Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “FATTY ACIDS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

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

At least 883 records · Page 49Linked to original sources
PubMed1991

High dietary linoleic acid affects the fatty acid compositions of individual phospholipids from tissues of Atlantic salmon (Salmo salar): association with stress susceptibility and cardiac lesion.

For 16 wk Atlantic salmon (Salmo salar) post-smolts were fed practical-type diets that contained either fish oil (FO) or sunflower oil (SO) as the lipid component. Both diets contained adequate (n-3) polyunsaturated fatty acids (PUFA). All the phospholipids of heart and liver from SO-fed fish had increased levels of 18:2(n-6), 20:2(n-6) and 20:3(n-6); phosphatidyl choline (PC) and phosphatidyl ethanolamine (PE) also had increased 20:4(n-6). There was a general decrease in 20:5(n-3) in the phospholipids, reflected in an increase in the 20:4(n-6)/20:5(n-3) ratio, especially in PC and PE. The fatty acid compositions of phospholipids from brain and retina were much less affected by dietary linoleate than those of heart and liver. Fish fed SO developed severe heart lesions that caused thinning of the ventricular wall and muscle necrosis. The fish fed SO also were susceptible to a transportation-induced shock syndrome that caused 30% mortality. These results establish that a diet with a low (n-3)/(n-6) ratio can cause changes in fatty acid metabolism that are deleterious to the health of salmonid fish, especially when subjected to stress.

Animals↗
PubMed1992

Incomplete fatty acid oxidation. The production and epimerization of 3-hydroxy fatty acids.

3-Hydroxydicarboxylic acids are major urinary metabolites derived from fatty acid metabolism. These compounds are produced from the omega-oxidation of 3-hydroxy fatty acids. The production of the precursor 3-hydroxy fatty acids from incomplete beta-oxidation of fatty acids in rat liver mitochondria was investigated. Independent of the chain length or the concentration of fatty acid substrates, the accumulation of 3-hydroxyacyl intermediates was relatively constant at the concentration of 3-5 nmol/mg of mitochondrial protein. The extent of the incomplete oxidation was the same in Percoll gradient-purified mitochondria. Rotenone treatment increased the production of 3-hydroxy fatty acids. 3-Hydroxy fatty acids did not exist as pure L-enantiomer as expected from beta-oxidation. Instead, these metabolites were epimerized to a near racemic mixture of D- and L-isomers with a slightly dominant D-isomer (58 +/- 3%). By using deuterium-isotope labeling, the mechanism of epimerizartion was shown to be a rapid dehydration-rehydration through trans-2-enoyl-CoA. In addition, cis-3 and trans-3 fatty acids were produced; these metabolites were derived from the isomerization of trans-2-enoyl-CoA. Epimerase and isomerase were thought to be enzymes involved in the oxidation of unsaturated fatty acids. Current data have shown that the metabolism of these acids is actually through NADPH-dependent reduction pathways. The activities of epimerase and isomerase detected in rat liver mitochondria possibly function mainly in the metabolism of saturated fatty acids in a reverse role to the conventional concept.

Animals↗
PubMed1997

Effect of omega 3 fatty acid on plasma lipids, cholesterol and lipoprotein fatty acid content in NIDDM patients.

This study was conducted to examine the effect of omega 3 fatty acid supplementation on plasma lipid, cholesterol and lipoprotein fatty acid content of non-insulin-dependent diabetic individuals consuming a higher (0.65, n = 10) or lower (0.44, n = 18) ratio of dietary polyunsaturated to saturated fatty acid (P/S). The participants were initially given an olive oil supplement (placebo) equivalent to 35 mg of 18:1. kg body weight-1.day-1 for 3 months. This was followed by two omega 3 supplement periods in a randomized crossover. In these 3-month periods, participants were given a linseed oil supplement equivalent to 35 mg of 18:3 omega 3.kg body weight-1.day-1 or a fish oil supplement equivalent to 35 mg of 20:5 omega 3 + 22:6 omega 3.kg body weight-1. day-1. At the end of each supplement period, a blood sample was drawn from each participant for lipid, lipoprotein, insulin, glucagon and C-peptide analyses. At the end of each 3-month period a 7-day dietary record was completed to calculate dietary fat intake and P/S ratio. Results indicate that fish oil significantly reduced plasma triacylglycerol level (p < 0.05) and increased 20:5 omega 3 and 22:6 omega 3 content of all lipoprotein lipid classes. Linolenic acid supplementation had no effect on plasma triacylglycerol level, but it increased 18:3 omega 3 content of lipoprotein cholesterol ester fractions (p < 0.05). A slight increase in 20:5 omega 3, but not 22:6 omega 3, content was noted in lipoprotein lipid classes as a result of 18:3 omega 3 supplementation. LDL and HDL cholesterol, insulin, glucagon and C-peptide levels were not affected by either omega 3 supplement. It is concluded that a modest intake of omega 3 fatty acids, such as could be obtained from consuming fish regularly, will reduce plasma triglyceride level without affecting LDL or HDL cholesterol levels.

