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PubMed2005

Genetic modification of essential fatty acids biosynthesis in Hansenula polymorpha.

The Delta(6)-desaturase gene isoform II involved in the formation of gamma-linolenic acid (GLA) was identified from Mucor rouxii. To study the possibility of alteration of the synthetic pathway of essential fatty acids in the methylotrophic yeast, Hansenula polymorpha, the cloned gene of M. rouxii under the control of the methanol oxidase (MOX) promoter of H. polymorpha, was used for genetic modification of this yeast. Changes in flux through the n-3 and n-6 pathways in the transgenic yeast were observed. The proportion of GLA varied dramatically depending on the growth temperature and media composition. This can be explained by the effects of either substrate availability or enzymatic activity. In addition to the potential application for manipulating the fatty acid profile, this study provides an attractive model system of H. polymorpha for investigating the deviation of fatty acid metabolism in eukaryotes.

Alcohol Oxidoreductases↗
PubMed1987

Soybean oil emulsion administration during parenteral nutrition in the preterm infant: effect on essential fatty acid, lipid, and glucose metabolism.

To examine the effect of a soybean oil emulsion on essential fatty acid, lipid, and glucose metabolism, preterm infants were randomized to receive 0.5 g/kg/d lipid for 5 days (n = 10, group 1) or 0.5 increased to 2.0 g/kg/d over 5 days (n = 11, group 2). Triene/tetraene ratios did not change in group 1, but decreased in group 2. In both groups, plasma phospholipid linoleate (percent and micrograms per milliliter) increased, the increase being greater in group 2. In both groups, percent content of arachidonate and 5,8,11-eicosatrienoate decreased, and that of oleate remained unchanged. In contrast, absolute content of arachidonate and oleate tended to increase, and that of 5,8,11-eicosatrienoate remained unchanged. At a lipid intake of 0.5 g/kg/d, no infants had hyperlipemia. When lipid intake exceeded 1.0 g/kg/d, the frequency of hypertriglyceridemia (triglycerides greater than 200 mg/dL) and free fatty acidemia, with the free fatty acid/molar albumin ratio exceeding 6:1, increased. Plasma glycerol increased slightly, but was substantially less than the rise in enzymatically determined triglycerides. Hyperglycemia was self-limiting and did not require alteration in dextrose intake. Thus, (1) infusion of a soybean oil emulsion at 0.5 to 2.0 g/kg/d maintains essential fatty acid status and phospholipid arachidonate concentrations; (2) significant hyperlipemia occurs when lipid intake exceeds 1.0 g/kg/d; (3) hyperglycemia associated with lipid infusion tends to be self-limiting and may not require alteration in lipid or dextrose intake; and (4) enzymatically determined triglycerides may be used to monitor lipid tolerance, provided that allowance is made for a small but systematic overestimation resulting from the rise in plasma glycerol.

8,11,14-Eicosatrienoic Acid↗
PubMed1982

Vitamin D-mediated intestinal calcium transport. Effects of essential fatty acid deficiency and spin label studies of enterocyte membrane lipid fluidity.

Vitamin D-3 and its metabolites regulate the transport of calcium across the intestinal epithelial cell via a mechanism which is as yet unknown. The purpose of this study was to evaluate the effect of an essential fatty acid deficiency on vitamin D-stimulated intestinal calcium transport as measured by both in vivo and in vitro techniques. We also describe in this report a procedure for the isolation of chick intestinal epithelial cell brush border and basal lateral membranes and an assessment of the effect of dietary vitamin D on the lipid fluidity of these membranes. An essential fatty acid deficiency in both vitamin D-replete and deficient chicks resulted in a decrease in intestinal mucosal levels of linoleic acid, with a compensatory increase in the levels of the short chain fatty acid, myristic acid, and the unsaturated fatty acids, palmitoleic and eicosatrienoic acids. An essential fatty acid deficiency did not affect the ability of vitamin D-deficient chicks to respond to vitamin D with a 2-fold increase in serum calcium and a 4-5-fold increase in intestinal calcium transport, measured in vivo. However, an essential fatty acid deficiency resulted in an inability of vitamin D to increase calcium efflux in vitamin D-deficient chick ileum as measured under in vitro conditions. Dietary vitamin D resulted in no detectable change in the protein composition in either the brush border or basal lateral membranes as evidenced by SDS-polyacrylamide electrophoresis. In addition, vitamin D did not alter the levels of brush border membrane cholesterol or lipid phosphorus (0.27 +/- 0.03 and 0.19 +/- 0.01 mumol/mol protein, respectively). Brush border and basal lateral membranes were labeled with the 5-nitroxide stearate spin probe I(12,3). The polarity of the environment of the probe in the brush border membranes is much greater than that of the basal lateral membranes. In addition, the lipid environment of the brush border membrane is much less fluid (S = 0.650) that that of the basal lateral membrane (S = 0.583). The data concerning membrane lipid fluidity is qualitatively similar to fluorescence polarization studies of rat intestinal epithelial cell membranes and confirms the concept that a given cell may contain plasma membrane regions having discrete lipid structures/fluidities. Dietary vitamin D had no detectable effect on the lipid fluidity or polarity in either the brush border or basal lateral membranes. The results do not support a role for an alteration in essential fatty acid composition or gross changes in the lipid fluidity of the brush border or basal lateral membranes as mechanisms by which vitamin D regulates intestinal calcium transport.

