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PubMed1993

Arachidonic acid and other unsaturated fatty acids alter membrane potential in PC12 and bovine adrenal chromaffin cells.

The action of arachidonic acid and other fatty acids on membrane potential in PC12 and bovine chromaffin cells was investigated using a membrane potential-sensitive fluorescent dye. Arachidonic acid (1-40 microM) provoked dose-dependent membrane hyperpolarization, thereby reducing hyperpolarization induced by the K(+)-selective ionophore valinomycin. Other cis-unsaturated fatty acids, but not lipoxygenase products or the saturated fatty acid palmitic acid, also affected membrane potential. Tetraethylammonium blocked the arachidonic acid-induced hyperpolarization. These data suggest that cis-unsaturated fatty acids alter membrane potential in PC12 and bovine chromaffin cells by modulating K+ conductances. Valinomycin-generated hyperpolarization had no effect on agonist-induced Ca2+ influx into bovine chromaffin cells, whereas preincubation with arachidonic acid and other cis-unsaturated fatty acids blocked Ca2+ influx and secretion. We propose a model where internally generated fatty acids act as a feedback to desensitize the stimulated cell via inhibition of receptor-dependent Ca2+ influx and induction of membrane hyperpolarization.

Animals↗
PubMed1988

Magnesium deprivation or short-term essential fatty acid deficiency in rats: effects on serum lipids, platelet fatty acid composition and arachidonic acid incorporation into platelet phospholipids.

The aim of this study was to evaluate the effect of short-term magnesium or essential fatty acid (EFA) deficiencies on plasma lipids, platelet fatty acid composition and [1-14C] arachidonic acid incorporation into platelet phospholipids. Weanling rats were fed purified diets (casein 20%, sucrose 70.5%, lipid 5%) for two weeks. The control and magnesium-deficient diets included corn oil as lipid source. The EFA-deficient diet included hydrogenated coconut oil. The fatty acid composition of serum lipids confirmed the linoleic acid deprivation in the EFA-deficient group. Significant changes in platelet fatty acid composition occurred in this limited period of time and arachidonic acid incorporation into platelet lipids was markedly increased. Magnesium deficiency induced hyperlipaemia. A significant decrease in the percentage of arachidonic acid in total serum lipids was observed, but fatty acid profile appeared quite different in the two deficiencies. In magnesium-deficient rats, the alteration in fatty acid composition of serum lipids was not associated with similar changes in fatty acid composition of platelet lipids. Arachidonic acid incorporation into platelet lipids was markedly increased in magnesium deficient animals as compared to control group. Relatively more arachidonic acid was incorporated into phosphatidylcholine and phosphatidylinositol when magnesium-deficient or EFA-deficient animals were compared to the control group.

Animals↗
PubMed1985

"Ex vivo" influence of fatty acids from plasma cholesterol and triglycerides on the fatty acid pattern of platelets.

We have studied "ex vivo", in 92 normal subjects, the influence of fatty acids (FA) that esterify plasma cholesterol and triglycerides on the fatty acid composition of phospholipids, triglycerides and free fatty acid fractions in platelets. High and significant correlations (p less than 0.001) were found for some of the platelet phospholipid FA and the same FA that esterify plasma cholesterol [18:1 (r = 0.56); 18:2 (r = 0.71) and 20:5 (r = 0.42)] and plasma triglycerides [18:1 (r = 0.57) and 18:2 (r = 0.66)]. Some significant correlations were also found between some of the platelet triglyceride FA and the same FA that esterify plasma phospholipids [18:1 (r = 0.58)], triglycerides [18:1 (r = 0.51), 18:2 (r = 0.52)] cholesterol [18:1 (r = 0.44)] and plasma free fatty acids [18:1 (r = 0.39); 18:2 (r = 0.40)]. By evaluating these results in conjunction with those of an earlier study, it can be concluded that "in vivo" the FA from different plasma lipid fractions and especially those esterifying the plasma cholesterol and phospholipid fractions, can influence the FA composition of platelet phospholipids in normal subjects. In trying to interpret the role played by plasma lipids in platelet lipids, it may be of interest to take into account the interrelationships found in this study.

