Journal articles on the topic 'Phospholipid fatty acid'
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1
Rudzite, Vera, Edite Jurika, Gabriele Baier-Bitterlich, Helmut Wachter, and Dietmar Fuchs. "Effect of Sepiapterin, 7,8-Dihydrobiopterin, 5,6,7,8-Tetrahydrobiopterin and Xanthopterin on Cholesterol and Phospholipid Content and Phospholipid Biosynthesis in vitro." Pteridines 6, no. 2 (May 1995): 69–73. http://dx.doi.org/10.1515/pteridines.1995.6.2.69.
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Summary Incorporation of fatty acids into phospholipids has been investigated using samples of rat live tissue homogenate, Krebs-Ringer-phosphate buffer (pH = 7A) containing 0.3% albumin, farry acid mixture and glycerol. The addition of sepiapterin, 7,8-dihydrobiopterin and 5.6.7.8-tetrahydrobiopterin (5 and 30 pmol g wet weight) to incubation medium induced a decrease of saturated (stearic acid) and an increase of polyunsaturated (arachidonic acid) fatty acids incorporation into phospholipids. Cholesterol content decreased, but phospholiplid content did not change in samples containing sepiapterin, 7,8-dihydrobiopterin and 5,6,7,8-tetrahydrobiopterin. No changes of fatty acid incorporation into phospholipids as well as of the content of cholesterol and phospholipids were observed in samples after the addition of xanthopterin (4 and 20 nmol/g wet weight) to incubation medium for phospholipid biosynthesis in vitro. The observations made by incubation with 7,8-dihydrobiopterin, 5,6,7,8-tetrahydrobiopterin and sepiapterin where in opposite to those made earlier employing neopterin and using the same incubation procedure.
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Rudzite, Vera, Edite Jurika, Gilbert Reibnegger, Günter Weiss, Helmut Wachter, and Dietmar Fuchs. "Influence of Kynurenine, Neopterin, Noradrenaline and Pyridoxal-5-Phosphate on Cholesterol and Phospholipid Content and Phospholipid Biosynthesis in vitro." Pteridines 4, no. 3 (August 1993): 126–30. http://dx.doi.org/10.1515/pteridines.1993.4.3.126.
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Summary Incorporation of fatty acids into phospholipids has been investigated using samples of rat liver tissue homogenate, Krebs-Ringer-phosphate buffer (pH = 7.4) containing 0.3% albumin, fatty acid mixture and glyceroL The addition of L-kynurenine (4 nmol/g wet weight), D-eryhro-neopterin (5 and 30 pmol/g wet weight) and noradrenaline (4 nmol/g wet weight) to incubation medium induced an increase of saturated (palmitic acid) and decrease of poly-unsaturated (linoleic and arachidonic acid) fatty acids incorporation into phospholipids. The increase of saturated fatty acids incorporation into phospholipids was more pronounced after addition of neopterin and noradrenaline to the incubation medium while the decrease of linoleic and arachidonic acid synthesis was stimulated most with kynurenine. Moreover, kynurenine stimulated whereas neopterin depressed the oleic acid incorporation into phospholipids. These changes of fatty acid incorporation into phospholipids were followed by increase of cholesterol content in samples containing kynurenine, neopterin or noradrenalin. In contrast, phospholipid content decreased in samples containing kynurenine or noradrenalin, hut was not altered by supplementation of neopterin. Since the addition of kynurenine and neopterin to incubation medium for isolated fog heart resulted in an increased noradrenaline and decreased pyridoxal-5-phosphate content in the tissue, we also added pyridoxal-5-phosphate (4 nmol/g wet weight) to incubation medium for phospholipid biosynthesis. No change of the fatty acid incorporation into phospholipids as welI as the content of phospholipids and cholesterol in samples was observed.
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Reibel, D. K., B. O'Rourke, K. A. Foster, H. Hutchinson, C. E. Uboh, and R. L. Kent. "Altered phospholipid metabolism in pressure-overload hypertrophied hearts." American Journal of Physiology-Heart and Circulatory Physiology 250, no. 1 (January 1, 1986): H1—H6. http://dx.doi.org/10.1152/ajpheart.1986.250.1.h1.
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The content and fatty acyl composition of phospholipids were examined in pressure-overload hypertrophied hearts. Cardiac hypertrophy was induced in rats by abdominal aortic constriction. Twenty-one days postconstriction the content of myocardial phosphatidylcholine (PC), sphingomyelin, and phosphatidylinositol (PI) was significantly elevated by 10, 10, and 20%, respectively. The essential fatty acid, linoleic acid, was markedly reduced in PC, phosphatidylethanolamine (PE), PI, and cardiolipin (CL) of hypertrophied hearts. The associated changes in fatty acyl composition were specific for the individual phospholipid class as evidenced by a significant elevation of palmitic acid in PC, docosahexaenoic acid in PE and oleic acid in CL. Alterations in fatty acyl composition of phospholipids were associated with no change in the composition of cardiac triglycerides, cardiac free fatty acids or serum lipids. The fatty acyl composition of phospholipids was also altered in pressure-overload hypertrophied hearts of cats, as evidenced by a reduction of linoleic acid and an elevation of arachidonic acid in total phospholipids. These findings demonstrate that changes in phospholipid metabolism occur in the pressure-overloaded mammalian heart. Such alterations may contribute to altered membrane function in the hypertrophied myocardium.
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Paoletti, Luciana, Ying-Jie Lu, Gustavo E. Schujman, Diego de Mendoza, and Charles O. Rock. "Coupling of Fatty Acid and Phospholipid Synthesis in Bacillus subtilis." Journal of Bacteriology 189, no. 16 (June 8, 2007): 5816–24. http://dx.doi.org/10.1128/jb.00602-07.
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ABSTRACT plsX (acyl-acyl carrier protein [ACP]:phosphate acyltransferase), plsY (yneS) (acyl-phosphate:glycerol-phosphate acyltransferase), and plsC (yhdO) (acyl-ACP:1-acylglycerol-phosphate acyltransferase) function in phosphatidic acid formation, the precursor to membrane phospholipids. The physiological functions of these genes was inferred from their in vitro biochemical activities, and this study investigated their roles in gram-positive phospholipid metabolism through the analysis of conditional knockout strains in the Bacillus subtilis model system. The depletion of PlsX led to the cessation of both fatty acid synthesis and phospholipid synthesis. The inactivation of PlsY also blocked phospholipid synthesis, but fatty acid formation continued due to the appearance of acylphosphate intermediates and fatty acids arising from their hydrolysis. Phospholipid synthesis ceased following PlsC depletion, but fatty acid synthesis continued at a high rate, leading to the accumulation of fatty acids arising from the dephosphorylation of 1-acylglycerol-3-P followed by the deacylation of monoacylglycerol. Analysis of glycerol 3-P acylation in B. subtilis membranes showed that PlsY was an acylphosphate-specific acyltransferase, whereas PlsC used only acyl-ACP as an acyl donor. PlsX was found in the soluble fraction of disrupted cells but was associated with the cell membrane in intact organisms. These data establish that PlsX is a key enzyme that coordinates the production of fatty acids and membrane phospholipids in B. subtilis.
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Calder, P. C., P. Yaqoob, D. J. Harvey, A. Watts, and E. A. Newsholme. "Incorporation of fatty acids by concanavalin A-stimulated lymphocytes and the effect on fatty acid composition and membrane fluidity." Biochemical Journal 300, no. 2 (June 1, 1994): 509–18. http://dx.doi.org/10.1042/bj3000509.