Animals↗
PubMed1996

Biomarkers of essential fatty acid consumption and risk of prostatic carcinoma.

Animal studies have suggested that omega-6 fatty acids found in vegetable oils may promote prostate cancer. Our goal was to use erythrocyte membrane and adipose tissue fatty acid composition as biomarkers to investigate whether essential fatty acids modulated prostate cancer risk. An outpatient clinic-based study of 89 cases and 38 controls was conducted in North Carolina between July 1989 and December 1991. Cases were recruited from a university-based urology outpatient clinic. Eligible cases were more than 45 years of age and had histological confirmation of a prostate cancer diagnosis within 1 year of entry into the study. Controls were histologically confirmed free of prostate cancer. Erythrocyte membranes from venous blood and adipose tissue fatty acids from s.c. fat samples were analyzed in batches using capillary gas chromatography. Unconditional logistic regression analysis was used to calculate odds ratios for the association of each fatty acid with prostate cancer while controlling for potential confounders. Linoleic acid consumption was positively associated with prostate cancer risk. The odds ratios comparing the first and fourth quartiles of linoleic acid consumption were 3.54 (95% confidence interval, 1.0-12.53) with P trend < 0.04 for erythrocyte membranes, and 2.47 (95% confidence interval, 0.66-9.26) with P trend < 0.08 for adipose tissue. These data suggest that linoleic acid consumption may increase prostate cancer risk, which is consistent with results from animal experiments. Linoleic acid is found in vegetable oils used in cooking and in cereals, snack foods, and baked goods. Our data failed to demonstrate consistently a protective effect of marine omega-3 fatty acids on prostate cancer.

Adipose Tissue↗
PubMed1977

Essential fatty acid deficiency associated with total parenteral nutrition.

Essential fatty acid deficiency is a clinical and biochemical entity encountered in both adults and children. Especially at risk are those patients maintained by fat-free total parenteral nutrition. Linoleic acid is the substance most responsible for the deficien state and essential to its correction. A ratio of trienoic-tetraenoic fatty acids of 0.4 or greater is diagnositc of a chemical deficiency. A severe deficiency affects polyunsatured fatty acids, in both plasma and tissues and, thus, many systems of the body. Mulitple blood transfusions have not proved sufficient to correct chemical deficiency. A recently marketed, commercially available fat supplement, however, may be useful in preventing the problem.

Animals↗
PubMed1982

Development and characterization of a tissue culture cell line with essential fatty acid deficiency.

We have developed an essential fatty acid-deficient cell line from a parental cell line, HSDM1C1, which metabolizes arachidonic acid to prostaglandin E2 (PGE2). This cell line, designated EFD-1, is depleted of arachidonate, is unable to synthesize PGE2 in response to bradykinin, and has changes in fatty acid composition characteristic of tissues from animals with essential fatty acid deficiency. Within 15 min of repletion by arachidonate, the ability to synthesize PGE2 is restored. Linoleate also is able to restore PGE2 synthesis, indicating that deficient cells contain both the rate-limiting delta 6 desaturase enzyme and the delta 5 desaturase enzyme, which are required to form arachidonate. When parental cells are incubated in lipid-free medium, there is rapid induction of the ability to convert linoleate to arachidonate. Arachidonate prevents this induction, suggesting that icosanoid precursor availability controls the rate of arachidonate formation.