Adult↗
PubMed2006

Effect of n-3 and n-6 polyunsaturated fatty acids on lymphocyte proliferation, interleukin production and phospholipid fatty acids composition in type 2 diabetic and healthy subjects in Jordan people.

Dietary lipid manipulation may affect a great number of immune parameters, such as lymphocyte proliferation, cytokine synthesis. In this study, lymphocytes of diabetic type 2 were incubated with different polyunsaturated fatty acid (docosahexaenoic, eicosapentaenoic, arachidonic acid) for investigated their effect on lymphoproliferation response, the concentration of interleukin 2 produced in each essay and phospholipid fatty acid composition of lymphocyte membrane. Our results found that the concanavalin A and insulin increase significantly the proliferative response while eicosapentaenoic, arachidonic and docosahexaenoic acid inhibited that by different degrees: 47%, 37% and 19%, respectively, for healthy subjects and 39%, 29% and 13% for diabetes. However, the concentration of IL-2 produced in presence of either docosahexaenoic, eicosapentaenoic or arachidonic acid was significantly reduced by 36%, 32% and 39%, respectively, in controls while 16%, 15% and 23%, respectively, in diabetics. On the other hand, the tested fatty acids demonstrated a major impact on the fatty acid composition of different phospholipid fractions of lymphocyte membrane but these fractions were different in their response to each fatty acid examined. For instance, the addition of docosahexaenoic acid to culture media was accompanied with a predominant composition of docosahexaenoic acid in phospholipid fractions. Also, our results showed a notable increased proportion of arachidonic, eicosapentaenoic and docosahexaenoic acids in control phospholipid fractions than those of diabetic.

Arachidonic Acid↗
PubMed1980

Stereochemistry in the formation of 9-hydroxy-10,12-octadecadienoic acid and 13-hydroxy-9,11-octadecadienoic acid from linoleic acid by fatty acid cyclooxygenase.

9-Hydroxy-10,12-octadecadienoic acid and 13-hydroxy-9,11-octadecadienoic acid are formed from linoleic acid upon incubation with the microsomal fraction of homogenates of the sheep vesicular gland (Hamberg, M. and Samuelsson, B. (1967) J. Biol. Chem. 242, 5344-5354. This communication is concerned with the stereochemical aspects of the conversion. The ratio between the 9- and 13-hydroxy isomers was 77:23. Steric analysis of the individual isomers showed that the hydroxyl group of both isomers had mainly the L configuration, i.e. 9L:9D, 79:21 and 13L:13D, 9- and 13-hydroxyoctadecadienoates which had largely lost the tritium label (6% and 7% retention of tritium relative to precursor, respectively) showing that the hydrogen which is removed from C-11 during the conversion has the L (pro-S) configuration.

Animals↗
PubMed2000

Bronchial asthma: information on phytotherapy with essential fatty acids. Interactions between essential fatty acids and steroid hormones.

The pharmacological treatment of bronchial asthma is based on the inhalation of bronchodilative beta2 agonists and steroid hormones. In view of the therapeutic successes obtained with evening primrose oil in the treatment of neurodermatitis in children, the question arises whether this phytotherapeutic substitution therapy could at least partly replace symptomatic pharmacotherapy in bronchial asthma. It is shown that this will only be successful if one dispenses with the anti-inflammatory effect of the treatment with steroid hormones.

Asthma↗
PubMed1997

Dietary supplementation with gamma-linolenic acid alters fatty acid content and eicosanoid production in healthy humans.