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The fatty acid compositions of the neutral lipid and phospholipid fractions of rat lymph node lymphocytes were characterized. Stimulation of rat lymphocytes with the T-cell mitogen concanavalin A resulted in significant changes in the fatty acid composition of both neutral lipids and phospholipids (a decrease in the proportions of stearic, linoleic and arachidonic acids and an increase in the proportion of oleic acid). Membrane fluidity was measured using nitroxide spin-label e.s.r., and increased during culture with concanavalin A. Culturing the lymphocytes in the absence of mitogen did not affect fatty acid composition or membrane fluidity. The uptake and fate of palmitic, oleic, linoleic and arachidonic acids were studied in detail; there was a time-dependent incorporation of each fatty acid into all lipid classes but each fatty acid had a characteristic fate. Palmitic and arachidonic acids were incorporated principally into phospholipids whereas oleic and linoleic acids were incorporated in similar proportions into phospholipids and triacylglycerols. Oleic acid was incorporated mainly into phosphatidylcholine, palmitic and linoleic acids were incorporated equally into phosphatidylcholine and phosphatidylethanolamine, and arachidonic acid was incorporated mainly into phosphatidylethanolamine. Supplementation of the culture medium with particular fatty acids (myristic, palmitic, stearic, oleic, linoleic, alpha-linolenic, arachidonic, eicosapentaenoic or docosahexaenoic acid) led to enrichment of that fatty acid in both neutral lipids and phospholipids. This generated lymphocytes with phospholipids differing in saturated/unsaturated fatty acid ratio, degree of polyunsaturation, index of unsaturation and n - 6/n - 3 ratio. This method allowed the introduction into lymphocyte phospholipids of fatty acids not normally present (e.g. alpha-linolenic) or usually present in low proportions (eicosapentaenoic and docosahexaenoic). These three n - 3 polyunsaturated fatty acids replaced arachidonic acid in lymphocyte phospholipids. Fatty acid incorporation led to an alteration in lymphocyte membrane fluidity: palmitic and stearic acids decreased fluidity whereas the unsaturated fatty acids increased fluidity. It is proposed that the changes in lymphocyte phospholipid fatty acid composition and membrane fluidity brought about by culture in the presence of polyunsaturated fatty acids are responsible for the inhibition of lymphocyte functions caused by these fatty acids.
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Rudzite, Vera, Edite Jurika, Bernhard Widner, and Dietmar Fuchs. "Similarity Between the Action of Pteridines and Tryptophan Metabolites on Lipid Metabolism." Pteridines 10, no. 3 (August 1999): 133–40. http://dx.doi.org/10.1515/pteridines.1999.10.3.133.
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Abstract Incorporation of fatty acids into phospholipids has been investigated using samples of rat liver tissue homogenate, Krebs-Ringer-phosphate buffer (pH=7.4) containing 0.3% albumin, fatty acid mixture and glycerol. The addition of anthranilic acid (2.2 and 4 nmol/g wet weight), kynurenic acid (4 and 40 nmol/ g wet weight), xanthurenic acid (4 and 40 nmol/g wet weight), picolinic acid (0.2 and 2 nmol/g wet weight) induced an increase of saturated and a decrease of polyunsaturated fatty acids incorporation into phospholipids as well as an eleyation of choksterol concentration in samples used for phospholipid biosynthesis in vitro. These changes were similar to those observed after addition of kynurenine and neopterin to the same test system, An inverse relationship has been observed after addition of nicotinic acid to samples used for phospholipid biosynthesis in vitro. Nicrotinic acid induced .1 decrease of saturated and an increase of unsaturated fatty acids incorporation into phospholipids as well as decrease of cholesterol concentration in samples, These changes were similar to those observed after addition of 3-hydroxykynurenine, 3-hydroxyanthranilic acid, quinolinic, acid, 5,6],8-tetrahydrobiopterin and its precursors to the same test system used rex phospholipid biosynthesis in vitro. In parallel anthranilic acid, kynurenic acid, xanthurenic acid and picolinic acid decrease while nicotinic acid increases membrane fluidity in the studied concentrations.
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Ferreira, Raphael, Paulo Gonçalves Teixeira, Verena Siewers, and Jens Nielsen. "Redirection of lipid flux toward phospholipids in yeast increases fatty acid turnover and secretion." Proceedings of the National Academy of Sciences 115, no. 6 (January 22, 2018): 1262–67. http://dx.doi.org/10.1073/pnas.1715282115.
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Bio-based production of fatty acids and fatty acid-derived products can enable sustainable substitution of petroleum-derived fuels and chemicals. However, developing new microbial cell factories for producing high levels of fatty acids requires extensive engineering of lipid metabolism, a complex and tightly regulated metabolic network. Here we generated a Saccharomyces cerevisiae platform strain with a simplified lipid metabolism network with high-level production of free fatty acids (FFAs) due to redirected fatty acid metabolism and reduced feedback regulation. Deletion of the main fatty acid activation genes (the first step in β-oxidation), main storage lipid formation genes, and phosphatidate phosphatase genes resulted in a constrained lipid metabolic network in which fatty acid flux was directed to a large extent toward phospholipids. This resulted in simultaneous increases of phospholipids by up to 2.8-fold and of FFAs by up to 40-fold compared with wild-type levels. Further deletion of phospholipase genes PLB1 and PLB2 resulted in a 46% decrease in FFA levels and 105% increase in phospholipid levels, suggesting that phospholipid hydrolysis plays an important role in FFA production when phospholipid levels are increased. The multiple deletion mutant generated allowed for a study of fatty acid dynamics in lipid metabolism and represents a platform strain with interesting properties that provide insight into the future development of lipid-related cell factories.
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Diez, E., F. H. Chilton, G. Stroup, R. J. Mayer, J. D. Winkler, and A. N. Fonteh. "Fatty acid and phospholipid selectivity of different phospholipase A2 enzymes studied by using a mammalian membrane as substrate." Biochemical Journal 301, no. 3 (August 1, 1994): 721–26. http://dx.doi.org/10.1042/bj3010721.
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Previous studies using phospholipid mixed vesicles have demonstrated that several types of phospholipase A2 (PLA2) enzymes exhibit different selectivity for fatty acids at the sn-2 position, for the type of chemical bond at the sn-1 position or for the phosphobase moiety at the sn-3 position of phospholipids. In the present study, we have utilized natural mammalian membranes from U937 monocytes to determine whether two purified 14 kDa PLA2 isoenzymes (Type I, Type II) and a partially purified 110 kDa PLA2 exhibit substrate selectivity for certain fatty acids or phospholipids. In these studies, arachidonic acid (AA) release from membranes was measured under conditions where the remodelling of AA mediated by CoA-independent transacylase (CoA-IT) activity has been eliminated. In agreement with the mixed-vesicle models, AA was the major unsaturated fatty acid hydrolysed from membranes by the 110 kDa PLA2, suggesting that this PLA2 is selective in releasing AA from natural membranes. By contrast, Type I and Type II PLA2s were less selective in releasing AA from phospholipids and released a variety of unsaturated fatty acids at molar ratios that were proportional to the ratios of these fatty acids in U937 microsomal membranes. Examination of AA release from phospholipid classes indicated that all three enzymes released AA from the major AA-containing phospholipid classes (phosphatidylethanolamine, phosphatidylcholine, and phosphatidylinositol) of U937 membranes. The 110 kDa PLA2 released AA from phospholipid subclasses in ratios that were proportional to the AA content within phospholipid classes and subclasses of U937 membranes. These data suggested that the 110 kDa PLA2 shows no preference either for the sn-1 linkage or for the sn-3 phosphobase moiety of phospholipids. By contrast, Type I and Type II PLA2s preferentially released AA from ethanolamine-containing phospholipids and appeared to prefer the 1-acyl-linked subclass. Taken together, these data indicate that the 110 kDa PLA2 selectively releases AA from U937 membranes, whereas Type I and Type II PLA2 release a variety of unsaturated fatty acids. Furthermore, the 110 kDa PLA2 releases the same molar ratios of AA from all major phospholipid subclasses, whereas Type I and Type II PLA2s show some specificity for phosphatidylethanolamine when these enzymes are incubated with a complex mammalian membrane substrate.
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PURDON, A. David, and Stanley I. RAPOPORT. "Energy requirements for two aspects of phospholipid metabolism in mammalian brain." Biochemical Journal 335, no. 2 (October 15, 1998): 313–18. http://dx.doi.org/10.1042/bj3350313.
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Previous estimates have placed the energy requirements of total phospholipid metabolism in mammalian brain at 2% or less of total ATP consumption. This low estimate was consistent with the very long half-lives (up to days) reported for fatty acids esterified within phospholipids. However, using an approach featuring analysis of brain acyl-CoA, which takes into account dilution of the precursor acyl-CoA pool by recycling of fatty acids, we reported that half-lives of fatty acids in phospholipids are some 100 times shorter (min–h) than previously thought. Based on these new estimates of short half-lives, palmitic acid and arachidonic acid were used as prototype fatty acids to calculate energy consumption by fatty acid recycling at the sn-1 and sn-2 positions of brain phospholipids. We calculated that the energy requirements for reacylation of fatty acids into lysophospholipids are 5% of net brain ATP consumption. We also calculated ATP requirements for maintaining asymmetry of the aminophospholipids, phosphatidylserine and phosphatidylethanolamine across brain membrane bilayers. This asymmetry is maintained by a translocase at a stoichiometry of 1 mol of ATP per mol of phospholipid transferred in either direction across the membrane. The energy cost of maintaining membrane bilayer asymmetry of aminophospholipids at steady-state was calculated to be 8% of total ATP consumed. Taken together, deacylation–reacylation and maintenance of membrane asymmetry of phosphatidylserine and phosphatidylethanolamine require about 13% of ATP consumed by brain as a whole. This is a lower limit for energy consumption by processes involving phospholipids, as other processes, including phosphorylation of polyphosphoinositides and de novo phospholipid biosynthesis, were not considered.