Animals↗
PubMed1977

Absence of the biochemical symptoms of essential fatty acid deficiency in surgical patients undergoing protein sparing therapy.

The biochemical symptoms of essential fatty acid deficiency appear within 7 to 10 days of fat-free total parenteral nutrition using glucose-amino acid mixtures. The linoleic acid (C18:2W6) content of all plasma lipid fractions decreases greatly and plasma eicosatrienoic acid (C20:3W9) increases. We have measured the fatty acid composition of the plasma lipid fractions in six surgical patients receiving parenteral nutritional solutions containing only amino acids, and completely free of glucose, before and after 10 to 14 days of such therapy. Biochemical symptoms of essential fatty acid deficiency did not occur. The fatty acid composition of all plasma lipid fractions remained unchanged after this time period. Mobilization of linoleic acid from the adipose tissue occurred with this treatment in contrast to the inhibition of lipolysis of adipose tissue triglyceride produced by continuous infusions of hypertonic glucose-amino acid mixtures.

Adult↗
PubMed2003

An enzyme electrode based on lipoxygenase immobilized in gelatin for selective determination of essential fatty acids.

An enzyme electrode for the specific determination of omega-3 and omega-6 fatty acids from the mixture of essential fatty acids (EFAs) was developed by using lipoxygenase (LOX) (EC 1.13.11.12) from soy beans in combination with a dissolved oxygen (DO) probe. The enzyme electrode showed different sensitivities for linoleic (LA) and alpha-linolenic acids (ALA), the most common essential fatty acids. Enzyme electrode response depends linearly on LA concentration between 12.8-160.5 microM and ALA concentration between 3.8-18.9 microM in borate buffer, 0.2 M at pH 9.0. However, in phosphate buffer 0.2 M at pH 6.0 linearity is in the range of 7.5-22.5 microM of ALA concentration at 5 minutes response times. Moreover, maximum electrode response was found in borate buffer at pH 9.0 and 30 degrees C.

Biosensing Techniques↗
PubMed1991

Is there a role for dietary essential fatty acids in gastroduodenal mucosal protection?

A great deal is known about methods to diminish intragastric acid concentration, but far less is known about the ability of the gastroduodenal mucosa to resist injury or accelerate its healing. One group of compounds that plays a key role in the endogenous ability of the mucosa to protect itself against injury and perhaps to accelerate healing is the prostaglandins (PGs). The gastroduodenal mucosa synthesizes PGs from fatty acids precursors--predominantly linoleic and arachidonic. PGE1 or PGE2 have been shown to possess cytoprotective activity in the stomach and duodenum. In laboratory animals, linoleic acid feeding increased PG synthesis and diminished injury. When presented in a detergent solubilized form, arachidonic acid can also provide acute protection against injury by alcohol, bile acids, and aspirin. Arachidonic acid can also promote angiogenic response and thereby, perhaps, accelerate the healing process. Epidemiological evidence points toward a parallel between the decrease in peptic ulcer disease virulence and incidence and the total ingestion of linoleic acid by the population in the U.S. and the United Kingdom. Therefore, dietary essential fatty acids may play a key role in mucosal defense and restitution, and perhaps in the diminished incidence and virulence of peptic ulcer disease in the Western world.

Animals↗
PubMedDate not supplied

Long-term deficiency of essential fatty acids in rats and its effect on brain recovery.

1. Nineteen-day old rats were fed an essential fatty acid deficient diet for 37 weeks, thereby making them essential fatty acid deficient for at least 24 weeks. The weights of their brains were 33% less than those of rats on control diets. 2. When the deficient rats were rehabilitated for ten weeks on a diet containing 5% by weight corn oil as a source of essential fatty acids, the weights of their brains were still 30% less than those of the controls. 3. Analysis of the brain lipids showed that, there was a large reduction in the proportions of cerebrosides and sphingomyelin in essential fatty acid deficiency. 4. Essential fatty acid deficiency was also characterised by the appearance of a high proportion of eicosatrienoic acid (20:3) and the reduction of arachidonic acid (20:4) and the other essential fatty acids. 5. Rehabilitation for a period of 10 weeks did not reverse these changes in brain composition. 6. It is considered that the feeding of essential fatty acid deficient diet to rats for a prolonged period of time causes retardation of brain maturity and makes the brain resistant to later dietary manipulations.

