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PubMed1997

Enhancement of neutrophil-mediated killing of Plasmodium falciparum asexual blood forms by fatty acids: importance of fatty acid structure.

Effects of fatty acids on human neutrophil-mediated killing of Plasmodium falciparum asexual blood forms were investigated by using a quantitative radiometric assay. The results showed that the antiparasitic activity of neutrophils can be greatly increased (>threefold) by short-term treatment with fatty acids with 20 to 24 carbon atoms and at least three double bonds. In particular, the n-3 polyenoic fatty acids, eicosapentaenoic and docosahexaenoic acids, and the n-6 fatty acid, arachidonic acid, significantly enhanced neutrophil antiparasitic activity. This effect was >1.5-fold higher than that induced by an optical concentration of the known agonist cytokine tumor necrosis factor alpha (TNF-alpha). At suboptimal concentrations, the combination of arachidonic acid and TNF-alpha caused a synergistic increase in neutrophil-mediated parasite killing. The fatty acid-induced effect was independent of the availability of serum opsonins but dependent on the structure of the fatty acids. The length of the carbon chain, degree of unsaturation, and availability of a free carboxyl group were important determinants of fatty acid activity. The fatty acids which increased neutrophil-mediated killing primed the enhanced superoxide radical generation of neutrophils in response to P. falciparum as detected by chemiluminescence. Scavengers of oxygen radicals significantly reduced the fatty acid-enhanced parasite killing, but cyclooxygenase and lipoxygenase inhibitors had no effect. These findings have identified a new class of immunoenhancers that could be exploited to increase resistance against Plasmodium species.

Adjuvants, Immunologic↗
PubMed1996

Amino acid and fatty acid compositions of Adenopus breviflorus benth seed.

The amino acid and fatty acid contents of Adenopus breviflorus benth seed (locally called egwoli) with and without hull were determined. The results for the amino acid analysis showed that the seed is a good source of most of the essential amino acids and comparable to those of soya bean. The total essential amino acids of the whole seed amounted to 53.7% while that of the dehulled seed is 51.4%. Linoleic acid is the predominant fatty acid with values of 60.7 and 58.8% for whole and dehulled seeds oil respectively. It is observed that the total unsaturated fatty acid is about 80.1% for the whole seeds and 77.2% for the dehulled seeds.

Amino Acids↗
PubMed1977

Effect of prolonged glucose infusion on total serum fatty acids and free fatty acids in the rat.

This investigation evaluates the effect of prolonged glucose infusion on triglycerides and the composition in total serum fatty acids and free fatty acids in the rat. Glucose infusion over a period of 4 days leads to the following changes: serum triglyceride concentrations are two to three times elevated and serum insulin levels rise 10 times after 12 hours, followed by a steady decrease. Chain elongation is depressed in serum free fatty acids and even more in total serum fatty acids. In serum free fatty acids monodesaturation is unaltered whereas it is highly stimulated in total serum fatty acids. These alterations correlate with the changes of hepatic total fatty acids and do not correlate with changes of fatty acids from epididymal fat pads. The alterations reflect a specific carbohydrate-induced effect on hepatic fatty acid desaturation and chain elongation. They do not support the idea that serum free fatty acids are mainly secreted from the storage pool of adipose tissue; yet, they may have been newly synthesized in fat cells or even in the liver.

Animals↗
PubMed1998

Conjugated linoleic acids alter bone fatty acid composition and reduce ex vivo prostaglandin E2 biosynthesis in rats fed n-6 or n-3 fatty acids.