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Rudzite, Vera, Edite Jurika, Matthias Jäger, and Dietmar Fuchs. "Impairment of Lipid Metabolism Due to Deficiency of Pyridoxal-5-phosphate and/or Activated Immune system: its Interpretation." Pteridines 11, no. 4 (November 2000): 107–20. http://dx.doi.org/10.1515/pteridines.2000.11.4.107.
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Abstract Impairment of lipid metabolism due to excess metabolite accumulation induced by pyridoxal-5-phosphate (P-5-P)-deficiency and/or stimulated immune system has been studied and interpreted. Decreased amounts of phospholipids as well as deviations in phospholipid classes and fatty acid composition of phospholipids have been demonstrated due to kynurenine accumulation in the blood of P-5-P-deficient cardiovascular patients and white rats as well as in cardiovascular patients with activated immune system identified by an increased neopterin concentration in the blood (dilated cardiomyopathy). The addition of P-5-P to the incubation medium for phospholipid biosynthesis in vitro did not change fatty acid incorporation into phospholipids, whereas it normalised fatty acid incorporation into phospholipids in liver homogenates received from P-5-P-deficient rats: The addition of kynurenine, neopterin and noradrenalin (accumulated m isolated heart tissue after addition of kynurenine and neopterin to incubation medium for isolated heart) to incubation medium for phospholipid biosynthesis in vitro induced an increase of saturated and a decrease of polyunsaturated fatty acid incorporation into phospholipids. These changes in fatty acid incorporation into phospholipids were followed by increased cholesterol concentrations in samples and an increased cholesterol/phospholipid ratio. Our results suggest that these changes in lipids are characteristic for decreased membrane fluidity, depressed cell cycle and lowered possibility of phospholipids to keep cholesterol in solution. P-5-P-deficiency is also accompanied with excess accumulation of homocysteine in the blood. The addition of L-homocysteine to the incubation medium for phospholipid biosynthesis in vitro was followed by inverse changes in fatty acid incorporation into phospholipids when compared with kynurenine, neopterin and noradrenalin. L-homocysteine induced a decrease of saturated and an increase of polyunsaturated fatty acid incorporation into phospholipids. The cholesterol concentration decreased in samples and the cholesterol/ phospholipid ratio decreased, too . These findings suggest that changes in lipids induced by L-homocysteine are characteristic for increased membrane fluidity and stimulated cell cycle. In this study, we have observed a similar effect to L-homocysteine effect when L-homocysteine, L-tryptophan and 5,6,7,8-tetrahydrobiopterin were added to the incubation medium for phospholipid biosynthesis in vitro. The comparison of our results with data from the literature allows to suggest that excess metabolite accumulation due to activated formation and inactivated catabolism of it plays a significant role in quantitative and qualitative changes of lipids, especially phospholipids, and therefore participates in the regulation of membrane fluidity, cell cycle of normal and malignant cells as well as in keeping cholesterol in the state of solution.
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Yousef, I. M., S. Barnwell, F. Gratton, B. Tuchweber, A. Weber, and C. C. Roy. "Liver cell membrane solubilization may control maximum secretory rate of cholic acid in the rat." American Journal of Physiology-Gastrointestinal and Liver Physiology 252, no. 1 (January 1, 1987): G84—G91. http://dx.doi.org/10.1152/ajpgi.1987.252.1.g84.
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The factors modulating the maximum secretory rate of cholic acid were investigated. Rats were infused intravenously with cholic acid in measured stepwise increasing doses (1, 2, 3, and 4 mumol X min-1 X 100 g body wt-1). Each dose was infused for 30 min and bile samples were collected every 10 min. Bile flow, bile acid, cholesterol, individual biliary phospholipids, and the fatty acid profiles of the biliary phospholipids were determined. Microsomal and bile canalicular membrane-enriched fractions were isolated from cholic acid-treated rats at the end of the experiment. Membranes were analyzed for cholesterol, phospholipid, and phospholipid fatty acid composition. During cholic acid infusion, the secretion rates of bile acid, cholesterol, phospholipid, and bile flow initially increased and then declined. No evidence of liver cell damage was observed by light or electron microscopy. Maximum phospholipid secretion rate (13.5 nmol X min-1 X g-1) occurred before peak bile flow and bile acid secretory rate maximum (4.72 microliter X min-1 X g-1 and 375 nmol X min-1 X g-1). When phospholipid output declined, the proportion of sphingomyelins and phosphatidylethanolamine relative to phosphatidylcholine increased. This was also reflected in the fatty acid composition. Cholic acid infusion caused a decline in microsomal and bile canalicular membrane phospholipid content without affecting their phospholipid composition. Depletion of membrane phospholipid resulted in an increase in the cholesterol:phospholipid ratio, which is suggested to be the underlying mechanism for modulating cholic acid secretion.
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Rudzite, Vera, Edite Jurika, Gabriele Baier-Bitterlich, Bernhard Widner, Gilbert Reibnegger, and Dietmar Fuchs. "Pteridines and Lipid Metabolism." Pteridines 9, no. 2 (May 1998): 103–12. http://dx.doi.org/10.1515/pteridines.1998.9.2.103.
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Summary The effect of 9 different pteridines on fatty acid incorporation into phospholipids as well as on cholesterol and phospholipid content was compared in vitro using rat liver homogenate, Krebs-Ringer phosphate buffer containing 0.3 % albumin (pH=7.4), fatty acid mixture and glycerol. D-neopterin (5-30 pmol/g) induced an increase of saturated, a decrease of unsaturated fatty acids incorporation into phospholipids and elevated the cholesterol content in samples. The phospholipid amount in samples remained unchanged. Sepiapterin, 7,8-dihydrobiopterin, 5,6,7,8-tetrahydrobiopterin, biopterin, monapterin and 7,8-dihydroneopterin addition to samples induced an inverse relationship: a decrease of saturated, an increase of unsaturated fatty acid, especially arachidonic acid, incorporation into phospholipids and the decrease of cholesterol content in samples. The phospholipid amount in samples remained unchanged or increased. Lipid metabolism was not altered after addition of xanthopterin and isoxanthopterin to samples. It was suggested that neopterin decreased membrane fluidity, prevented cell cycle, induced cell dystrophy and apoptosis, and promoted the cholesterol precipitation while tetrahydrobiopterin, its precursors, biopterin, monapterin and dihydroneopterin increased membrane fluidity, stimulated cell cycle, prevented cholesterol precipitation. The data point to a potential role of increased neopterin concentrations in vivo to support atherosclerosis development and progression whereas the other pteridines may have a protective effect. Moreover, these pteridines can also promote cell transformation.
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Rzehak, Peter, Joachim Heinrich, Norman Klopp, Linda Schaeffer, Sebastian Hoff, Günther Wolfram, Thomas Illig, and Jakob Linseisen. "Evidence for an association between genetic variants of the fatty acid desaturase 1 fatty acid desaturase 2 (FADS1 FADS2) gene cluster and the fatty acid composition of erythrocyte membranes." British Journal of Nutrition 101, no. 1 (May 15, 2008): 20–26. http://dx.doi.org/10.1017/s0007114508992564.
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The present study gives further evidence for the recently found association between variants of the fatty acid desaturase 1 fatty acid desaturase 2 (FADS1 FADS2) gene cluster and PUFA in blood phospholipids and explores this association for cellular fatty acids in erythrocyte membranes. In a subgroup of adults participating in the Bavarian Nutrition Survey II, a cross-sectional population-based study conducted in Bavaria, Germany, allelic variation in three selected loci of the FADS1 FADS2 gene cluster was analysed and used for haplotype construction. Associations with plasma phospholipid PUFA (n 163) and PUFA in erythrocyte membranes (n 535) were investigated by regression analysis. All haplotypes of the original five-loci haplotypes of our previous study could be replicated. In addition, associations with serum phospholipid PUFA were confirmed in the present data set. Although less pronounced, associations between FADS1 FADS2 haplotypes and PUFA in erythrocyte membranes, particularly arachidonic and dihomo-γ-linolenic acid, could be established. We provide the first replication of the association of the FADS1 FADS2 gene cluster with PUFA in blood phospholipids. For the first time, such associations were also shown for PUFA in cell membranes.
