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PubMed1992

Effect of lysophospholipids, arachidonic acid and other fatty acids on regulation of Ca2+ transport in permeabilized pancreatic islets.

The immediate reaction products of PLA2-mediated hydrolysis of phospholipids were tested for their ability to induce Ca2+ mobilization from internal stores in permeabilized ob/ob mouse pancreatic islets. Lysophospholipids and unsaturated fatty acids increased the free Ca2+ concentration in the incubation medium of permeabilized ob/ob mouse pancreatic islets. The potency of the lysophospholipids decreased in the following order: lysophosphatidylcholine = lysophosphatidylglycerol much greater than lysophosphatidylinositol greater than lysophosphatidylserine much greater than lysophosphatidylethanolamine. Arachidonic acid and palmitoleic acid had a potency comparable to lysophosphatidylinositol, while palmitic acid was ineffective. The Ca(2+)-mobilizing effect of inositol-1,4,5-trisphosphate (IP3) in permeabilized islet cells was additive to the lysophospholipid effect, indicating different sites of action. Both Ca(2+)-mobilizing effects were counteracted by the polyamine spermine, while the presence of Mg2+ shifted the Ca2+ concentrations to higher levels. Since not only an activation of a phospholipase C but also an activation of a phospholipase A2 with subsequent generation of lysophospholipids and free fatty acids is reported to occur in glucose-induced insulin secretion, the interaction of the phospholipase C reaction product IP3 with a lysophospholipid or an unsaturated fatty acid may affect the extent and duration of the rise in the free cytoplasmic Ca2+ concentration responsible for initiation of insulin secretion.

Animals↗
PubMed1982

Effects of dietary long-chain fatty acids on the rat biosynthesis of unsaturated fatty acids in the rat.

Menhaden oil (ME) was included in semisynthetic diets to study the effect of long-chain fatty acids, mainly 20:5n3 and 22:6n3, on the biosynthesis of polyunsaturated fatty acids and on the 6- and 9-desaturase activities in liver microsomes. Five experimental diets, with the following fat supplements, were fed to male rats from weaning for a period of 33 weeks: 5% safflower oil (SAF) + 10% hydrogenated coconut oil (HCO), 5% SAF + 5% HCO + 5% ME, 5% SAF + 10% ME, 15% HCO and 5% HCO + 10% ME. The last two diets were deficient in linoleic acid. The three nondeficient diets contained similar amounts of linoleic acid. Including ME in the diets depressed the 6- and 9-desaturase activities, especially in the linoleic acid--deficient rats. The synthesis of 20:4n6, 22:4n6 and 22:5n6 were depressed. These effects were related to the preferential accumulation of dietary 20:5n3 and 22:6n3 in the liver microsomes, as compared to the n6 fatty acids. It is hypothesized that dietary 20:5n3 and 22:6n3 increase the minimum requirement for linoleic acid in the diet.

Animals↗
PubMed1999

Modification of release rates of cyclosporin A from polyl(L-lactic acid) microspheres by fatty acid esters and in-vivo evaluation of the microspheres.

Biodegradable microspheres containing cyclosporin A (CyA, cyclosporine) were prepared using poly(L-lactic acid) (PLA) and poly(lactide-co-glycolide)(PLGA) by a solvent evaporation method. CyA was efficiently entrapped in PLA, PLGA(50/50) and PLGA(75/25) microspheres in a range of 81-85%. CyA released constantly from PLA microspheres without any lag time, whereas the drug from PLGA(50/50) and PLGA(75/25) microspheres was released after lag time of about 1 and 3 weeks, respectively. Addition of fatty acid esters enhanced the release rates of CyA from PLA microspheres. In-vivo study was performed using rats with adjuvant-induced arthritis. PLA microspheres with ethyl myristate sustained high blood levels of CyA compared with the microspheres with no additives over 4 weeks. In addition, the PLA microspheres improved the symptoms such as the decrease in body weight and the increase in paw swelling occurred by adjuvant-induced arthritis in rats. Consequently, the release rate of CyA from PLA microspheres can be improved by adding fatty acid esters and PLA microspheres with fatty acid esters seem to be a useful dosage form for autoimmune disease therapy.