Cholesterol, HDL↗
PubMed1993

Inhibition of fatty acid synthesis in rat hepatocytes by exogenous polyunsaturated fatty acids is caused by lipid peroxidation.

Rat hepatocyte long-term cultures were utilized to investigate the impact of different polyunsaturated fatty acids (PUFA) on the insulin-induced de novo fatty acid synthesis in vitro. The addition of 0.5 mM albumin-complexed oleic, linoleic, columbinic, arachidonic, eicosapentaenoic or docosahexaenoic acid resulted in a marked suppression of fatty acid synthesis. By evaluation of cell viability (determined as the leakage of lactate dehydrogenase (LDH) it turned out, that the antioxidant used (50 microM alpha-tocopherol phosphate) had a low antioxidant activity, resulting in cytotoxic effects by the peroxidized PUFA. Arachidonic acid and eicosapentaenoic acid showed a dose- and time-dependent cytotoxicity. Two other antioxidants: 50 microM alpha-tocopherol acid succinate and 1 microM N,N'-diphenyl-1,4-phenylenediamine, both proved more efficient than alpha-tocopherol phosphate. There was a significant correlation between LDH-leakage and inhibition of fatty acid synthesis. Lipid peroxidation, measured as thiobarbituric acid-reactive substances, also showed a significant correlation with the degree of inhibition of fatty acid synthesis. Furthermore, PUFA had no inhibitory effect on fatty acid synthesis when peroxidation was minimized by the use of proper antioxidants. These data indicate that PUFA in vitro inhibit the insulin-induced de novo fatty acid synthesis in hepatocytes from starved rats, due to cytotoxic effects caused by lipid peroxidation.

Animals↗
PubMed1983

Medium-chain fatty acid synthesis by goat mammary-gland fatty acid synthetase. The effect of limited proteolysis.

Fatty acid synthetase from goat mammary gland was subjected to limited proteolysis by trypsin and elastase. Both proteolytic enzymes selectively cleaved the chain-terminating thioester hydrolase component from the enzyme complex, leaving all other partial activities intact in the core peptides. Trypsin, but not elastase, caused extensive degradation of the released thioester hydrolase. The released thioester hydrolase could be purified to homogeneity by gel filtration. The molecular weight was estimated as 29 000 and the enzyme showed only significant hydrolytic activity toward long-chain acyl-CoA esters. The core peptides retained the ability to synthesize medium-chain acyl-CoA esters in the presence of 2,6-di-O-methyl-alpha-cyclodextrin. The results conclusively show that the terminating thioester hydrolase of goat mammary-gland fatty acid synthetase is not involved in termination of medium-chain-length fatty acid synthesis by this enzyme.

Animals↗
PubMedDate not supplied

[The effect of diets containing omega-3 polyunsaturated fatty acids on biochemical indicators and the fatty acid composition of the cell membranes in patients with ischemic heart disease and hereditary hyperlipidemia].

A decrease in content of total cholesterol, triglycerides, fibrinogen, and atherogeneity index as well as increase in fibrinolytic activity and prolongation of the hemorrhage time were observed in blood serum of 20 patients with ischemic heart disease and hyperlipidemia of the IIa and IIb types maintained on anti-atherosclerotic diet containing 20 g of ichthyenic oil within 4 weeks. Relative content of polyunsaturated fatty acids omega 6 was decreased while the content of omega 3 fatty acids was distinctly increased in erythrocytes and blood platelets membranes, thus demonstrating the high efficiency of ichthyenic oil.