To understand the in vivo metabolism of dietary gamma-linolenic acid (GLA), we supplemented the diets of 29 volunteers with GLA in doses of 1.5-6.0 g/d. Twenty-four subjects ate controlled eucaloric diets consisting of 25% fat; the remaining subjects maintained their typical Western diets. GLA and dihomo-gamma-linolenic acid (DGLA) increased in serum lipids of subjects supplemented with 3.0 and 6.0 g/d; serum arachidonic acid increased in all subjects. GLA supplementation with 3.0 and 6.0 g/d also resulted in an enrichment of DGLA in neutrophil phospholipids but no change in GLA or AA levels. Before supplementation, DGLA was associated primarily with phosphatidylethanolamine (PE) of neutrophil glycerolipids, and DGLA increased significantly in PE and neutral lipids after GLA supplementation. Extending the supplementation to 12 wk did not consistently change the magnitude of increase in either serum or neutrophil lipids in subjects receiving 3.0 g/d. After GLA supplementation, A23187-stimulated neutrophils released significantly more DGLA, but AA release did not change. Neutrophils obtained from subjects after 3 wk of supplementation with 3.0 g/d GLA synthesized less leukotriene B4 (P < 0.05) and platelet-activating factor. Together, these data reveal that DGLA, the elongase product of GLA, but not AA accumulates in neutrophil glycerolipids after GLA supplementation. The increase in DGLA relative to AA within inflammatory cells such as the neutrophil may attenuate the biosynthesis of AA metabolites and may represent a mechanism by which dietary GLA exerts an anti-inflammatory effect.

8,11,14-Eicosatrienoic Acid↗
PubMed1984

Inhibition of fatty acid oxidation and decrease of oxygen consumption of working rat heart by 4-bromocrotonic acid.

Nonesterified fatty acids (NEFA), glucose and lactate are major fuels for myocardial energy production. The ratio of energy produced and oxygen consumed, which can be expressed as ATP/O ratio, is different for each substrate: e.g. 3.17 for glucose and 2.83 for palmitate. Direct measurements, however, have shown that the difference of oxygen consumption is about twice as great as theoretically expected. This difference is of little significance under aerobic conditions, but may be important when oxygen supply is restricted. Numerous attempts have been made to reduce oxygen consumption by activating carbohydrate oxidation or inhibiting fatty acid metabolism. As the rate of fatty acid oxidation has been shown to depend on arterial concentrations of NEFA and albumin, this may be one point of control. Further approaches such as increasing the arterial levels of glucose, insulin and potassium, have been controversially discussed. As 4-bromocrotonic acid has been found to inhibit the fatty acid oxidation in isolated rat heart mitochondria [8], this might be an effective agent to save oxygen by reducing the rate of fatty acid oxidation in intact hearts.

Animals↗
PubMed1996

Very-long-chain n-3 fatty acids as biomarkers for intake of fish and n-3 fatty acid concentrates.

We examined how supplementation with very-long-chain n-3 fatty acids was reflected in the concentration of these fatty acids in plasma phospholipids of 363 Norwegian men and women. The concentration of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) in plasma phospholipids was significantly higher among individuals supplemented with n-3 fatty acids after the supplementation period than before. We also examined the relation between dietary intake of fatty acids measured with a 180-item quantitative food-frequency questionnaire and the concentration of the same fatty acids in plasma phospholipids in 579 men and women. Correlation coefficients between plasma phospholipid fatty acids and dietary intake of fatty acids were 0.51 and 0.49 for EPA and DHA, respectively. The correlation between fish intake and n-3 fatty acids in plasma phospholipids was 0.37. These results suggest that dietary intake measured with our food-frequency questionnaire may be used to predict the biological availability of some of the essential n-3 fatty acids.

Adolescent↗
PubMed1995

Lipolysis-induced partitioning of free fatty acids to lipoproteins: effect on the biological properties of free fatty acids.