Animals↗
PubMed1983

Arachidonic acid and other fatty acids inhibit secretion from sea urchin eggs.

Massive secretion at the egg surface follows fertilization of sea urchin eggs or parthenogenetic activation by the calcium ionophore A23187. The secretory products are used to construct the fertilization envelope around the egg. Arachidonic acid prevents the raising of the fertilization envelope induced by either sperm or A23187. We developed a secretion assay based on the ability of A23187 to raise fertilization envelopes from the surface of unfertilized eggs. Arachidonate delays the onset of this reaction in a dose-dependent fashion. 5 microM arachidonate produces a two-fold delay in the standard assay. In contrast, the propagation of secretion over the surface of the egg is unaffected at all concentrations that have been tested. Some closely related fatty acids (e.g. 11, 14, 17 C20:3 and linoleate, 9, 12 C18:2) share with arachidonate the ability to inhibit secretion, whereas others (e.g., 8, 11, 14 C20:3 and linolenate, 9, 12, 15 C18:3) do not. The results are not easily reconciled with a cyclooxygenase- or a lipoxygenase-mediated action. Despite the sensitivity of this phenomenon to small changes in fatty acid structure, it is suggested that the fatty acids exert their effect by altering the structure or dynamics of the membrane lipid bilayer.

Animals↗
PubMed1996

Glucuronic acid-conjugated dihydroxy fatty acids in the urine of patients with generalized peroxisomal disorders.

Urine extracts from children diagnosed with generalized peroxisomal disorders were screened by continuous flow-negative ion fast atom bombardment-mass spectrometry. In 45 of 60 children with generalized peroxisomal disorders, we observed one or more intense ions (m/z 489, 505, 461, and others) that are infrequently found in children with cholestatic liver disease or normal children. Compounds giving rise to these ions were isolated using reverse phase and anion exchange chromatography. After appropriate derivatization and/or methanolysis the compounds were analyzed using capillary gas chromatography-mass spectrometry. The major compounds were found to be 12,13-dihydroxy-9-octadecenoic acid and 9,10-dihydroxy-12-octadecenoic acid, with one of the hydroxyl groups in glycosidic linkage with glucuronic acid. Minor compounds were glucuronic acid conjugates of 9,10-dihydroxy-octadecanoic acid, and 12,13-dihydroxy-6,9-, 15,16-dihydroxy-9,12-, and 9, 10-dihydroxy-12,15-octadecadienoic acids. A series of hexadecanoic, hexadecenoic, and hexadecadienoic acid glucuronides which appear to be beta-oxidation products of the C18 fatty acids were also observed, with the major species being 10, 11-dihydroxy-7-hexadecenoic acid glucuronide. In all, 16 C16 and C18 dihydroxy fatty acids were identified by gas chromatography-mass spectrometry. A series of at least 11 trihydroxy fatty acids was also observed but not fully characterized. Measurement of these compounds may prove to be useful in the diagnosis of some peroxisomal disorders.

Child↗
PubMed1994

Red blood cell membrane dynamics in schizophrenia. II. Fatty acid composition.

Fatty acid compositions were determined in red blood cell (RBC) ghost membranes of schizophrenic patients before and after haloperidol withdrawal, as well as with age-matched normal male control subjects (n = 22). Patients on haloperidol (HD) received treatment in doses between 5 and 20 mg/day for at least 5 weeks (n = 24). Drug-free patients (n = 19) were free of all psychotropic medications for an average of 40 days. A highly significant decrease in the levels (nmol/ml packed RBC) of polyunsaturated fatty acids (PUFAs), particularly 18:2(n - 6) and 20:4(n - 6), was found in both HD-treated and drug-free patients. This decrease remained in those patients who had withdrawn from HD for more than 5 weeks (n = 10). Concomitantly, the percentage of saturated and monoenoic fatty acids to total fatty acids increased significantly in schizophrenic patients. The resultant fatty acid profile consequently lowers the unsaturation index (UI), which represents the average number of double bonds per fatty acid molecule, in RBC ghost membranes of schizophrenic patients. Furthermore, the decreases in UI were significantly correlated to the increases in "structure order" of RBC ghost membranes as measured by the steady-state fluorescence anisotropy (rs) in normal control and drug-free schizophrenic subjects. Therefore, it is likely that decreased levels of PUFAs in schizophrenic patients might result from a defective uptake of 18:2(n - 6) into RBC membrane phospholipids. Since fatty acid composition of membrane phospholipids affects the relative degree of membrane fluidity, the present results lend further support that RBC membrane dynamics are altered in schizophrenia.