This study evaluated the effects of conjugated linoleic acids (CLA) on tissue fatty acid composition and ex vivo prostaglandin E2 (PGE2) production in rats given diets varying in n-6 and n-3 fatty acids. Four groups of rats were given a basal semipurified diet (AIN-93G) containing 70 g/kg of added fat for 42 d. The fat treatments were formulated to contain CLA (0 vs. 10 g/kg of diet) and n-6 (soybean oil having an n-6/n-3 ratio of 7.3) and n-3 fatty acids (menhaden oil + safflower oil having an n-6/n-3 ratio of 1.8) in different ratios in a 2 x 2 factorial design. Fatty acids in liver, serum, muscle, heart, brain, spleen, and bone (cortical, marrow, and periosteum) were analyzed by capillary gas-liquid chromatography. The various dietary lipid treatments did not affect growth; however, CLA improved feed efficiency. The CLA isomers were found in all rat tissues analyzed although their concentrations varied. Dietary CLA decreased the concentrations of 16:1n-7, 18:1, total monounsaturates and n-6 fatty acids, but increased the concentrations of n-3 fatty acids (22:5n-3 and 22:6n-3), and saturates in the tissues analyzed. Ex vivo PGE2 production in bone organ culture was decreased by n-3 fatty acids and CLA. We speculate that CLA reduced the concentration of 18:1 fatty acids by inhibiting liver delta9-desaturase activity. The fact that CLA lowered ex vivo PGE2 production in bone organ culture suggests that these conjugated fatty acids have the potential to influence bone formation and resorption.

Animal Feed↗
PubMed1983

Effects of amphotericin B and cholera toxin on intestinal transport in the rat. An in vivo model for the effects of dihydroxy bile acids and fatty acids on intestinal transport.

In vivo perfusion experiments were performed in the rat jejunum and colon to test the hypothesis that the changes in intestinal solute transport induced by dihydroxy bile acids and fatty acids are the result of the combined effects of fluid secretion and enhancement of mucosal permeability. The hypothesis predicts that absorption of organic solutes will be reduced in inverse relationship to the absorption rates under control conditions and that absorption of small, nonabsorbable solutes such as mannitol will be enhanced by these agents. Fluid secretion was induced either by administering cholera toxin or by increasing the osmolality of the perfusion solution to 365 mOsm/L. Permeability was enhanced by adding amphotericin B, 50 micrograms/ml, to the perfusion solutions. The isotonic perfusion solutions contained 11.2 mM glucose and 4 mM triethylene, tetraethylene, pentaethylene, and hexaethylene glycol or mannitol as probes of passive permeability. In the jejunum cholera toxin induced fluid and electrolyte secretion and reduced organic solute absorption to a small but significant degree (p less than 0.05). Amphotericin B alone enhanced absorption of organic solutes, water, and electrolytes (p less than 0.01). In the presence of fluid secretion induced by an osmotic load, only absorption of triethylene and pentaethylene glycol was reduced. Addition of amphotericin B after exposure to cholera toxin or to the hypertonic solutions resulted in a further significant reduction of absorption of glucose and ethylene glycols (p less than 0.05). The combination of amphotericin B and cholera toxin resulted in enhanced absorption of mannitol (p less than 0.02). Similarly, 5 mM deoxycholate enhanced jejunal absorption of mannitol (p less than 0.01) and reduced the absorption of glucose and the low-molecular-weight ethylene glycols (p less than 0.01). In the colon the administration of amphotericin B after the exposure to cholera toxin resulted in enhanced absorption of glucose (p less than 0.05) in spite of continuing fluid secretion. The combination of fluid secretion and enhancement of mucosal permeability, therefore, reproduced all in vivo effects of bile acids and fatty acids on intestinal transport of organic solutes.

Amphotericin B↗
PubMed2001

Replacement of dietary saturated fatty acids by trans fatty acids lowers serum HDL cholesterol and impairs endothelial function in healthy men and women.