Free fatty acids (FFA) released during the lipolysis of triglyceride (TG)-rich lipoproteins in vivo are generally believed to be bound to serum albumin. When hypertriglyceridemic (HTG) sera were lipolyzed in vitro by purified bovine milk lipoprotein lipase (LpL), there was an 11- to 18-fold increase in serum FFA levels, and a major portion (> 80%) of the FFA in serum was partitioned to lipoprotein fractions. The greatest portion (33%) of FFA in lipolyzed HTG serum was associated with newly formed flocculent remnants that banded just below low density lipoproteins (LDL) in the density gradient tube. Very low density lipoprotein (VLDL), LDL, and high density lipoprotein (HDL) fractions in lipolyzed HTG serum contained 18- to 29-times more FFA molecules than those in prelipolysis serum. Analysis of the fatty acyl chain composition of FFA in lipolyzed HTG serum showed that the extent of partitioning of saturated FFA into the lipoprotein fractions relative to that of polyunsaturated FFA was about 4.5- to 11-times greater than that partitioned into the free protein fraction; most (84%) of FFA partitioned into flocculent remnants were saturated fatty acids. In vivo lipolysis of TG-rich lipoproteins in HTG subjects, induced by heparinization, resulted in only a small (2.8-fold) increase in serum FFA and little or no increase in the partitioning of FFA to lipoproteins. However, in vitro incubation of the postheparin serum at 37 degrees C for 90 min resulted in a 2.9- to 6.8-fold increase in the serum FFA level and the partitioning of > 66% of total serum FFA into lipoprotein fractions. Studies of the interaction of various plasma fractions from control and in vitro lipolyzed HTG serum with cultured mouse peritoneal macrophages (MPM) showed that FFA partitioned to lipoprotein fractions were highly cytotoxic to cultured MPM, whereas FFA partitioned to albumin at a 10 x greater concentration were not cytotoxic. The cytotoxic potencies of FFA bound to lipoproteins and albumin were further compared after in vitro incorporation of FFA (oleic acids) into LDL and to albumin. FFA bound to LDL but not to albumin were cytotoxic to cultured MPM; the cytotoxicity of FFA bound to LDL was more closely related to the FFA to LDL-cholesterol molar ratio than to the total FFA concentration in the culture dish. The ability of FFA bound to LDL and albumin to induce foam cell formation was studied in THP-1 monocyte-derived macrophages, which were less susceptible to cytotoxicity produced by FFA bound to LDL than MPM.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1975

Fatty acid biosynthesis in Erlich cells. The mechanism of short term control by exogenous free fatty acids.

We have examined the mechanism by which extracellular free fatty acids regulate fatty acid biosynthesis in Ehrlich ascites tumor cells. De novo biosynthesis in intact cells was inhibited by stearate greater than oleate greater than palmitate greater than linoleate. The amount of citrate and long chain acyl-CoA in the cells was not changed appreciably by the addition of free fatty acids to the incubation medium, indicating than free fatty acids do not regulate fatty acid biosynthesis by changing the total intracellular content of these metabolites. By measuring the incorporation of labeled free fatty acids into acyl-CoA, however, it was determined that the fatty acid composition of the acyl-CoA poolwas changed dramatically to reflect the composition of the exogenous free fatty acids. The relative inhibitory effects of different free fatty acids appear to depend on the ability of their acyl-CoA derivatives to regulate acyl-CoA carboxylase activity. The acyl-CoA concentration needed to produce 50% inhibition of purified Ehrlich cell carboxylase was found to be 0.68 mum for stearoyl-CoA, 1.6 mum for oleoyl-CoA, 2.2 mum for palmitoyl-CoA, 23 mum for myristoyl-CoA, 30 mum for lauroyl-CoA, and 37 mum for linoleoyl-CoA. In contrast to their effects on de novo synthesis, all of the free fatty acids added except stearate stimulated chain elongation in intact cells. Microsomal chain elongation, the major system for elongation in Ehrlich cells, also was regulated by the composition of the cellular acyl-CoA pool. Lauroyl-CoA, myristoyl-CoA, and palmitoyl-CoA were good substrates for elongation by isolated microsomes; oleoyl-CoA, and linoleoyl-CoA were intermediate; and stearoyl-CoA was a very poor substrate. We conclude that free fatty acids regulate fatty acid biosynthesis by changing the composition of the cellular acyl-CoA pool. These changes control the rate of malonyl-CoA production and, because of the acyl-CoA substrate specificity of the microsomal elongation system, modulate the amount of malonyl-CoA used for chain elongation.