Adult↗
PubMed1991

Dietary n-6 fatty acids inhibit the incorporation of dietary n-3 fatty acids in thrombocyte and serum phospholipids in humans: a controlled dietetic study.

The effect of a high dietary intake of n-6 fatty acids (36 g daily) vs a low intake (4-6 g daily) on the incorporation of fatty acids from a dietary supplementation of n-3 fatty acids (6 g daily) was studied for 8 weeks in 15 healthy, normolipaemic volunteers. The importance of a high (43.6) vs a low (20.6) energy percentage from fat was also investigated in the participants on a low n-6 intake. Fatty acid analyses of serum and thrombocyte phospholipids showed a marked increase in docosahexaenoic acid (22:6 (n-3), DHA) and especially eicosapentaenoic acid (20:5 (n-3), EPA) in both the high and low n-6 groups after 14 days, but the changes were significantly greater in the low n-6 diet groups. Changes of the ratio between EPA and arachidonic acid (20:4 (n-6), AA) in phospholipids followed an identical pattern in serum and thrombocytes. This indicates that thrombocytes are influenced by the fatty acid composition in serum. The results showed that incorporation of n-3 fatty acids in phospholipids was reduced by a high intake of dietary n-6 fatty acids in the cells and lipid fractions studied. The observed effect of dietary n-6 fatty acids was independent of the energy percentage provided by dietary fat. In order to obtain an optimal effect of n-3 supplementation, the intake of linoleic acid has to be considered and kept at a low level. The serum content of cholesterol was unaffected, but the concentration of triacylglycerol was reduced during the supplementation period.

Adult↗
PubMed1980

Effects of exogenous fatty acid concentration on glucagon-induced changes in hepatic fatty acid metabolism.

Studies were conducted to clarify the relationship between the external fatty acid concentration and glucagon in the regulation of hepatic fatty acid metabolism. Hepatocytes from fed rats were incubated with increasing concentrations of oleate (up to 1 mM) in the presence and absence of glucagon and the time sequence of changes in cellular malonyl-CoA levels, fatty acid synthesis, fatty acid oxidation, and ketogenesis were measured. At low concentrations of fatty acid the effect of glucagon was to abolish malonyl-CoA synthesis and lipogenesis and to produce a marked stimulation of fatty acid oxidation and ketogenesis. Similar effects were obtained with high concentrations of fatty acid in the absence of glucagon and, under these conditions, the additional presence of the hormone produced little further response. The results are consistent with the concept that the rate of fatty acid oxidation in liver is dictated largely by the relative concentrations of long-chain acyl-CoA (substrate for carnitine acyltransferase I) and malonyl-CoA (inhibitor of the transferase). They also indicate that the preemptive effect of fatty acids on glucagon-induced changes in fatty acid metabolism stems from their ability to reduce the tissue malonyl-CoA content, probably through long-chain acyl-CoA suppression of acetyl-CoA carboxylase.

Animals↗
PubMed1997

Diet-induced changes in liver and bile but not brain fatty acids can be predicted from differences in plasma phospholipid fatty acids in formula- and milk-fed piglets.