We tested whether trans fatty acids and saturated fatty acids had different effects on flow-mediated vasodilation (FMD), a risk marker of coronary heart disease (CHD). Consumption of trans fatty acids is related to increased risk of CHD, probably through effects on lipoproteins. Trans fatty acids differ from most saturated fatty acids because they decrease serum high-density lipoprotein (HDL) cholesterol, and this may increase the risk of CHD. We fed 29 volunteers 2 controlled diets in a 2x4-week randomized crossover design. The "Trans-diet" contained 9.2 energy percent of trans fatty acids; these were replaced by saturated fatty acids in the "Sat-diet." Mean serum HDL cholesterol after the Trans-diet was 0.39 mmol/L (14.8 mg/dL), or 21% lower than after the Sat-diet (95% CI 0.28 to 0.50 mmol/L). Serum low density lipoprotein and triglyceride concentrations were stable. FMD+SD was 4.4+/-2.3% after the Trans-diet and 6.2+/-3.0% after the Sat-diet (difference -1.8%, 95% CI -3.2 to -0.4). Replacement of dietary saturated fatty acids by trans fatty acids impaired FMD of the brachial artery, which suggests increased risk of CHD. Further studies are needed to test whether the decrease in serum HDL cholesterol caused the impairment of FMD.

Adult↗
PubMed2000

[Mechanisms for tissue transport of fatty acids].

Fatty acids (FA) play an important role in energy metabolism. They are not only used as substrates for energy production but are also involved in many other metabolic pathways. However, the exact mechanisms by which FA are taken up by the cells are not yet fully understood. Fatty acids circulating in blood cross the cell membranes partly via a mechanism facilitated by plasma membrane proteins and partly via a passive diffusion mechanism, the former mechanism being of major importance.

Animals↗
PubMed1983

Excessive intake of 13-cis retinoic acid and fatty acid composition of tissues.

The effects of feeding an excess of 13-cis retinoic acid on the fatty acid composition of tissues were studied. Groups of male, weanling, Sprague-Dawley rats were fed diets containing 0, 100 and 300 mg 13-cis retinoic acid per kilogram diet. Rats were killed 4 weeks after feeding the diets, and the fatty acid composition of total lipids in plasma, liver, kidney, heart and lung was determined. Changes in fatty acid patterns were observed primarily in plasma and liver. The proportions of 16:1, 18:1 and 20:3 omega 6 were generally higher, whereas those of 20:4 were lower. The fatty acid composition of kidney, heart and lung lipids was not appreciably changed. The results on fatty acid changes in liver suggest that 13-cis retinoic acid may be modifying the activities of desaturating enzymes.

Animals↗
PubMed1984

The effects of trans fatty acids on fatty acyl delta 5 desaturation by human skin fibroblasts.

The effectiveness of different fatty acids as inhibitors of fatty acyl delta 5 desaturation activity in human skin fibroblasts has been investigated. When incubated with 2.25 microM [14C] eicosatrienoate (20:3 omega 6) in otherwise lipid-free medium, these cells rapidly incorporate the radiolabeled fatty acid into cellular glycerolipids and desaturate it to produce both [14C] arachidonate and [14C]docosatetraenoate. The delta 5 desaturation activity can be enhanced by prior growth of the cells without serum lipids. Elaidate (9t-18:1) is a potent inhibitor of delta 5 desaturation while trans-vaccenate (11t-18:1) is virtually without effect. Oleate and linoleate are only mildly inhibitory. Linoelaidate (9t,12t-18:2) is more inhibitory than linoleate but significantly less effective than elaidate. The effects of elaidate can be readily overcome by increasing the concentration of exogenous eicosatrienoate. Studies with a variety of trans monounsaturates of differing chain lengths indicate that the omega 9 trans fatty acids are potent inhibitors of delta 5 desaturation, while omega 7 trans fatty acids are relatively ineffective. Intact human fibroblasts could thus be important in characterizing novel fatty acids as selective inhibitors of arachidonate synthesis in vivo.

Arachidonic Acids↗
PubMed1997

Intake of a diet high in trans monounsaturated fatty acids or saturated fatty acids. Effects on postprandial insulinemia and glycemia in obese patients with NIDDM.

