗

Distribution of 14C after oral administration of [1-14C]linoleic acid in rats fed different levels of essential fatty acids.

Rats from an inbred Sprague-Dawley strain were fed semisynthetic diets with a low [0.3 energy percent (en %)], normal (3 en %) or high (10 en %) content of essential fatty acids (EFA) for at least three generations. Twenty-nine- to 33-day-old male rats were given a single intragastric dose of [1-14C]linoleic acid in olive oil, and the respiratory CO2, urine and feces were collected for 46 hours (expt 1) or 20 hours (expt 2). The 14C activity in respiratory CO2, feces, urine and the carcass was determined in both experiments. In experiment 2 it was also measured in samples of the brown fat, liver, adrenals, white fat, skeletal muscles and brain. In both experiments the rats fed the low EFA diet retained significantly more 14C activity than the rats fed the normal or high EFA diets. In all groups the concentration of label was highest in the brown fat and the adrenals, but the above differences among the groups with respect to 14C retention were mainly observed in the liver, skeletal muscles and brain.

Adipose Tissue↗