The fatty acid composition of plasma phospholipids differs between infants fed formula and infants fed human milk, but the extent to which this is accompanied by differences in tissue phospholipid fatty acids is unclear. This paper describes analysis of plasma, liver and brain fatty acids from piglets fed one of seven formulas, varying in saturated, monounsaturated, (n-6) and (n-3) fatty acids or sow milk from birth for 18 d. Bile fatty acids were analyzed because they are secreted from liver and may be an important source of fatty acids for intestinal lipoprotein synthesis. The results were used to determine the relation between diet-related differences in plasma phospholipid fatty acids and those in brain, liver and bile. Where significant associations were found, prediction limits were constructed to assess the usefulness of analysis of plasma phospholipid fatty acids to predict diet-induced changes in tissue fatty acids. The proportions (g/100 g fatty acids) of 16:0, 18:0, 18:1, 18:2(n-6) and 20:4(n-6) in plasma phospholipids were significantly associated with the proportions of the same fatty acids in liver and bile, but not brain. The results show a reasonably precise, predictable association between plasma and liver, and plasma and bile fatty acids. Brain 20:4(n-6) and 22:6(n-3), in contrast, were not reliably associated with plasma phospholipid 20:4(n-6) and 22:6(n-3) for piglets fed milk or formula providing about 1.5% energy as 18:3(n-3).

Animal Feed↗
PubMed1999

Structure and dynamics of the fatty acid binding cavity in apo rat intestinal fatty acid binding protein.

The structure and dynamics of the fatty acid binding cavity in I-FABP (rat intestinal fatty acid binding protein) were analyzed. In the crystal structure of apo I-FABP, the probe occupied cavity volume and surface are 539+/-8 A3 and 428 A2, respectively (1.4 A probe). A total of 31 residues contact the cavity with their side chains. The side-chain cavity surface is partitioned according to the residue type as follows: 36-39% hydrophobic, 21-25% hydrophilic, and 37-43% neutral or ambivalent. Thus, the cavity surface is neither like a typical protein interior core, nor is like a typical protein external surface. All hydrophilic residues that contact the cavity-with the exception of Asp74-are clustered on the one side of the cavity. The cavity appears to expand its hydrophobic surface upon fatty acid binding on the side opposite to this hydrophilic patch. In holo I-FABP the fatty acid chain interactions with the hydrophilic side chains are mediated by water molecules. Molecular dynamics (MD) simulation of fully solvated apo I-FABP showed global conformational changes of I-FABP, which resulted in a large, but seemingly transient, exposure of the cavity to the external solvent. The packing density of the side chains lining the cavity, studied by Voronoi volumes, showed the presence of two distinctive small hydrophobic cores. The MD simulation predicts significant structural perturbations of the cavity on the subnanosecond time scale, which are capable of facilitating exchange of I-FABP internal water.

Animals↗
PubMed1986

Inhibition of fatty acid mobilization by arterial free fatty acid concentration.

Subcutaneous, inguinal adipose tissue from dogs was perfused with blood in which the free fatty acid (FFA) concentration was varied corresponding to FFA/albumin molar ratios between 1 and 6. Otherwise the composition of the perfusate was kept constant. In order to stimulate lipolysis, isoprenaline and theophyllamine were added to the perfusate. A raise in arterial FFA/albumin molar ratio was without influence on lipolysis (as reflected in the release of glycerol), but reduced the FFA release indicating an increased re-esterification. At FFA/albumin ratios above 3 a marked increase in vascular resistance was seen. This increase was partly reversible within the time of a perfusion. When lipolysis is stimulated in the intact organism, the effects of increasing arterial FFA/albumin ratio on re-esterification and vascular resistance may serve as feedback mechanisms regulating FFA mobilization.

Adipose Tissue↗
PubMed1998

Effects of feeding Lunaria oil rich in nervonic and erucic acids on the fatty acid compositions of sphingomyelins from erythrocytes, liver, and brain of the quaking mouse mutant.

