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 523 records · Page 29Linked to original sources
PubMed1987

Effects of essential fatty acid deficiency on mouse brain development.

The effect of essential fatty acid (EFA) deficiency on the activities of several membrane-bound enzymes was examined in the brains of C57BL/6J mice. Pregnant females were placed on an EFA-deficient diet during the last week of gestation and their progeny were examined at intervals up to 16 weeks after birth. Early signs of the deficiency, such as reduced body and brain weight, were noted in the mice on the experimental diet. The fatty acid ratio of 20:3w9/20:4w6, a biochemical index of EFA deficiency, rose progressively in the deficient brains from 0.17 at 4 weeks to 0.68 at 16 weeks. Only one of the membrane-bound enzymes studied, i.e. ATPase, demonstrated any consistent significant alteration in specific activity as a consequence of the deficiency. The accumulation of myelin, as measured by the levels of myelin basic protein, was reduced from the earliest age studied. These findings suggest that EFA deficiency does not exert a general, nonspecific effect on all membranes in the brain and that hypomyelination is a major effect of EFA deficiency on brain development.

Animals↗
PubMedDate not supplied

Effect of essential fatty acids on tumor cells.

An earlier study showed that essential fatty acids and their metabolites can kill tumor cells in vitro. This tumoricidal action can be correlated to an increase in generation of free radicals in the tumor cells. Evening primrose oil (EPO) is a rich source of linoleic acid and gamma-linolenic acid. We report that EPO can kill tumor cells both in vitro and in vivo. This tumoricidal action of EPO was associated with a threefold increase in superoxide generation. One of the factors that is capable of interfering with the cytotoxic action of fatty acids appears to be the protein content of the medium. Fatty acids can bind to protein and thus prevent their cytotoxic action.

Animals↗
PubMed1980

Incidence of urothelial tumors in rats deficient in essential fatty acids.

Wistar rats were fed a diet deficient in essential fatty acids (EFA). Control animals received the same diet to which was added 5% corn oil, a source of EFA. The experimental group showed clinical and chromatographic evidences of EFA deficiency. Groups of deficient and control animals were killed at various periods up to 100 weeks of age. Of 43 EFA-deficient rats, 8 (18.6%) had papillary transitional cell tumors of the urinary tract. None of the 36 controls had tumors (P less than 0.01). In 7 animals, tumors were found in the renal pelvis and upper portion of the ureter; in one, the tumor was in the bladder. The tumors were more frequent at the end of the first year of life and after the first year of life, with no significant sex differences. Tumors showed various degrees of differentiation and a trend toward bilateral involvement. Subepithelial and muscle invasion of tumor was noted in 5 rats. Most tumors were polycentric, and carcinomas in situ were seen. Atypical hyperplasias were found in 35% of the EFA-deficient rats and in 3% of the controls. Typical hyperplasias were seen in 63% of the EFA-deficient rats and in 72% of the controls, Renal calcifications, congestion, inflammation, and hydronephrosis were also seen. No significant differences other than congestion were found in both groups. Our results suggest that the mechanisms regulating proliferation of urothelial cells are upset in EFA-deficient rats; this favors the appearance of atypical hyperplasias and tumors. Therefore, EFA deficiency in the rat may be a useful model for the study of the causes and pathogenesis of human urothelial cancer.

Animals↗
PubMed1989

Relation between essential fatty acid metabolism and gastrointestinal symptoms in cystic fibrosis.

Studies in our laboratory have supported the hypothesis, that the basic defect in cystic fibrosis increases the metabolism of essential fatty acids and thereby gradually gives rise to essential fatty acid deficiency, which is a well documented finding in most cases with this disease. Both the increased metabolism--giving high liberation of arachidonic acid and its metabolic products, i.e. different eicosanoids--and the subsequent essential fatty acid deficiency will cause gastrointestinal symptoms and the sequence of this development will mirror the natural history of the disease. Clinical data and results from animal research are discussed in relation to gastrointestinal symptoms and signs of cystic fibrosis.