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Fuhrmann, H., and H. P. Sallmann. "Phospholipid fatty acids of brain and liver are modified by α-tocopherol and dietary fat in growing chicks." British Journal of Nutrition 76, no. 1 (July 1996): 109–22. http://dx.doi.org/10.1079/bjn19960013.
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Dietary fatty acids modify phospholipid fatty acids in brain and liver of growing chickens post-hatching.The effect of vitamin E deficiency on this process is unknown and may be relevant to the pathogenesis of chick nutritional encephalomalacia (NE). Therefore laying hens received a diet low in vitamin E (10 mg α-tocopherol/kg feed). Resulting chicks were assigned to nine dietary groups each fed with either oleic (18:ln-9, 58 g/kg), linoleic (18:2n-6, 57 g/kg) or linolenic (18:3n-3, 56 g/kg) acid together with 5, 25 or 125 mg α-tocopherol/kg feed. NE affecting the cerebellum only occurred in the group given linoleic acid and 5 mg α-tocopherol/kg.In l-d-old chicks and after 1 and 2 weeks the phospholipid fatty acid composition of liver, cerebrum and cerebellum (additionally after 3 weeks) was determined. The feed fatty acids were incorporated into the liver very efficiently during the first week of life. Unsaturation of liver membranes decreased in the orderdietary linolenic >linoleic >oleic acid. In liver, also, the effect of α-tocopherol supplementation on phospholipid fatty acids was most pronounced. Theunsaturation index increased during deficiency, whereas n-9 fatty acids decreased. In the chicken brain the alterations were delayed and less distinct. The cerebellum phospholipids were rich in n-9 fatty acids and as a whole more saturated in comparison with the cerebrum. Cerebellar unsaturation increased when linolenic or linoleic acid was given. However, NE-producing dietary conditions were not accompanied by specific alterations in cerebellar phospholipid fatty acids due to the α-tocopherol content of the diet. Rather the alterations of membrane fatty acids in the liver seem to play a role in the pathogenesis of NE.
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Brooks, S., G. T. Clark, S. M. Wright, R. J. Trueman, A. D. Postle, A. R. Cossins, and N. M. Maclean. "Electrospray ionisation mass spectrometric analysis of lipid restructuring in the carp (Cyprinus carpio L.) during cold acclimation." Journal of Experimental Biology 205, no. 24 (December 15, 2002): 3989–97. http://dx.doi.org/10.1242/jeb.205.24.3989.
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SUMMARY Cold acclimation of carp from 30°C to 10°C causes a restructuring of liver microsomal phospholipids characterised by increased proportions of monounsaturated fatty acid in phosphatidylcholine (PC) and phosphatidylethanolamine (PE). Here, we have used electrospray ionisation mass spectrometry (ESI-MS) to determine the patterns of alteration to individual molecular species compositions of PC, PE and phosphatidylinositol (PI) in response to gradually decreasing temperature. The results demonstrate that cold induces precise changes to a limited number of phospholipid species, and that these changes are distinct and different for each phospholipid class. The major change for PC was increased 16:1/22:6, but for PE the species that increased was 18:1/22:6. By contrast, the PI species that increased during cold acclimation were characterised by an sn-1 monounsaturated fatty acid in combination with arachidonoyl or eicosapentaenoyl fatty acid at the sn-2 position. Analysis of acyl distribution indicates that cold only caused the accumulation of monounsaturated fatty acids at the sn-1 and not at the sn-2 position of phospholipids. These results highlight the tight and restricted range of modifications that membranes make to their phospholipid composition in response to thermal stress.
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Aznar, Justo, Teresa Santos, and Juana Vallés. "“Ex Vivo” Influence of Fatty Acids from Plasma Cholesterol and Triglycerides on the Fatty Acid Pattern of Platelets." Thrombosis and Haemostasis 54, no. 03 (1985): 669–74. http://dx.doi.org/10.1055/s-0038-1660094.
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SummaryWe 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 <0.001) were found for some of the platelet phospholipid FA and the same FA that esterify plasma cholesterol [18:11 (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 (1), 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.
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Hsiao, L. L., R. J. Howard, M. Aikawa, and T. F. Taraschi. "Modification of host cell membrane lipid composition by the intra-erythrocytic human malaria parasite Plasmodium falciparum." Biochemical Journal 274, no. 1 (February 15, 1991): 121–32. http://dx.doi.org/10.1042/bj2740121.
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The phospholipid and fatty acid compositions of the host infected erythrocyte plasma membrane (IEPM) have been determined for erythrocytes infected with the human malaria parasite Plasmodium falciparum. IEPM were prepared by selective lysis of the host erythrocyte (but not of the parasite membranes) with 0.1% saponin, followed by differential centrifugation. The purity of the IEPM was determined by measuring the membrane-specific enzyme markers acetylcholinesterase, glutamate dehydrogenase and lactate dehydrogenase, and by immunoelectron microscopy using monoclonal antibodies specific for human erythrocyte glycophorin A (4E7) and for a 195 kDa parasite membrane glycoprotein (Pf6 3B10.1). Both approaches demonstrated that the host erythrocyte plasma membrane preparation was free from contamination by parasite membranes. During intra-erythrocytic development of the parasite, the phospholipid composition of the erythrocyte membrane was strikingly altered. IEPM contained more phosphatidylcholine (38.7% versus 31.7%) and phosphatidylinositol (2.1% versus 0.8%) and less sphingomyelin (14.6% versus 28.0%) than normal uninfected erythrocytes. Similar alterations in phospholipid composition were determined for erythrocyte membranes of parasitized cells isolated by an alternative method utilizing polycationic polyacrylamide microbeads (Affigel 731). The total fatty acid compositions of the major phospholipids in IEPM were determined by g.l.c. The percentage of polyunsaturated fatty acids in normal erythrocyte phospholipids (39.4%) was much higher than in phospholipids from purified parasites (23.3%) or IEPM (24.0%). The unsaturation index of phospholipids in IEPM was considerably lower than in uninfected erythrocytes (107.5 versus 161.0) and was very similar to that in purified parasites (107.5 versus 98.5). Large increases in palmitic acid (C16:0) (from 21.88% to 31.21%) and in oleic acid (C18:1) (from 14.64% to 24.60%), and major decreases in arachidonic acid (C20:4) (from 17.36% to 7.85%) and in docosahexaenoic acid (C22:6) (from 4.34% to 1.8%) occurred as a result of infection. The fatty acid profiles of individual phospholipid classes from IEPM resembled in many instances the fatty acid profiles of parasite phospholipids rather than those of uninfected erythrocytes. Analysis of IEPM from P. falciparum-infected erythrocytes (trophozoite stage) revealed that, during intra-erythrocytic maturation of the parasite, the host erythrocyte phospholipid composition was markedly refashioned. These alterations were not dependent on the method used to isolate the IEPM, with similar results obtained using either a saponin-lysis method or binding to Affigel beads. Since mature erythrocytes have negligible lipid synthesis and metabolism, these alterations must occur as a result of parasite-directed metabolism of erythrocyte lipids and/or trafficking of lipids between the parasite and erythrocyte membranes.
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Dise, C. A., J. M. Clark, C. J. Lambersten, and D. B. Goodman. "Hyperbaric hyperoxia reversibly inhibits erythrocyte phospholipid fatty acid turnover." Journal of Applied Physiology 62, no. 2 (February 1, 1987): 533–38. http://dx.doi.org/10.1152/jappl.1987.62.2.533.