Cell Membrane↗
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↗
PubMed1965

EFFECT IN THE COW OF INTRARUMINAL INFUSIONS OF VOLATILE FATTY ACIDS AND OF LACTIC ACID ON THE SECRETION OF THE COMPONENT FATTY ACIDS OF THE MILK FAT AND ON THE COMPOSITION OF BLOOD.

1. The effects in the cow of intraruminal infusions of acetic acid, propionic acid or butyric acid on the secretion of the component fatty acids of the milk fat, and of these acids and of lactic acid on the composition of the blood plasma of the jugular vein, have been studied. 2. The infusion of acetic acid or butyric acid increased the yield of the C(4)-C(16) acids of milk fat but decreased the yield of C(18) acids. The infusion of propionic acid decreased the yields of all major component acids except palmitic acid and possibly lauric acid. 3. The changes in the concentrations in blood plasma of glucose and of ketone bodies were consistent with the glucogenic effect of propionic acid and the ketogenic effects of butyric acid and acetic acid. The effects of lactic acid were not consistent from cow to cow. Only with the infusion of acetic acid was a significant increase in the concentration of total volatile fatty acids in blood plasma found. Infusions of butyric acid and of propionic acid tended to depress the concentration of citric acid in the blood plasma and infusion of acetic acid increased it. No consistent effects of the infused acids on the concentration in blood plasma of esterified cholesterol, free cholesterol, triglyceride or phospholipid were observed. 4. The possibility is discussed that the effects of the infused acids on milk-fat secretion are caused through an alteration of the concentrations of precursors of milk fat in mammary arterial blood.

Acetates↗
PubMed1998

The helical domain of intestinal fatty acid binding protein is critical for collisional transfer of fatty acids to phospholipid membranes.

Fatty acid binding proteins (FABPs) exhibit a beta-barrel topology, comprising 10 antiparallel beta-sheets capped by two short alpha-helical segments. Previous studies suggested that fatty acid transfer from several FABPs occurs during interaction between the protein and the acceptor membrane, and that the helical domain of the FABPs plays an important role in this process. In this study, we employed a helix-less variant of intestinal FABP (IFABP-HL) and examined the rate and mechanism of transfer of fluorescent anthroyloxy fatty acids (AOFA) from this protein to model membranes in comparison to the wild type (wIFABP). In marked contrast to wIFABP, IFABP-HL does not show significant modification of the AOFA transfer rate as a function of either the concentration or the composition of the acceptor membranes. These results suggest that the transfer of fatty acids from IFABP-HL occurs by an aqueous diffusion-mediated process, i.e., in the absence of the helical domain, effective collisional transfer of fatty acids to membranes does not occur. Binding of wIFABP and IFABP-HL to membranes was directly analyzed by using a cytochrome c competition assay, and it was shown that IFABP-HL was 80% less efficient in preventing cytochrome c from binding to membranes than the native IFABP. Collectively, these results indicate that the alpha-helical region of IFABP is involved in membrane interactions and thus plays a critical role in the collisional mechanism of fatty acid transfer from IFABP to phospholipid membranes.

Animals↗
PubMed1982

A comparative study on the effect of cis (oleic, linoleic) and trans (elaidic, linoelaidic) fatty acids on the in vitro prostaglandin biosynthesis in human blood platelets from (1-14C) arachidonic acid.

Dietary fatty acids affect the synthesis and thus ultimate availability of prostaglandin precursors. During processing of edible fats a significant portion of the naturally occurring cis fatty acids is changed to the respective trans isomers. Trans fatty acids could have a wide variety of effects including their effect on prostaglandin synthesis. A comparative study on the effect of cis (oleic and linoleic) fatty acids and their corresponding trans isomers (elaidic and linoelaidic acids) on the in vitro prostaglandin biosynthesis in human blood platelets was made. Linoleic acid (0.5, 1.0 mM) showed the same effect on the various arachidonic acid (AA) metabolites as reported earlier by us, that is, increased generation of prostaglandins and thromboxanes and reduced amounts of HHT and HETE (26). Linoelaidic acid at these two concentrations had the same effect but to a lesser extent. Both linoleic and linoelaidic acids at 0.25 mM concentration reduced TxB2 formation. Oleic and elaidic acids (0.5, 1.0 mM) decreased the formation of TxB2 though not significantly. With oleic acid, the results in respect of other AA metabolites were similar to those reported by us earlier (26). MDA was reduced significantly in the presence of linoleic, linoelaidic and oleic acids; cis isomers being more effective. In the presence of linoleic and linoelaidic acids, prostaglandin endoperoxides were reduced significantly; there was no change in the presence of oleic and elaidic acids. Thus fatty acids seem to affect the platelet cyclo-oxygenase activity; this being more pronounced in the case of cis fatty acids compared to their trans isomers. Reduction in cyclo-oxygenase activity also depends upon the number of double bonds in the acids.