Cystic Fibrosis↗
PubMed1998

Lipid content and essential fatty acid (EFA) composition of mature Congolese breast milk are influenced by mothers' nutritional status: impact on infants' EFA supply.

OBJECTIVE: To measure the lipid content and the fatty acid (FA) composition of breast milk as part of a nutritional survey of the essential fatty acid (EFA) status of 5 months old Congolese infants. DESIGN: Cross sectional nutrition survey. SETTING: A suburban district of Brazzaville (capital of the Congo). SUBJECTS: A random sample of nursing mothers and their 5 months old infants (n = 102). Data collection procedures: The mothers were questioned on their socio-economic status, dietary habits, and their body mass index (BMI) was measured. Breast milk samples were collected from each mother. Milk lipid content and fatty acid composition were determined. RESULTS: Compared with milk from various countries, Congolese women's mature breast milk was low in lipid (28.70+/-11.33 g/L) but rich in 8:0-14:0 FAs (25.97+/-8.17% of total FAs) and in polyunsaturated FAs (PUFAs), particularly n-3 PUFAs (2.39+/-0.68% of total FAs, mainly 18:3 and 22:6). This was associated with the frequent consumption of high-carbohydrate foods (processed cassava roots, wheat bread, doughnuts) known to enhance 8:0-14:0 FA biosynthesis, and with that of foods providing n-6 and n-3 EFAs such as freshwater and saltwater fish, vegetable oil, green leafy vegetables, and high-fat fruit (peanuts, avocado, bushbutter). These foods were traditionally and locally produced. Milk lipid content was negatively related with mothers' BMI (P < 0.01) and varied with the frequency of consumption of certain foods corresponding to distinct dietary patterns. CONCLUSIONS: Lipid content and FA composition of Congolese breast milk were dependent on mother's nutritional status. However, despite an adequate EFA composition of breast milk, partially breast-fed 5 months old Congolese infants probably did not get enough n-6 and n-3 EFAs from breast milk to meet their EFA requirements.

Adult↗
PubMed1981

Effects of dietary essential fatty acids on murine mammary gland development.

Removal of unsaturated fatty acids from the diet of female C3H mice resulted in the gradual onset of essential fatty acid deficiency. Upon reaching the deficient state, alveolar components of the mammary gland began to regress as did the ovarian corpora lutea. An increase in the viscosity of microsomal membranes and a decrease in the number of prolactin binding sites also occurred concomitantly as the deficient state increased in severity. Modification of fats with the diet changes the fluidity of cellular membranes. This appears to alter the functionality of the membrane-associated receptors and their subsequent ability to respond to circulating hormones.

Animals↗
PubMed2000

The pathology of essential fatty acid deficiency: is it cell adhesion mediated?

For almost 70 years, essential fatty acid deficiency has been known to be associated with skin disorders, vessel abnormalities, and increased tumorigenesis. However, the underlying molecular and cellular mechanism is largely unknown. Recently, it has been reported that essential fatty acids regulate cell adhesion by modifying the expression of cell adhesion molecules. These findings may provide molecular explanations for those phenomena seen in EFAD and this paper aims to discuss these relationships and raise points for further discussion.

Animals↗
PubMed1983

The effect of essential fatty acid and specific vitamin supplements on vascular sensitivity in the mid-trimester of human pregnancy.

Vascular sensitivity to angiotensin II was determined in the mid-trimester of pregnancy in women after taking a diet with supplemented essential fatty acids and vitamins. The essential fatty acids linoleic and dihommogammalinolenic acid were administered as evening primrose oil capsules (Efamol) for one week prior to the study. Vascular sensitivity was then determined in response to 4, 8 and 16 ng kg-1 min-1 angiotensin II. Vitamin supplements (Efavit) were given with the Efamol capsules. Seven women have been studied, and their vascular sensitivity compared with controls on normal diet. The vascular sensitivity was significantly reduced in all the patients on essential fatty acid supplements, and all values fell below the mean of the control group.