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The present study is one component of a comprehensive investigation of oxygen tolerance of tissues and organs in normal human subjects. The focus of this study was the acylation of membrane phospholipid in situ by erythrocytes. Activation of exogenous [9,10–3H]oleic acid to acyl thioester and transesterification of the acyl thioester into phospholipid by intact human erythrocytes incubated in vitro decreased 30% after exposure of 10 human subjects to hyperbaric hyperoxia (100% O2, 3 ATA, 3.5 h). Partial recovery of activity could be detected when additional cells were obtained from these subjects and assayed in vitro 24 h after cessation of exposure. No significant change in membrane phospholipid fatty acid composition was detected under these conditions. The reduced glutathione content of intact erythrocytes increased by 15% after hyperbaric hyperoxia and remained elevated 24 h after exposure. In isolated membranes prepared from the same cells activation of [9,10–3H]oleic acid to acyl thioester and its transesterification into phospholipid did not change after hyperoxia. Since the ability of intact cells to replace oxidized fatty acids in membrane phospholipids via deacylation and reacylation in situ may be necessary for the maintenance of membrane integrity during exposure to oxidative stress, the decrease in [9,10–3H]oleic acid incorporation by human erythrocytes detected in vitro after hyperbaric hyperoxia in vivo may reflect an early event in the pathogenesis of oxygen-induced cellular injury and may be a useful index for assessment of the tolerance of tissues to hyperoxia.
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McHowat, Jane, Michael H. Creer, Kristine K. Hicks, Janet H. Jones, Raetreal McCrory, and Richard H. Kennedy. "Induction of Ca-independent PLA2 and conservation of plasmalogen polyunsaturated fatty acids in diabetic heart." American Journal of Physiology-Endocrinology and Metabolism 279, no. 1 (July 1, 2000): E25—E32. http://dx.doi.org/10.1152/ajpendo.2000.279.1.e25.
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Diabetes-induced changes in phospholipase A2(PLA2) activity have been measured in several tissues but are undefined in diabetic myocardium. We measured ventricular PLA2 activity in control, streptozotocin-induced diabetic, and insulin-treated diabetic rats and characterized myocardial phospholipids to determine whether diabetes altered myocardial phospholipid metabolism. Increased membrane-associated Ca2+-independent PLA2 (iPLA2) activity was observed in diabetes that was selective for arachidonylated phospholipids. Increased iPLA2 activity was accompanied by an increase in choline lysophospholipids. Diabetes was associated with marked alterations in the phospholipid composition of the myocardium, characterized by decreases in esterified arachidonic and docosahexaenoic acids and increases in linoleic acid. The decrease in polyunsaturated fatty acids was confined to diacylphospholipids, whereas the relative amount of these fatty acids in plasmalogens was increased. Diabetes-induced changes in PLA2 activity, lysophospholipid production, and alterations in phospholipid composition were all reversed by insulin treatment of diabetic animals. Diabetes-induced changes in membrane phospholipid content and phospholipid hydrolysis may contribute to some of the alterations in myocardial function that are observed in diabetic patients.
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Hueso, P., L. Zancada, F. Pérez-Díez, F. Sánchez-Juanes, J. M. Alonso, and L. A. García-Pardo. "Phospholipid classes and fatty acid composition of ewe’s and goat’s milk." Grasas y Aceites 64, no. 3 (May 28, 2013): 304–10. http://dx.doi.org/10.3989/gya.095312.
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Tsofina, L. M., and E. N. Mokhova. "Effect of Palmitic and Lauric Acids on the Phospholipid Bilayer Membrane Conductivity." Bioscience Reports 18, no. 2 (April 1, 1998): 91–95. http://dx.doi.org/10.1023/a:1020136327022.
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Palmitic acid increased the conductivity of BLM from mitochondrial phospholipids when they were dissolved in a mixture of decane and chlorodecane, and was ineffective when phospholipids were dissolved in decane. Lauric acid produced an increase in the membrane conductivity independently of the phospholipid type in the membrane-forming solutions (mitochondrial phospholipids, asolectin, lecithin with cholesterol) and their solvents (decane or decane with chlorodecane). The results show that discrepancies between published data concerning fatty acid effects on the BLM conductivity may be explained by differences in phospholipids, their solvents and fatty acid used.
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Klingler, Mario, and Berthold Koletzko. "Novel methodologies for assessing omega-3 fatty acid status – a systematic review." British Journal of Nutrition 107, S2 (May 17, 2012): S53—S63. http://dx.doi.org/10.1017/s0007114512001468.
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Over the last few decadesn-3 long chain polyunsaturated fatty acid status became of special interest for scientists. Biochemical measures on then-3 fatty acid status vary depending on body compartment assessed and measures chosen. Plasma phospholipids and red blood cell membrane phospholipids are mainly used asn-3 fatty acid status marker. The conventional analysis of phospholipid fatty acids involves lipid extraction and consecutive chromatographic separation of phospholipids from other lipid fractions, which is time-consuming and costly. In recent years, different investigators have tried to overcome these limitations by using other biological markers or by modifying the analytical procedures used to assessn-3 fatty acid status. The aim of this systematic review was to provide an overview on these novel analytical methods developed for the fatty acid quantification by gas chromatography, highlights the methodological limitations, and discusses advantages or disadvantages of the biological markers used. Seventeen papers were identified that fulfilled the inclusion criteria. New opportunities arise from sensitive and precise high-throughput methodologies for assessment of plasma total lipid and plasma glycerophospholipid fatty acids, as well as cheek cell fatty acid composition.
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Aerde, John E. Van, and M. T. Clandinin. "Controversy in fatty acid balance." Canadian Journal of Physiology and Pharmacology 71, no. 9 (September 1, 1993): 707–12. http://dx.doi.org/10.1139/y93-105.
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It is uncertain whether preterm infants can synthesize C20 and C22 (ω−6) and (ω−3) fatty acids required for structural lipids. Dietary intake of CI8:2ω−6 and C18:3ω−3 in formulae lacking long-chain polyunsaturated fatty acids can result in reduced levels of C20 and C22 homologues in membrane phospholipids as compared with breast-fed infants. Supplementation of fish oil has been shown to alleviate this problem in part only, as synthesis and incorporation of arachidonic acid into membrane phospholipids is reduced. Presently, infant formulae do not contain C20 and C22 fatty acids. Feeding an experimental infant formula with a balance between C20 and C22 (ω−6) and (ω−3) fatty acids within the range of human milk results in plasma phospholipid levels of C20 and C22 long-chain polyunsaturated (ω−6) and (ω−3) fatty acids similar to those in breast-fed infants. On the basis of clinical studies and evolutionary data, an increase of the linolenic and a decrease of the linoleic acid content in infant formula are suggested. Balanced incorporation of both (ω−6) and (ω−3) long-chain polyunsaturated fatty acids seems advisable in view of the lack of knowledge concerning the neonate's ability to chain elongate and desaturate essential fatty acids. Recommendations for the essential fatty acid content of preterm infant formula are suggested.Key words: essential fatty acids, long-chain polyunsaturated fatty acids, infant formula, fish oil, desaturation.
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Baker, R. Roy, and Zou Dao Loh. "Fatty acid release in incubations of serum with synaptosome and myelin subfractions of brain." Biochemistry and Cell Biology 68, no. 1 (January 1, 1990): 148–53. http://dx.doi.org/10.1139/o90-020.
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To study lipid breakdown in brain membranes following hemorrhage, synaptosome and myelin fractions isolated from rat brain were incubated with rat serum. After 3 h in vitro at 37 °C, 0.43 and 0.26 μmol of fatty acid were released in incubations containing synaptosomes (1.37 μmol phospholipid) or myelin (1.23 μmol phospholipid), respectively, in the presence of 0.25 mL serum. Less than 0.05 μmol of fatty acid was liberated in incubations containing only serum, synaptosomes, or myelin. For synaptosomes and serum, docosahexaenoate was the principal fatty acid released (28 mol% of total) after 3 h of incubation. This fatty acid and arachidonate made up 43 mol% of the liberated fatty acid. The presence of free docosahexaenoate was of interest, as this fatty acid is particularly enriched in phosphatidylserine and phosphatidylethanolamine, phospholipids found in the cytoplasmic half of the synaptosomal plasma membrane and in interior synaptosomal membranes. In incubations of serum and myelin, oleate was the major free fatty acid produced in 30 min to 3 h of incubation (29–35 mol% of total). After 3 h, docosahexaenoate contributed 20 mol% to the total. The release of fatty acids from the membranes may be mediated by serum phospholipase(s) or possibly by activated endogenous lipolytic activities.Key words: fatty acid, serum, synaptosome, myelin, phospholipase A2.
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Mahajan, Sandeep, and G. K. Khuller. "Cerulenin inhibition of lipid synthesis and its reversal by exogenous fatty acids in Mycobacterium smegmatis ATCC 607." Canadian Journal of Biochemistry and Cell Biology 63, no. 2 (February 1, 1985): 85–90. http://dx.doi.org/10.1139/o85-012.