Feeding an oil from Lunaria biennis rich in 22:1n-9 and 24:1n-9 to homozygous quaking (qk.qk) mice caused a large increase in the percentage of 24:1n-9 and corresponding decreases in the percentage of 24:0 and 22:0 in sphingomyelins from liver, erythrocytes, and milk. Brain sphingomyelin from 2-wk-old qk.qk pups born to qk.qk mothers maintained on the Lunaria oil had essentially normal percentage of 24:1n-9 and 18:0, in contrast to pups born to mothers maintained on a control oil rich in 18:1n-9 whose brain sphingomyelin had a markedly reduced percentage of 24:1n-9 and an increased percentage of 18:0. After 2 wk and up to and beyond weaning, the qk.qk pups from Lunaria-fed mothers weaned on to the Lunaria diet had a markedly decreased percentage of 24:1n-9 in their brain sphingomyelin, accompanied by an increased percentage of 18:0, as compared to heterozygous quaking mice. However, the percentage of 24:1n-9 in brain sphingomyelin in qk.qk pups weaned on to the Lunaria diet continued throughout this period (2-8 wk postbirth) to be significantly higher than in qk.qk pups weaned on to the control diet. We conclude that dietary 24:1n-9 influences the fatty acid composition of brain sphingomyelin in qk.qk mice, but only via the mother in pre- or early postnatal animals. We further consider that the dietary effects may be elicited mainly in the sphingomyelin of nonmyelinated brain cells, and that the nervonic acid in myelin sphingomyelin may be formed mainly by chain elongation in oligodendrocytes from shorter chain fatty acid precursors.

Animal Nutritional Physiological Phenomena↗
PubMed2003

Supplementation with fish oil affects the association between very long-chain n-3 polyunsaturated fatty acids in serum non-esterified fatty acids and soluble vascular cell adhesion molecule-1.

We have investigated the effect of fish oil supplementation on the association between serum non-esterified fatty acid (NEFA) pattern and atherosclerotic activity. We studied correlations between serum non-esterified very long-chain eicosapentaenoic (EPA), docosahexaenoic acid (DHA) and arachidonic acid (AA) and biochemical markers of endothelial activation before and after 18-months intervention with fish oil supplementation. The fish oil supplementation consisted of 2.4 g of EPA and DHA per day, with corn oil as placebo. Elderly men ( n =171) with high risk for coronary heart disease were divided into four intervention groups in a factorial design: fish oil supplementation ( n =44), dietary intervention ( n =42), fish oil supplementation+dietary intervention ( n =47) or placebo ( n =38). The composition of fasting NEFA was analysed before and after intervention by GLC. Circulating endothelial markers were analysed by ELISA. A statistically significant positive correlation between the change in serum non-esterified DHA and soluble vascular cell adhesion molecule-1 (sVCAM-1) was found in the pooled group that received fish oil supplementation ( n =91; Spearman's correlation coefficient r =0.24, P =0.02). No such correlation was found in the pooled group without fish oil supplementation ( n =80). Furthermore, there was a significant negative correlation between the change in serum non-esterified EPA and the relative change in sVCAM-1 in the group that did not receive fish oil supplementation ( r =-0.34, P =0.002). No such correlation was found in the group with fish oil supplementation. We conclude that large increase in serum non-esterified EPA and DHA, which can only be attained by supplementation, might increase inflammation in vascular endothelium. A moderate dietary increase in fish oil intake may, however, have an effect on decreasing inflammatory markers.

Aged↗
PubMed1979

Effects of essential fatty acid deficiency, and various levels of dietary polyunsaturated fatty acids, on humoral immunity in mice.

Six experiments were conducted to determine the influence of an essential fatty acid deficient diet (EFAD), and various levels of dietary polyunsaturated fatty acids, on humoral immunity in mice. The results indicated that: 1) Consumption of diets deficient in essential fatty acids (0% corn oil) significantly reduced the humoral response. This reduction was demonstrated after feeding the essential fatty acid deficient diet for only 28 days; and preceded the effects of essential fatty acid deficiency on growth or appearance. 2) Reduced antibody response was demonstrated against T-cell dependent and T-cell independent antigens, and in both primary and secondary responses of mice fed the essential fatty acid deficient diet. 3) After 56 days of feeding the EFAD diet (0% corn oil), mice switched to the control diet (13% corn oil) for 7 days demonstrated full recovery of the humoral response. 4) Diets containing various levels of polyunsaturated fatty acids (from 2 to 70% of energy from corn oil) did not adversely affect the humoral response. The results support the hypothesis that essential fatty acids play a crucial role in maintaining the functional integrity of humoral immunity.