Acetyl Coenzyme A↗
PubMed2006

Translocation of long chain fatty acids across the plasma membrane--lipid rafts and fatty acid transport proteins.

Translocation of long chain fatty acids across the plasma membrane is achieved by a concert of co-existing mechanisms. These lipids can passively diffuse, but transport can also be accelerated by certain membrane proteins as well as lipid rafts. Lipid rafts are dynamic assemblies of proteins and lipids, that float freely within the two dimensional matrix of the membrane bilayer. They are receiving increasing attention as devices that regulate membrane function in vivo and play an important role in membrane trafficking and signal transduction. In this review we will discuss how lipid rafts might be involved in the uptake process and how the candidate proteins for fatty acid uptake FAT/CD36 and the FATP proteins interact with these domains. We will also discuss the functional role of FATPs in general. To our understanding FATPs are indirectly involved in the translocation process across the plasma membrane by providing long chain fatty acid synthetase activity.

Animals↗
PubMed1993

cis-9,cis-15-octadecadienoic acid: a novel fatty acid found in higher plants.

An unusual fatty acid, cis-9,cis-15-octadecadienoic acid, has been identified in the pulp lipids of mango (Mangifera indica L.) grown in the Philippines. To our knowledge, the occurrence of cis-9,cis-15-octadecadienoic acid in higher plant lipids has not been previously reported. The structure confirmation was based on the results of chromatographic (capillary GC, argentation thin-layer) and spectrometric (GC-MS, infrared, ultraviolet) analysis and chemical treatment. This butylene-interrupted dienoic fatty acid is concentrated in the pulp part of mango fruit and occupies 5.4% of total acyl groups in the pulp lipids; whereas a common octadecadienoic acid, linoleic acid, is a minor component (1.1%) in the same lipids. If a trivial name is desired, it is suggested that cis-9,cis-15-octadecadienoic acid be called "mangiferic" acid.

Chromatography, Gas↗
PubMed1992

Arachidonic acid regulates unsaturated fatty acid synthesis in lymphocytes by inhibiting stearoyl-CoA desaturase gene expression.

This work was based upon the observation that a reduction in the level of serum, provided to murine lymphocytes in culture, augmented endogenous unsaturated fatty acid (UFA) synthesis. Since the phospholipids of BW5147 cells grown in 1% serum were especially deficient in arachidonic acid (20:4), and given the findings of previous workers, we suspected that the availability of exogenous 20:4 in serum might correlate with the squelching of UFA synthesis. Indeed, after a 5 h exposure to 4-28 microM 20:4, the 20:4 content of BW5147 cell phospholipids increased from 1% to 15% of the total fatty acids with a coincident reduction in 18:1 synthesis to approx. 30% of starting values. Subsequent studies were done to define the mechanism by which 20:4 down-regulates 18:1 synthesis. The results indicated that 20:4 inhibited endogenous 18:1 synthesis by reducing stearoyl-CoA desaturase (SCD) enzyme activity. Moreover, as determined by Northern blot analyses, the inhibitory effect of 20:4 on stearoyl-CoA desaturase activity coincided with decreased stearoyl-CoA desaturase mRNA levels. Exposure of BW5147 cells to either 20:4, actinomycin D, or both, resulted in a temporal decay of stearoyl-CoA desaturase mRNAs with half-lives ranging from 4.0 h to 4.4 h. Such a similarity in decay times implied that 20:4 regulates stearoyl-CoA desaturase expression by inhibiting transcription. This was confirmed by nuclear run-on studies in which 20:4 was found to inhibit transcription of nascent stearoyl-CoA desaturase mRNA. Collectively, these findings implicate 20:4 as an important regulator of stearoyl-CoA desaturase gene expression, and hence UFA synthesis, in lymphoid cells.

Animals↗