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Cerulenin inhibited the lipid synthesis of Mycobacterium smegmatis ATCC 607 over the range of 0.5–1.8 μg/mL with complete inhibition at 1.8 μg/mL, as monitored by [14C]glycerol incorporation into lipids. Exogenous fatty acids failed to restore the lipid synthesis at 1.8 μg/mL; however, the addition of palmitic acid to the growth medium partially restored the lipid synthesis when cerulenin concentration was decreased to 1.6 μg/mL. Fatty acid analysis of cerulenin plus palmitic acid supplemented cultures revealed that exogenously supplied fatty acid was incorporated into cellular phospholipids. Further investigations with 1.6 μg/mL of cerulenin and [14C]acetate and [32P]orthophosphoric acid showed that cerulenin inhibited the synthesis of saturated plus unsaturated fatty acids and phospholipids. Pulse–chase studies with [14C]acetate revealed decreased synthesis and degradation of each of the phospholipid components.
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SUNDSTRÖM, BJÖRN, GUNNAR JOHANSSON, HEIDI KOKKONEN, TOMMY CEDERHOLM, and SOLVEIG WÅLLBERG-JONSSON. "Plasma Phospholipid Fatty Acid Content Is Related to Disease Activity in Ankylosing Spondylitis." Journal of Rheumatology 39, no. 2 (December 15, 2011): 327–33. http://dx.doi.org/10.3899/jrheum.110575.
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Objective.To investigate fatty acid composition in the diet, plasma phospholipids, and adipose tissue in a cohort of patients with ankylosing spondylitis (AS), and to determine their correlations to disease activity and blood lipids in a cross-sectional study.Methods.Diet was assessed using a food frequency questionnaire in 66 patients with AS. Polyunsaturated fatty acids in plasma phospholipids and gluteal adipose tissue were measured using gas chromatography. Disease status was quantified using the Bath Ankylosing Spondylitis Disease Activity Index (BASDAI), erythrocyte sedimentation rate (ESR), high sensitivity C-reactive protein, and proinflammatory cytokines.Results.Diet did not correlate with disease activity assessed by the BASDAI, but there were negative correlations between the dietary intake of long-chain omega-3 fatty acids and ESR (rs = –0.27, p < 0.05). The plasma phospholipid content of arachidonic acid correlated significantly with the BASDAI score (rs = 0.39, p < 0.01). There were correlations between the intake of long-chain omega-3 fatty acids and high-density lipoproteins and serum triglycerides (rs = 0.26 and rs = –0.25, respectively, p < 0.05).Conclusion.There was a positive correlation between levels of arachidonic acid in plasma phospholipids and disease activity assessed by BASDAI in patients with AS. A Western diet does not appear to influence this correlation, but seems to affect blood lipids involved in atherogenic processes.
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Furtado, Beqari, and Campos. "Comparison of the Utility of Total Plasma Fatty Acids Versus those in Cholesteryl Ester, Phospholipid, and Triglyceride as Biomarkers of Fatty Acid Intake." Nutrients 11, no. 9 (September 3, 2019): 2081. http://dx.doi.org/10.3390/nu11092081.
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Total plasma fatty acids or those in cholesteryl ester and phospholipids are often used to reflect fatty acid intake in epidemiological studies, but their relative performance as biomarkers of intake has not been clearly evaluated within a single population. The assessment of fatty acids in plasma fractions is more labor intensive. Thus, their use as biomarkers of dietary intake needs to be justified. Dietary intake was assessed in 200 population-based controls from a case-control study of diet and heart disease in Costa Rica by a validated food frequency questionnaire (FFQ). Fatty acids in fasting whole plasma and plasma fractions (cholesteryl ester, phospholipid, and triglyceride + free fatty acid) were measured in the 200 controls by the same laboratory using gas chromatography with flame ionization detection (GC-FID). We compared the plasma and plasma fractions data with the FFQ and adipose fatty acid profile using partial Spearman correlations to assess utility as biomarkers of intake and exposure. We found that whole plasma was equally or more strongly correlated with the FFQ and adipose fatty acid profile than either cholesteryl ester or phospholipid in most of the established markers of dietary intake, including dairy (15:0 and 17:0) and seafood (eicosapentaenoic acid and docosahexaenoic acid). Of the three plasma fractions, only fatty acids in the plasma triglyceride + free fatty acid fraction had stronger correlations with dietary intake than whole plasma. In our study population, fatty acids measured in fasting whole plasma perform as good as or better than those measured in plasma fractions as biomarkers for dietary fatty acid intake. Thus, the fractionation of plasma to evaluate long-term fatty acid intake may not be warranted.
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Starodub, O., C. A. Jolly, B. P. Atshaves, J. B. Roths, E. J. Murphy, A. B. Kier, and F. Schroeder. "Sterol carrier protein-2 localization in endoplasmic reticulum and role in phospholipid formation." American Journal of Physiology-Cell Physiology 279, no. 4 (October 1, 2000): C1259—C1269. http://dx.doi.org/10.1152/ajpcell.2000.279.4.c1259.
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Although sterol carrier protein-2 (SCP-2; also called nonspecific lipid transfer protein) binds fatty acids and fatty acyl-CoAs, its role in fatty acid metabolism is not fully understood. L-cell fibroblasts stably expressing SCP-2 were used to resolve the relationship between SCP-2 intracellular location and fatty acid transacylation in the endoplasmic reticulum. Indirect immunofluorescence double labeling and laser scanning confocal microscopy detected SCP-2 in peroxisomes > endoplasmic reticulum > mitochondria > lysosomes. SCP-2 enhanced incorporation of exogenous [3H]oleic acid into phospholipids and triacylglycerols of overexpressing cells 1.6- and 2.5-fold, respectively, stimulated microsomal incorporation of [1-14C]oleoyl-CoA into phosphatidic acid in vitro 13-fold, and exhibited higher specificity for unsaturated versus saturated fatty acyl-CoA. SCP-2 enhanced the rate-limiting step in microsomal phosphatidic acid biosynthesis mediated by glycerol-3-phosphate acyltransferase. SCP-2 also enhanced microsomal acyl-chain remodeling of phosphatidylethanolamine up to fivefold and phosphatidylserine twofold, depending on the specific fatty acyl-CoA, but had no effect on other phospholipid classes. In summary, these results were consistent with a role for SCP-2 in phospholipid synthesis in the endoplasmic reticulum.
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Boberg, M., L. B. Croon, I. B. Gustafsson, and B. Vessby. "Platelet fatty acid composition in relation to fatty acid composition in plasma and to serum lipoprotein lipids in healthy subjects with special reference to the linoleic acid pathway." Clinical Science 68, no. 5 (May 1, 1985): 581–87. http://dx.doi.org/10.1042/cs0680581.
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1. The fatty acid composition in platelet phospholipids and in the plasma lipid esters as well as the serum lipoprotein lipid concentrations were determined in 67 healthy male subjects in order to establish the relationships between blood lipids and platelets. 2. A positive correlation was found between the concentrations of the triglyceride rich serum lipoprotein lipids and the relative percentage of saturated and monounsaturated fatty acids in plasma. The correlations were also positive between the serum high density lipoprotein-cholesterol concentration and the relative content of linoleic acid in the plasma cholesterol esters and phospholipids. 3. Negative correlations were found between the relative percentage of saturated and monounsaturated fatty acids in the plasma lipid esters versus linoleic acid in plasma and in the platelets. On the other hand there were positive correlations between linoleic acid in the plasma lipid esters and in the platelet phospholipids. These results indicate a direct dietary influence on the platelet phospholipid fatty acid composition. 4. The correlations between the fatty acids of the n −6 series within plasma and platelets as well as between plasma and platelets indicate that a high linoleic acid content is not associated with an increased arachidonic acid concentration. The results also indicate that the limiting metabolic step in the conversion of linoleic acid into arachidonic acid may be located at different levels in plasma and in the platelets.
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Schneiter, Roger, Verena Tatzer, Gabriela Gogg, Erich Leitner, and Sepp Dieter Kohlwein. "Elo1p-Dependent Carboxy-Terminal Elongation of C14:1Δ9 to C16:1Δ11 Fatty Acids inSaccharomyces cerevisiae." Journal of Bacteriology 182, no. 13 (July 1, 2000): 3655–60. http://dx.doi.org/10.1128/jb.182.13.3655-3660.2000.