8,11,14-Eicosatrienoic Acid↗
PubMed1996

Essential fatty acid deficiency and predisposition to lung disease in cystic fibrosis.

UNLABELLED: Essential fatty acid (EFA) deficiency is a predisposing factor for pulmonary infection with Staphylococcus aureus and Pseudomonas aeruginosa, the two major pathogenic microorganisms in cystic fibrosis (CF). OBJECTIVE: The goal of this study was to investigate the essential fatty acid status of CF patients from infancy to 20 years old. MATERIALS AND METHODS: Plasma fatty acid profiles for phospholipid (PL) were determined for cord (n = 6), 4 months (n = 40), 16 months (n = 25), 3 y (n = 8), 5-10 y (n = 10), and 10-20 y (n = 10) aged CF patients and compared to their respective control; cord (n = 22), 1-36 months (n = 38) and adult (n = 100). Significance was established by Student's t-test (p < 0.05). RESULTS: The plasma PL fatty acid profile for all CF patients, except cord, revealed consistent deficiency in omega 3 and omega 6 EFAs. These deficiencies were most marked at infancy and more pronounced for patients with meconium ileus. CONCLUSIONS AND RELEVANCE: EFA deficiency may contribute to the predisposition of CF infants to develop respiratory disease and to the excess cytotoxic activity found in bronchoalveolar lavage fluid at 2 months of age in the majority of screened infants.

Adult↗
PubMed2000

Essential fatty acids in early life: structural and functional role.

Essential fatty acids (EFA) are structural components of all tissues and are indispensable for cell membrane synthesis; the brain, retina and other neural tissues are particularly rich in long-chain polyunsaturated fatty acids (LCPUFA). These fatty acids serve as specific precursors for eicosanoids that regulate numerous cell and organ functions. Results from animal and recent human studies support the essential nature of n-3 EFA in addition to the well-established role of n-6 EFA for human subjects, particularly in early life. The most significant effects relate to neural development and maturation of sensory systems. Recent studies using stable-isotope-labelled tracers demonstrate that even preterm infants are able to form arachidonic acid (AA) and docosahexaenoic acid (DHA), but that synthesis is extremely low. Intracellular fatty acids or their metabolites regulate transcriptional activation of gene expression during adipocyte differentiation, and retinal and nervous system development. Regulation of gene expression by LCPUFA occurs at the transcriptional level and is mediated by nuclear transcription factors activated by fatty acids. These nuclear receptors are part of the steroid hormone receptor family. Two types of polyunsaturated fatty acid responsive transcription factors have been characterized, the peroxisome proliferator-activated receptor (PPAR) and the hepatic nuclear factor 4alpha. DHA also has significant effects on photoreceptor membranes involved in the signal transduction process, rhodopsin activation, and rod and cone development. Comprehensive clinical studies have shown that dietary supplementation with marine oil or single-cell oils, sources of LCPUFA, results in increased blood levels of DHA and AA, as well as an associated improvement in visual function in formula-fed premature infants to match that of human milk-fed infant. Recent clinical trials convincingly support LCPUFA supplementation of preterm infant formulations and possibly term formula to mimic human milk composition.

Animals↗
PubMed2005

Essential fatty acid deficiency in mice is associated with hepatic steatosis and secretion of large VLDL particles.