OBJECTIVE: High intake of trans fatty acids and saturated fatty acids (SFAs) is known to increase the risk of coronary heart disease. We studied the effects of diets enriched in various fatty acids on postprandial insulinemia and fasting serum levels of lipids and lipoproteins in obese patients with NIDDM. RESEARCH DESIGN AND METHODS: Sixteen obese NIDDM patients were studied in a free-living outpatient regimen. After a run-in period, the patients received three different isocaloric diets for 6 weeks using a randomized crossover design. The patients were instructed to keep the energy intake from carbohydrate and protein constant at 50 and 20 E% (percent of energy intake), respectively, on all three diets. The fat composition of the diets differed: saturated fat (SAT) diet (20 E% SFAs, 5 E% polyunsaturated fatty acids [PUFAs], and 5 E% monounsaturated fatty acids [MUFAs]) versus cis monounsaturated fatty acid (CMUFA) diet (20 E% cis-MUFAs, 5 E% PUFAs, and 5 E% SFAs) versus trans monounsaturated fatty acid (TMUFA) diet (20 E% trans-MUFAs, 5 E% PUFAs, and 5 E% SFAs). Fasting serum levels of lipids and lipoproteins were measured at baseline and in the fasting state before meal tolerance tests at the end of each study period. Insulin secretion was assessed from incremental serum insulin and C-peptide responses during the meal tests. RESULTS: BMI, waist-to-hip ratio, and glycemic control remained stable throughout the study. After meal stimulation, postprandial glycemic responses were similar on all diets; however, serum insulin and C-peptide responses were greater following the TMUFA and SAT diets than following the baseline or CMUFA diets (P < 0.05). No statistical difference was found in fasting levels of serum lipids (total cholesterol, triglyceride, phospholipid, and nonesterified fatty acids) or lipoproteins of HDL cholesterol, VLDL cholesterol, LDL cholesterol, and apolipoprotein B between diets. CONCLUSIONS: In the presence of unchanged glycemia, both dietary trans fatty acids and SFAs induce an increase in postprandial insulinemia in obese patients with NIDDM.

Blood Glucose↗
PubMed1994

A possible route for the release of fatty acid from fatty acid-binding protein.

A simulation of the release of fatty acid from intestinal fatty acid-binding protein was attempted, starting with the crystallographic model and using molecular-dynamic processes at different temperatures. The release of the ligand was observed only at high temperature, which perhaps makes the process unreliable in detail. Nevertheless, the overall behaviour of the protein, also confirmed by the simulation performed at room temperature, strongly supports the idea that the fatty acid leaves the protein through an opening formed by alpha-helix II and turns beta C-beta D and beta E-beta F. Additionally, it suggests a role for the lack of hydrogen bonds between the main chains of beta-strands D and E: this feature, observed in all the protein structures of this family which have currently been determined, seems to provide the structure with great flexibility, allowing the barrel to open and close without disruption of the hydrogen-bond network.

Carrier Proteins↗
PubMed2006

Biocatalytic acylation of carbohydrates with fatty acids from palm fatty acid distillates.

Palm fatty acid distillates (PFAD) are by-products of the palm oil refining process. Their use as the source of fatty acids, mainly palmitate, for the biocatalytic synthesis of carbohydrate fatty acid esters was investigated. Esters could be prepared in high yields from unmodified acyl donors and non-activated free fatty acids obtained from PFAD with an immobilized Candida antarctica lipase preparation. Acetone was found as a compatible non-toxic solvent, which gave the highest conversion yields in a heterogeneous reaction system without the complete solubilization of the sugars. Glucose, fructose, and other acyl acceptors could be employed for an ester synthesis with PFAD. The synthesis of glucose palmitate was optimized with regard to the water activity of the reaction mixture, the reaction temperature, and the enzyme concentration. The ester was obtained with 76% yield from glucose and PFAD after reaction for 74 h with 150 U ml(-1) immobilized lipase at 40 degrees C in acetone.

Acylation↗
PubMed1995

Incorporation of dietary n-3 fatty acids into the fatty acids of human adipose tissue and plasma lipid classes.