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ABSTRACT Saccharomyces cerevisiae medium-chain acyl elongase (ELO1) mutants have previously been isolated in screens for fatty acid synthetase (FAS) mutants that fail to grow on myristic acid (C14:0)-supplemented media. Here we report that wild-type cells cultivated in myristoleic acid (C14:1Δ9)-supplemented media synthesized a novel unsaturated fatty acid that was identified as C16:1Δ11 fatty acid by gas chromatography-mass spectroscopy. Synthesis of C16:1Δ11 was dependent on a functional ELO1 gene, indicating that Elo1p catalyzes carboxy-terminal elongation of unsaturated fatty acids (α-elongation). In wild-type cells, the C16:1Δ11elongation product accounted for approximately 12% of the total fatty acids. This increased to 18% in cells that lacked a functional acyl chain desaturase (ole1Δ mutants) and hence were fully dependent on uptake and elongation of C14:1. The observation thatole1Δ mutant cells grew almost like wild type on medium supplemented with C14:1 indicated that uptake and elongation of unsaturated fatty acids were efficient. Interestingly, wild-type cells supplemented with either C14:1 or C16:1 fatty acids displayed dramatic alterations in their phospholipid composition, suggesting that the availability of acyl chains is a dominant determinant of the phospholipid class composition of cellular membranes. In particular, the relative content of the two major phospholipid classes, phosphatidylethanolamine and phosphatidylcholine, was strongly dependent on the chain length of the supplemented fatty acid. Moreover, analysis of the acyl chain composition of individual phospholipid classes in cells supplemented with C14:1 revealed that the relative degree of acyl chain saturation characteristic for each phospholipid class appeared to be conserved, despite the gross alteration in the cellular acyl chain pool. Comparison of the distribution of fatty acids that were taken up and elongated (C16:1Δ11) to those that were endogenously synthesized by fatty acid synthetase and then desaturated by Ole1p (C16:1Δ9) in individual phospholipid classes finally suggested the presence of two different pools of diacylglycerol species. These results will be discussed in terms of biosynthesis of different phospholipid classes via either the de novo or the Kennedy pathway.
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Vistisen, Bodil, Lars Nybo, Xuebing Xu, Carl-Erik Høy, and Bente Kiens. "Minor amounts of plasma medium-chain fatty acids and no improved time trial performance after consuming lipids." Journal of Applied Physiology 95, no. 6 (December 2003): 2434–43. http://dx.doi.org/10.1152/japplphysiol.00118.2003.
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Medium-chain triacylglycerols (MCT) have a potential glycogen-saving effect during exercise due to rapid hydrolysis and oxidation. However, studies comparing intake of carbohydrates (CHO) plus 80–90 g MCT with intake of CHO alone have revealed different results. The present study tested performance after consumption of specific structured triacylglycerol, consisting of a mixture of medium-chain fatty acids and long-chain fatty acids, to prevent the adverse effects observed by MCT (pure medium-chain fatty acids) regarding gastrointestinal distress. Seven well-trained subjects cycled 3 h at 55% of maximum O2 uptake during which they ingested CHO or CHO plus specific structured triacylglycerols. Immediately after the constant-load cycling, the subjects performed a time trial of ∼50-min duration. Breath and blood samples were obtained regularly during the experiment. Fatty acid composition of plasma triacylglycerols, fatty acids, and phospholipids was determined. Performance was similar after administration of CHO plus specific structured triacylglycerol [medium-, long-, and medium-chain fatty acid (MLM)] compared with CHO (50.0 ± 1.8 and 50.8 ± 3.6 min, respectively). No plasma 8:0 was detected in the plasma lipid classes, but the amount of phospholipid fatty acids was significantly higher after CHO+MLM compared with CHO intake. The lacking time trial improvement after intake of medium-chain fatty acids might be due to no available 8:0 in the systemic circulation. A higher level of plasma phospholipid fatty acids in the CHO+MLM compared with the CHO group was probably due to endogenous phospholipid release into chylomicrons.
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Wang, H., H. M. Berschneider, J. Du, and D. D. Black. "Apolipoprotein secretion and lipid synthesis: regulation by fatty acids in newborn swine intestinal epithelial cells." American Journal of Physiology-Gastrointestinal and Liver Physiology 272, no. 5 (May 1, 1997): G935—G942. http://dx.doi.org/10.1152/ajpgi.1997.272.5.g935.
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The IPEC-1 newborn swine intestinal epithelial cell line was used to determine the effects of the uptake of various fatty acids on the secretion of apolipoprotein (apo) B and apo A-I, as well as triglyceride and phospholipid. Long-chain saturated fatty acids were taken up and stimulated triglyceride synthesis, and palmitic (16:0) and stearic (18:0) acids also stimulated phospholipid synthesis. However, these fatty acids did not enhance triglyceride, phospholipid, or apo B or apo A-I secretion. Oleic acid (18:1) was the most effective of all fatty acids tested in stimulating triglyceride synthesis and the secretion of triglyceride, phospholipid, and apo B. Linoleic (18:2) and linolenic (18:3) acids were no more effective than long-chain saturated fatty acids in stimulating these processes. With saturated fatty acids, apo A-I followed the same secretory pattern as apo B. However, among the unsaturated fatty acids, oleic acid was the least effective and linolenic acid was the most effective in stimulating apo A-I secretion. Basolateral secretion of lipid and apolipoproteins by differentiated IPEC-1 cells is differentially regulated by apical exposure to fatty acids.
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Williams, Christine M., and K. Maunder. "Effect of dietary fatty acid composition on inositol-, choline- and ethanolamine-phospholipids of mammary tissue and erythrocytes in the rat." British Journal of Nutrition 68, no. 1 (July 1992): 183–93. http://dx.doi.org/10.1079/bjn19920076.
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The present study investigated the effect of feeding maize-oil, olive-oil and fish-oil diets, from weaning to adulthood, on rat mammary tissue and erythrocyte phospholipid fatty acid compositions. Effects of diet on the relative proportions of membrane phospholipids in the two tissues were also investigated. Mammary tissue phosphatidylinositol (PI) fatty acids were unaltered by diet, but differences in phosphatidylethanolamine (PE) and, to a lesser extent, phosphatidylcholine (PC) fractions were found between animals fed on different diets from weaning. Differences observed were those expected from the dietary fatty acids fed; n-6 fatty acids were found in greatest amounts in maize-oil-fed rats, n-9 in olive-oil-fed rats, and n-3 in fish-oil-fed rats. In erythrocytes the relative susceptibilities of the individual phospholipids to dietary modification were: PE > PC > PI, but enrichment with n-9 and n-3 fatty acids was not observed in olive-oil- and fish-oil-fed animals and in PC and PE significantly greater amounts of saturated fatty acids were found when animals fed on olive oil or fish oil were compared with maize-oil-fed animals. The polyunsaturated: saturated fatty acid ratios of PE and PC fractions were significantly lower in olive-oil- and fish-oil-fed animals. No differences in the relative proportions of phospholipid classes were found between the three dietary groups. It is suggested that differences in erythrocyte fatty acid composition may reflect dietary-induced changes in membrane cholesterol content and may form part of a homoeostatic response the aim of which is to maintain normal erythrocyte membrane fluidity. The resistance of mammary tissue PI fatty acids to dietary modification suggests that alteration of PI fatty acids is unlikely to underlie effects of dietary fat on mammary tumour incidence rates.
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LI, Duo, Madeleine BALL, Melinda BARTLETT, and Andrew SINCLAIR. "Lipoprotein(a), essential fatty acid status and lipoprotein lipids in female Australian vegetarians." Clinical Science 97, no. 2 (June 18, 1999): 175–81. http://dx.doi.org/10.1042/cs0970175.