Arachidonic Acids↗
PubMed1998

Heterologously expressed acyl carrier protein domain of rat fatty acid synthase functions in Escherichia coli fatty acid synthase and Streptomyces coelicolor polyketide synthase systems.

INTRODUCTION: Fatty acid synthases (FASs) catalyze the de novo biosynthesis of long-chain saturated fatty acids by a process common to eubacteria and eukaryotes, using either a set of monofunctional proteins (Type II FAS) or a polypeptide containing several catalytic functions (Type I FAS). To compare the features of a Type I domain with its Type II counterpart we expressed and characterized an acyl carrier protein (ACP) domain of the Type I rat FAS. RESULTS: An ACP domain of rat FAS was defined that allows expression of a small percentage of active holo-ACP both in Escherichia coli, increasing fivefold upon co-expression with an E. coli holo-ACP synthase, and in Streptomyces coelicolor. The rat ACP domain functions with some components of the E. coli FAS, and can replace the actinorhodin polyketide synthase (PKS) ACP in S. coelicolorA3(2). Purification of the rat ACP domain from E. coli resulted in loss of its functionality. Purified apo-ACP could be converted to its holo-form upon incubation with purified E. coli holo-ACP synthase in vitro, however, suggesting that the loss of functionality was not due to a conformational change. CONCLUSIONS: Functionality of the recombinant rat ACP was shown in distantly related and diverse enzyme systems, suggesting that Type I and Type II ACPs have a similar conformation. A procedure was described that might permit the production of rat FAS holo-ACP for structural and further biochemical characterization.

Acyl Carrier Protein↗
PubMed1997

Threonine allele in codon 54 of the fatty acid binding protein 2 gene does not modify the fatty acid composition of serum lipids in obese subjects.

Intestinal fatty acid binding protein (I-FABP) participates in the metabolism of fatty acids in the intestinal enterocytes. Threonine encoding allele in codon 54 of the I-FABP gene has been suggested as regulating the absorption of long-chain fatty acids. We examined the fatty acid composition of serum lipid fractions and the concentration of serum free fatty acids after an overnight fast in obese subjects, aged 24-56 years, on their habitual diet. The body mass index of the subjects ranged from 29.7 to 43.3 kg m-2. Six subjects were homozygous for the Thr-54 allele of the I-FABP gene, 37 subjects were heterozygous for the Thr-54/Ala-54 allele and 24 subjects were homozygous for the Ala-54 allele. We did not find any consistent differences in the proportions of long-chain fatty acids in serum triglycerides, cholesterol esters or phospholipids, but the concentration of serum free fatty acids tended to be higher in subjects who were homozygous for the Thr-54 allele (P = 0.13, for trend). In conclusion, our findings suggest that a polymorphism at codon 54 of the I-FABP2 gene does not substantially modify the fatty acid composition of serum lipids in obese Finns.

Adult↗
PubMed2000

Effect of supplementation of arachidonic acid (AA) or a combination of AA plus docosahexaenoic acid on breastmilk fatty acid composition.

We investigated whether supplementation with arachidonic acid (20:4 omega 6; AA), or a combination of AA and docosahexaenoic acid (22:6 omega 3; DHA) would affect human milk polyunsaturated fatty acid (PUFA) composition. Ten women were daily supplemented with 300 mg AA, eight with 300 mg AA, 110 mg eicosapentaenoic acid (20:5 omega 3; EPA) and 400 mg DHA, for one week and eight women served as unsupplemented controls. Milk samples were collected on days 0, 1 and 7. The fatty acid composition of the milk was analyzed by capillary gas chromatography with flame ionisation detection. Supplementation with AA alone had no effect on breastmilk AA, but tended to reduce EPA and DHA levels. Administration of a combination of AA, EPA and DHA tended to increase both milk AA and long chain PUFA (LCPUFA)omega 3 content. A larger simultaneous increase of milk AA, DHA and EPA than observed in the present study can probably be accomplished by the use of a combination of a lower LCPUFA omega 6/LCPUFA omega 3 ratio and higher AA, EPA and DHA dosages.