The consumption of n-3 fatty acids from seafood has been related to a lower incidence of coronary artery disease. Adipose tissue composition has served as a biological marker of chronic ingestion of many dietary polyunsaturated fatty acids. However, the incorporation of n-3 fatty acids into the fat depots has not been studied in humans. Daily dietary supplementation with > or = 10 g n-3 fatty acids from fish oil for > 12 mo resulted in significantly greater 20:5n-3, 22:5n-3, and 22:6n-3 concentrations in fatty acids of adipose tissue, and a greater 20: 5n-3 fatty acid content in plasma lipid classes (cholesterol esters, phospholipids, and free fatty acids) of supplemented subjects compared with nonsupplemented control subjects. Combined values for all subjects indicated that fatty acid concentrations of n-3 plasma lipid classes, including 20:5n-3, 22:5n-3, 22:6n-3, and total n-3, significantly correlated with corresponding concentrations of fatty acids in adipose tissue. These findings indicate that the long-term ingestion of large amounts of n-3 fatty acids in humans resulted in their incorporation into the adipose tissue fatty acids. Incorporation of the fatty acids into adipose tissue warrants consideration for use in clinical studies requiring precise documentation of long-term n-3 fatty acid consumption.

Adipose Tissue↗
PubMed1980

Substrate control of termination of fatty acid biosynthesis by fatty acid synthetase from Brevibacterium ammoniagenes.

The pattern of fatty acids produced by the fatty acid synthetase complex of Brevibacterium ammoniagenes under several conditions was examined. The fatty acid synthetase obtained from B. ammoniagenes produced oleic acid as well as saturated fatty acids (palmitic and stearic acids). The relative proportions of palmitic to stearic acids varied over a wide range. Such alterations were dependent on the malonyl-CoA concentration and the ratio of acetyl-CoA to malonyl-CoA concentrations. At malonyl-CoA concentrations higher than 100 microM, stearic acid accounted for more than 90% of the saturated fatty acids and the pattern of fatty acid synthesized was independent on the ratio of acetyl-CoA to malonyl-CoA. At malonyl-CoA concentrations lower than 100 microM, raising the acetyl-CoA/malonyl-CoA ratio increased the percentage of palmitic acid. However, the proportion of oleic acid produced remained almost constant under all conditions tested.

Acetyl Coenzyme A↗
PubMed1989

Alkylthioacetic acids (3-thia fatty acids) as non-beta-oxidizable fatty acid analogues: a new group of hypolipidemic drugs. III. Dissociation of cholesterol- and triglyceride-lowering effects and the induction of peroxisomal beta-oxidation.

Previous work in this laboratory indicated that sulfur-substituted fatty acid analogues, 1.10-bis(carboxymethylthio)decane and alkylthioacetic acid, both non-beta-oxidizable compounds, and the beta-oxidizable alkylthiopropionic acid (1) caused, to different extents, dose-related hepatomegaly and proliferation of peroxisomes and enhanced peroxisomal fatty acid beta-oxidation. In the present study, treatment of normolipidemic rats with alkylthioacetic acid resulted in a dose- and time-dependent decrease in serum cholesterol and serum and liver triglycerides to an extent comparable to that of the 3-thiadicarboxylic acid. At hypolipidemic doses, alkylthioacetic acid caused no hepatomegaly, did not significantly alter peroxisome morphology, and only marginally affected peroxisomal beta-oxidation activity. Only at the highest, nonpharmacological doses of alkylthioacetic acid were these hepatic parameters increased, although to a lesser extent than by the 3-thiadicarboxylic acid. Hence, on the basis of dose- and time-related studies of the two compounds, data indicate that the hypotriglyceridemia and hypocholesterolemia were dissociated from induction of peroxisomal beta-oxidation and peroxisome proliferation. Palmitic acid and hexadecanedioic acid, both beta-oxidizable fatty acids, only marginally affected the serum and liver parameters. The beta-oxidizable fatty acid analogue, alkylthiopropionic acid lowered the serum triglycerides in normolipidemic rats. In contrast to the 3-thiadicarboxylic acid and alkylthioacetic acid, alkylthiopropionic acid treatment at hypolipidemic doses caused accumulation of triglycerides in the liver.