Animals↗
PubMed2002

Differential modulation of Toll-like receptors by fatty acids: preferential inhibition by n-3 polyunsaturated fatty acids.

Human subjects consuming fish oil showed a significant suppression of cyclooxygenase-2 (COX-2) expression in blood monocytes when stimulated in vitro with lipopolysaccharide (LPS), an agonist for Toll-like receptor 4 (TLR4). Results with a murine monocytic cell line (RAW 264.7) stably transfected with COX-2 promoter reporter gene also demonstrated that LPS-induced COX-2 expression was preferentially inhibited by docosahexaenoic acid (DHA, C22:6n-3) and eicosapentaenoic acid (EPA, C20:5n-3), the major n-3 polyunsaturated fatty acids (PUFAs) present in fish oil. Additionally, DHA and EPA significantly suppressed COX-2 expression induced by a synthetic lipopeptide, a TLR2 agonist. These results correlated with the preferential suppression of LPS- or lipopeptide-induced NF kappa B activation by DHA and EPA. The target of inhibition by DHA is TLR itself or its associated molecules, but not downstream signaling components. In contrast, COX-2 expression by TLR2 or TRL4 agonist was potentiated by lauric acid, a saturated fatty acid. These results demonstrate that inhibition of COX-2 expression by n-3 PUFAs is mediated through the modulation of TLR-mediated signaling pathways. Thus, the beneficial or detrimental effects of different types of dietary fatty acids on the risk of the development of many chronic inflammatory diseases may be in part mediated through the modulation of TLRs.

Animals↗
PubMed2005

Fatty acid synthesis is a target for antibacterial activity of unsaturated fatty acids.

Long-chain unsaturated fatty acids, such as linoleic acid, show antibacterial activity and are the key ingredients of antimicrobial food additives and some antibacterial herbs. However, the precise mechanism for this antimicrobial activity remains unclear. We found that linoleic acid inhibited bacterial enoyl-acyl carrier protein reductase (FabI), an essential component of bacterial fatty acid synthesis, which has served as a promising target for antibacterial drugs. Additional unsaturated fatty acids including palmitoleic acid, oleic acid, linolenic acid, and arachidonic acid also exhibited the inhibition of FabI. However, neither the saturated form (stearic acid) nor the methyl ester of linoleic acid inhibited FabI. These FabI-inhibitory activities of various fatty acids and their derivatives very well correlated with the inhibition of fatty acid biosynthesis using [(14)C] acetate incorporation assay, and importantly, also correlated with antibacterial activity. Furthermore, the supplementation with exogenous fatty acids reversed the antibacterial effect of linoleic acid, which showing that it target fatty acid synthesis. Our data demonstrate for the first time that the antibacterial action of unsaturated fatty acids is mediated by the inhibition of fatty acid synthesis.

Anti-Bacterial Agents↗
PubMed2005

Effect of randomly interesterified triacylglycerols containing medium- and long-chain fatty acids on energy expenditure and hepatic fatty acid metabolism in rats.

In our previous studies, medium- and long-chain triacylglycerols (MLCT), randomly interesterified triacylglycerols containing medium-chain and long-chain fatty acids in the same glycerol molecule, significantly reduced body fat accumulation in humans and rats. To clarify mechanism(s) for this effect of MLCT, we measured energy expenditure and hepatic fatty acid metabolism in rats by comparison with long-chain triacylglycerols (LCT) or medium-chain triacylglycerols (MCT). MLCT, compared with LCT, showed significantly lower body fat accumulation, higher 24-h energy expenditure and acyl-CoA dehydrogenase activity measured using octanoyl-CoA as a substrate, and similar lipogenic activity. MCT, compared with LCT, showed significantly higher energy expenditure, but fat accumulation was comparable. Additionally, MCT exhibited significantly higher lipogenic activity than the other oils. These data suggest that enhancement of energy expenditure and medium-chain fatty acids (MCFA) oxidation without activating de novo lipogenesis are responsible at least for the lower body fat accumulation in rats fed MLCT. The activation of hepatic lipogenesis by excessive intake of MCFA might counteract their preventive effects on body fat accumulation.

Acyl-CoA Dehydrogenase↗