Adult↗
PubMedDate not supplied

An experimental model of hypoxia on isolated rat heart in recirculating system: study of fatty acid metabolism with an iodinated fatty acid.

An experimental model of hypoxia was developed on isolated rat heart to study the effects of hypoxia on cardiac performance and metabolism. Fatty acid (FA) metabolism was explored by external detection with a labelled FA, iodohexadecenoic acid (IHA). Hearts, after 30 min preperfusion in an open system, were transferred in a recirculating system for 40 min and perfused with oleate, glucose, lactate, pyruvate and IHA, either in normoxia (pO2 = 660 mmHg) or in hypoxia (pO2 = 220 mmHg). After 40 min hypoxic recirculation, oxygen uptake and dynamic parameters, except the heart rate, decreased respectively by 56% and 44%, and remained constant throughout the perfusion. Glucose utilization increased 2 fold, endogenous glycogen fell by 50% and lactate + pyruvate production increased 3 fold, showing a stimulation of glycolysis. Oleate uptake decreased by 28%, while triglycerides content remained higher. The ATP/ADP ratio decreased by 24%. Conversely to oleate, IHA uptake was not significantly modified, but its intracellular fate showed a higher radioactivity in all lipid fractions: polar lipids, diglycerides, free FAs and triglycerides. beta oxidation of IHA, evidenced by iodide production, decreased by 39%. The external detection of cardiac radioactivity allowed us to obtain time-activity curves that were analyzed with a 4-compartment mathematical model. The data evidenced an esterification ratio significantly higher in hypoxia. The metabolism of IHA as estimated by the intracellular analysis or, in a non-invasive way, by external detection, was similar to the metabolism of oleate. Thus, lipid metabolism, in hypoxia, can be explored by external detection with IHA.

Animals↗
PubMed1976

Fatty acid binding protein. Role in esterification of absorbed long chain fatty acid in rat intestine.

Fatty acid binding protein (FABP) is a protein of 12,000 mol wt found in cytosol of intestinal mucosa and other tissues, which exhibits high affinity for long chain fatty acids. It has been suggested that FABP (which may comprise a group of closely related proteins of 12,000 mol wt) participates in cellular fatty acid transport and metabolism. Although earlier findings were consistent with this concept, the present studies were designed to examine its physiological function more directly. Everted jejunal sacs were incubated in mixed fatty acid-monoglyceride-bile acid micelles, in the presence or absence of equimolar concentrations of either of two compounds which inhibit oleate binding to FABP:flavaspidic acid-N-methyl-glucaminate and alpha-bromopalmitate. Oleate uptake, mucosal morphology, and oxidation of [14C]acetate remained unaffected by these agents, but oleate incorporation into triglyceride was inhibited by 62-64% after 4 min. The inhibition by flavaspidic acid was reversible with higher oleate concentrations. The effect of these compounds on enzymes of triglyceride biosynthesis was examined in intestinal microsomes. Neither flavaspidic acid nor alpha-bromopalmitate inhibited acyl CoA:monoglyceride acyl-transferase. Fatty acid:coenzyme A ligase activity was significantly enhanced in the presence of partially purified FABP, probably reflecting a physical effect on the fatty acid substrate or on the formation of the enzyme-substrate complex. Activity of the enzyme in the presence of 0.1 mM oleate was only modestly inhibited by equimolar flavaspidic acid and alpha-bromopalmitate, and this effect was blunted or prevented by FABP. We conclude that in everted gut sacs, inhibition of triglyceride synthesis by flavaspidic acid and alpha-bromopalmitate could not be explained as an effect on fatty acid uptake or on esterifying enzymes in the endoplasmic reticulum but rather can be interpreted as reflecting inhibition of fatty acid binding to FABP. These findings lend further support to the concept that FABP participates in cellular fatty acid transport and metabolism. It is also possible that FABP, by effecting an intracellular compartmentalization of fatty acids and acyl CoA, may play a broader role in cellular lipid metabolism.

Acids↗