Animals↗
PubMed1987

[Metabolism of free fatty acids in fatty tissue].

Hyperlipacidaemias play a role as etiological partial factor in the pathogenesis of various acute and chronic functional disturbances and are essentially the sequel of a disturbed metabolism of the free fatty acids of the fatty tissue. With regard to its clinical relevance a survey is given of the free fatty acid metabolism of the fatty tissue and its free fatty acid net balance as resultants from lipolysis and triglyceride synthesis is described. The author deals with the regulation of the lipolysis by cyclic mononucleotides, adenosine triphosphate, adenosine, fatty acids, ions, beta-hydroxybutyrate, lactate as well as hormones and finally with the control of the triglyceride synthesis.

Adipose Tissue↗
PubMed1985

Reciprocal effects of 5-(tetradecyloxy)-2-furoic acid on fatty acid oxidation.

Under certain incubation conditions 5-(tetradecyloxy)-2-furoic acid (TOFA) stimulated the oxidation of palmitate by hepatocytes, as observed by others. A decrease in malonyl-CoA concentration accompanied the stimulation of oxidation. Under other conditions, however, TOFA inhibited fatty acid oxidation. The observed effects of TOFA depended on the TOFA and fatty acid concentrations, the cell concentration, the time of TOFA addition relative to the addition of fatty acid, and the nutritional state of the animal (fed or starved). The data indicate that only under limited incubation conditions may TOFA be used as an inhibitor of fatty acid synthesis without inhibition of fatty acid oxidation. When rat liver mitochondria were preincubated with TOFA, ketogenesis from palmitate was slightly inhibited (up to 20%) at TOFA concentrations that were less than that of CoA, but the inhibition became almost complete (up to 90%) when TOFA was greater than or equal to the CoA concentration. TOFA had only slight or no inhibitory effects on the oxidation of palmitoyl-CoA, palmitoyl(-)carnitine, or butyrate. Since TOFA can be converted to TOFyl-CoA, the data suggest that the inhibition of fatty acid oxidation from palmitate results from the decreased availability of CoA for extramitochondrial activation of fatty acids. These data, along with previous data of others, indicate that inhibition of fatty acid oxidation by CoA sequestration is a common mechanism of a group of carboxylic acid inhibitors. A general caution is appropriate with regard to the interpretation of results when using TOFA in studies of fatty acid oxidation.

Animals↗
PubMed1982

[Effect of clofibric acid on fatty acid metabolism in HLP patients in the 2d half of life].

Ten patients with primary type IIb hyperlipoproteinemia and one hundred patients with primary type IV hyperlipoproteinemia (sixty-seven men and forty-three women aged forty-three to seventy-four) were treated with clofibric acid (Regadrin) for three years. Gas chromatographic analysis of the composition of cholesterol ester and triglyceride fatty acids in serum were done prior to and at four-month intervals during therapy. During treatment of type IIb and type IV hyperlipoproteinemia there was observed a decrease of palmitic, stearic, palmitoleic, oleic, and eicosane-tetraenoic acids as well as an increase of linoleic, linolenic, arachidonic, and eicosane-pentaenoic acids in the triglyceride fraction. These changes manifest themselves most conspicuously in the effect of clofibric acid upon the hepatogenic fatty acid metabolism (increased synthesis or reduced catabolization of polyunsaturated fatty acids and increased oxidation or reduced formation of monounsaturated and saturated fatty acids, increased esterification of polyenic acids). In addition, these is the possibility of selective displacement of saturated and monounsaturated fatty acids of the unsaturated fatty acids fraction as well as specific inhibition of their esterification with glycerol by clofibric acid. Treatment with clofibric acid over a long period of time may well give rise to additional reactions through influences exerted upon the insulin level.

Adult↗