Essential fatty acid (EFA) deficiency in mice decreases plasma triglyceride (TG) concentrations and increases hepatic TG content. We evaluated in vivo and in vitro whether decreased hepatic secretion of TG-rich very low-density lipoprotein (VLDL) contributes to this consequence of EFA deficiency. EFA deficiency was induced in mice by feeding an EFA-deficient (EFAD) diet for 8 wk. Hepatic VLDL secretion was quantified in fasted EFAD and EFA-sufficient (EFAS) mice using the Triton WR-1339 method. In cultured hepatocytes from EFAD and EFAS mice, VLDL secretion into medium was measured by quantifying [(3)H]-labeled glycerol incorporation into TG and phospholipids. Hepatic expression of genes involved in VLDL synthesis and clearance was measured, as were plasma activities of lipolytic enzymes. TG secretion rates were quantitatively similar in EFAD and EFAS mice in vivo and in primary hepatocytes from EFAD and EFAS mice in vitro. However, EFA deficiency increased the size of secreted VLDL particles, as determined by calculation of particle diameter, particle sizing by light scattering, and evaluation of the TG-to-apoB ratio. EFA deficiency did not inhibit hepatic lipase and lipoprotein lipase activities in plasma, but increased hepatic mRNA levels of apoAV and apoCII, both involved in control of lipolytic degradation of TG-rich lipoproteins. EFA deficiency does not affect hepatic TG secretion rate in mice, but increases the size of secreted VLDL particles. Present data suggest that hypotriglyceridemia during EFA deficiency is related to enhanced clearance of altered VLDL particles.

Animals↗
PubMed1990

The effects of maternal diabetes on placental transfer of essential and non-essential fatty acids in the rat.

Studies were performed on the transfer of essential and non-essential non-esterified fatty acids across the in-situ perfused placenta in normal and diabetic rats in late gestation. Results indicated that increasing maternal glycaemia is associated with a decrease in the unidirectional transfer of both essential and non-essential fatty acids. This reduced transfer is dependent upon the uteroplacental blood flow, which is compromised in the diabetic animals. The transfer of essential fatty acid was always twofold that of non-essential fatty acids regardless of the total amount of lipid transferred, indicating a selective mechanism for the transfer of these moieties.

Animals↗
PubMed1983

Role of linoleate as an essential fatty acid for the cat independent of arachidonate synthesis.

To determine the essential fatty acid (EFA) requirements of the cat, specific pathogen-free kittens were fed either a linoleate-deficient diet or one of two diets containing 5% safflower seed oil (SSO) with or without 0.2% tuna oil. The diets were fed for 82-101 weeks beginning at 3 months of age. The results showed that linoleate is an essential fatty acid for the cat. Linoleate deficiency resulted in reduced feed efficiency (in males), high rates of transepidermal water loss, poor skin and coat condition, and fatty liver. These manifestations of EFA deficiency were prevented by SSO. Tuna oil had no additional effect. Analyses of the fatty acid composition of plasma, erythrocytes and liver lipids revealed that linoleate deficiency caused changes that were qualitatively, but not quantitatively similar to EFA deficiency in the rat. When SSO was provided, linoleate was elongated and desaturated at the delta 5 position to form 20:2n6 and 20:3(5,11,14). However, there was negligible conversion of linoleate to arachidonate. These results indicate that linoleate has specific functions as an EFA, independent of arachidonate synthesis and prostaglandin formation.

Animals↗
PubMed2000

Essential fatty acid metabolism and its modification in atopic eczema.

Research from the 1930s to the 1950s established that a deficit of n-6 essential fatty acids (EFAs) leads to an inflammatory skin condition in both animals and humans. In a common inherited skin condition, atopic dermatitis (eczema), there was evidence of low blood EFA concentrations and of a therapeutic response to exceptionally high doses of linoleic acid. More recently, it has been established that there is no deficit of linoleic acid in atopic eczema. Concentrations of linoleic acid instead tend to be elevated in blood, milk, and adipose tissue of patients with atopic eczema, whereas concentrations of linoleic acid metabolites are substantially reduced. This suggests reduced conversion of linoleic acid to gamma-linolenic acid (GLA). In most but not all studies, administration of GLA has been found to improve the clinically assessed skin condition, the objectively assessed skin roughness, and the elevated blood catecholamine concentrations of patients with atopic eczema. Atopic eczema may be a minor inherited abnormality of EFA metabolism.

Adipose Tissue↗