Animals↗
PubMed1993

The role of essential fatty acids in neural development: implications for perinatal nutrition.

The brain is 60% structural lipid, which universally uses arachidonic acid (AA; 20:4n6) and docosahexaenoic acid (DHA; 22:6n-3) for growth, function, and integrity. Both acids are consistent components of human milk. Experimental evidence in animals has demonstrated that the effect of essential fatty acid deficiency during early brain development is deleterious and permanent. The risk of neurodevelopmental disorder is highest in the very-low-birth-weight babies. Babies born of low birth weight or prematurely are most likely to have been born to mothers who were inadequately nourished, and the babies tend to be born with AA and DHA deficits. Because disorders of brain development can be permanent, proper provision should be made to protect the AA and DHA status of both term and preterm infants to ensure optimum conditions for the development of membrane-rich systems such as the brain, nervous, and vascular systems.

Animals↗
PubMed1996

Involvement of (n-6) essential fatty acids and prostaglandins in liver lipid accumulation in Japanese quail.

OBJECTIVE: To investigate the involvement of (n-6) essential fatty acids, such as linoleic acid [18:2(n-6)] or gamma-linolenic acid [18:3(n-6)], and of prostaglandins on liver lipid accumulation in Japanese quail. DESIGN: Effects of graded amounts of aspirin, which inhibits prostaglandin synthesis, on liver weight were determined in experiment 1. Experiment 2 was designed to clarify the effect of dietary essential fatty acid sources and inhibition of prostaglandin synthesis on the liver fat and fatty acid profile. ANIMALS: Female Japanese quail. PROCEDURE: In experiment 1, from 1 to 3 weeks of age, birds were fed ad libitum the essential fatty acids-free or linoleic acid-adequate (2%) diets with graded amounts of aspirin (0, 0.1, 0.2, and 0.4%). In experiment 2, from 1 to 4 weeks of age, birds were fed the same amount of essential fatty acids-free, linoleic acid-adequate, or gamma-linolenic acid (0.4%) diets with (0.2%) or without aspirin. RESULTS: In experiment 1, in groups given the essential fatty acids-free diet, liver weight increased with an increase in dietary aspirin concentration. In experiment 2, gamma-linolenic acid completely prevented liver triacylglycerol and cholesterol accumulation induced by the essential fatty acids-free diet. Aspirin treatment significantly lowered plasma prostaglandin F2 alpha concentration, but did not affect liver lipid concentrations. In groups fed the essential fatty acids-free diets, however, aspirin treatment increased liver weight and liver triacylglycerol concentration by 20 and 40%, respectively. CONCLUSIONS: gamma-Linolenic acid or its metabolites, but not linoleic acid itself, are important factors in reducing fatty liver in Japanese quail with the essential fatty acids-deficient condition.

Animals↗
PubMed1992

Essential fatty acids in human colostrum.

We analyzed the colostrum of 11 mothers, consuming a normal hospital diet, for total fat content and various fatty acids. Three of the mothers had given birth four weeks prematurely. Total fat content of the colostrum ranged from 2.16 to 3.65 g/100 ml. The major fatty acids were palmitic acid (16:0) and oleic acid (18:1) (24.3 and 39.7% (w/w), respectively). The dominating polyunsaturated fatty acid was linoleic acid (18:2n-6) (11.5% of the total fatty acids). Linolenic acid (18:3n-3) and docosahexaenoic acid (22:6n-3) accounted for 0.7 and 0.6%, respectively, of the sum of total fatty acids. The ratio of polyunsaturated to saturated fatty acids was 0.42, ranging from 0.28 to 0.5, and the ratio of n-6/n-3 fatty acids was 6:1. Linoleic acid and linolenic acid were positively correlated with each other (p < 0.02), whereas palmitic acid was negatively correlated with oleic acid (p < 0.05). We conclude that the average human colostrum contains the recommended level and balance of the essential fatty acids required by the newborn baby.

Colostrum↗