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In the present study we investigated serum lipoprotein(a) [Lp(a)] levels, plasma lipids, the serum phospholipid polyunsaturated fatty acid profile and correlates of serum Lp(a) in healthy free-living female vegetarians (n = 50) and omnivores (n = 24) to assess differences which may have implications for cardiovascular risk. Dietary saturated fat and total plasma cholesterol were significantly lower in the vegetarians compared with omnivores. The mean serum Lp(a) concentration was lower in the vegetarians (171 mg/l) than in the omnivores (247 mg/l). The serum Lp(a) concentration was significantly negatively correlated with carbohydrate intake (as % of energy), and positively correlated with plasma total cholesterol. Compared with the omnivores, the vegetarians had significantly lower concentrations of 20:3,n-6, 20:4,n-6, 22:5,n-6, 20:5,n-3, 22:6,n-3 and total n-6 and n-3 polyunsaturated fatty acids, and a lower n-3/n-6 polyunsaturated fatty acid ratio, in serum phospholipids. Lower concentrations of plasma total cholesterol, serum phospholipid total fatty acids, total saturated fatty acids and arachidonic acid, and a tendency towards a lower serum Lp(a) concentration, in vegetarians may have beneficial effects on cardiovascular disease risk. However, the decreased concentration of serum phospholipid n-3 polyunsaturated fatty acids may potentially promote thrombotic risk. Based on the present data, it would seem appropriate for omnivores to reduce their dietary intake of total fat and saturated fat in order to decrease their plasma cholesterol, and vegetarians should perhaps increase their dietary intake of n-3 polyunsaturated fatty acids, and thus improve the balance of n-3/n-6, in order to reduce any thrombotic tendency that might increase their generally low risk of cardiovascular disease.
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Murray Skeaff, C., and Sonya Gowans. "Home use of margarine is an important determinant of plasma trans fatty acid status: a biomarker study." British Journal of Nutrition 96, no. 2 (August 2006): 377–83. http://dx.doi.org/10.1079/bjn20061737.
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The contribution of the home use of margarines, made with partially hydrogenated vegetables oils, to total trans fatty acid intake is difficult to determine using dietary assessment because food composition databases are incomplete for trans fatty acids; moreover, hidden fats in manufactured foods may be the predominant sources of trans fatty acids. The objective of our study was to determine, using plasma phospholipid trans fatty acid composition as a surrogate measure of exposure, whether the home use of margarine or butter is an important determinant of trans fatty acid status. We conducted a community-based (Dunedin, New Zealand), cross-sectional survey of people who consumed either margarine (n 65) or butter (n 64) but not both for home use. The levels of the 18:1 trans isomers commonly found in partially hydrogenated vegetable oils were all significantly higher in the plasma phospholipids of margarine compared with butter consumers, with the exception of 18:1n-7t, which did not differ. Among margarine consumers, the percentage of total fat from margarine was significantly correlated with levels of phospholipid 18:1n−6t, 18:1n-8t and 18:1n-1/t isomers (r 0·57–0·63, P<0·001) but only weakly with 18:1n-7t (r 0·30, P=0·016). The intake of fat from fast foods, bakery products or meat and meat products was not associated with plasma phospholipid trans isomeric composition. The home use of margarine, made with partially hydrogenated vegetable oils, is an important determinant of trans fatty acid exposure in New Zealand.
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WIGGINS, David, and Geoffrey F. GIBBONS. "Origin of hepatic very-low-density lipoprotein triacylglycerol: the contribution of cellular phospholipid." Biochemical Journal 320, no. 2 (December 1, 1996): 673–79. http://dx.doi.org/10.1042/bj3200673.
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When rat hepatocytes were cultured for 24 h in the absence of exogenous fatty acid, the amount of very-low-density lipoprotein (VLDL) triacylglycerol (TAG) secreted (114±14 µg/mg of cell protein) could not be accounted for by the mass of TAG lost from the cells (29±6.1 µg/mg of cell protein) during this period (n = 12). Of the balance (85±14 µg/mg; 94±15 nmol/mg), a maximum of only 37 nmol/mg of cell protein of TAG could be accounted for by fatty acids synthesized de novo. When labelled exogenous oleate (initial concentration, 0.75 mM) was present in the culture medium, the net gain in cellular plus VLDL TAG (253±38 µg/mg of cell protein per 24 h) was greater than that contributed by the exogenous fatty acid (155±18.2 µg/mg of cell protein, n = 5). Again, the balance (98.8±18.2 µg/mg of cell protein per 24 h) was too great to be accounted for by fatty acid synthesis de novo. In experiments in which cellular glycerolipids were prelabelled with [9,10(n)-3H]oleic acid, following removal of the labelled fatty acid, there was a net increase in labelled cellular plus VLDL TAG over the next 24 h. That cellular phospholipids are the source of a substantial part of the excess TAG synthesized is supported by the following evidence. (1) The loss of prelabelled cellular phospholipid during culture was greater than could be accounted for by secretion into the medium. (2) During culture of cells prelabelled with 1,2-di-[1-14C]palmitoyl phosphatidylcholine, a substantial amount of label was secreted as VLDL TAG. (3) In pulse–chase experiments, the kinetics of labelled phospholipid turnover were consistent with conversion into a non-phospholipid pool. The enzymology involved in the transfer of phospholipid fatty acids into TAG is probably complex, but the present results suggest that this pathway may represent an important route by which extracellular fatty acids are channelled into VLDL TAG.
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Rudzite, Vera, Edite Jurika, Janis Jirgensons, Inga Herpfer, Günter Weiss, Helmut Wachter, and Dietmar Fuchs. "The Influence of Kynurenine and Its Metabolites on Lipid Metabolism." Pteridines 8, no. 3 (September 1997): 201–5. http://dx.doi.org/10.1515/pteridines.1997.8.3.201.
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Summary Incorporation of fatty acids into phospholipids has been investigated using samples of rat liver tissue homogenate, Krebs-Ringer-phosphate buffer (pH=7.4) containing 0.3% albumin, fatty acid mixture and glycerol. The addition of L-kynurenine (4 nmoljg wet weight) to incubation medium induced an increase of palmitic, oleic and linolenic acid and decrease of linoleic and arachidonic acid incorporation into phospholipids. These changes of fatty acid incorporation into phospholipids were followed by increase of cholesterol and decrease of phospholipids content in samples. The addition of 3-hydroxykynurenine (1.8 and 4 nmoljg wet weight), 3-hydroxyanthranilic acid (2.2 and 4 nmoljg wet weight) ,1n..:l quinolinic acid (2.4 and 4 nmoljg wet weight) to incubation medium for phospholipid biosynthesis ill vitro induced a decrease of stearic, palrnitic and linoleic acid and an increase of oleic and especially arachidonic acid incorporation into phospholipids. These changes were accompanied by a decrease of cholesterol content in samples. The influence of kynurenine on fatty acid incorporation into phospholipids was similar to that of neopterin observed earlier. The other tryptophan degradation products behaved similar to the reduced pteridine derivatives. Our results allow to suggest that L-kynurenine decreases, while 3-hydroxykynurenine, 3-hydroxyanthranilic acid and quinolinic acid increase membrane fluidity in the studied concentrations.
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Wetzels, J. F., X. Wang, P. E. Gengaro, R. A. Nemenoff, T. J. Burke, and R. W. Schrier. "Glycine protection against hypoxic but not phospholipase A2-induced injury in rat proximal tubules." American Journal of Physiology-Renal Physiology 264, no. 1 (January 1, 1993): F94—F99. http://dx.doi.org/10.1152/ajprenal.1993.264.1.f94.
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We studied the effects of glycine (2 mM) on hypoxia-induced changes in phospholipids and fatty acids in isolated rat proximal tubules. In this preparation, 25 min of hypoxia caused cell injury, as reflected by the release of lactate dehydrogenase (LDH) (13.1 +/- 0.8 vs. 43.5 +/- 3.2%; P < 0.01). Hypoxia caused increases in fatty acids and in lysophospholipids. Glycine prevented the hypoxia-induced cell injury (LDH 13.1 +/- 0.8 vs. 11 +/- 0.7%; not significant) but did not attenuate the increases in fatty acids or lysophospholipids. In additional experiments, the effects of glycine on phospholipid changes and cell injury induced by exogenous phospholipase A2 (PLA2) were studied. PLA2 caused dramatic increases in fatty acids and lysophospholipids and mild cell injury; these effects were not influenced by glycine. In contrast, glycine attenuated increases in LDH release induced by exposing the tubules to exogenous arachidonic acid. In conclusion, glycine does not prevent the phospholipid degradation induced by either exogenous PLA2 or hypoxia in isolated proximal tubules and yet affords protection against hypoxia and exogenous arachidonic acid.
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Banaś, A., A. Dahlqvist, U. Ståhl, M. Lenman, and S. Stymne. "The involvement of phospholipid:diacylglycerol acyltransferases in triacylglycerol production." Biochemical Society Transactions 28, no. 6 (December 1, 2000): 703–5. http://dx.doi.org/10.1042/bst0280703.
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We have characterized three CoA-independent types of enzyme, phospholipases, phospholipid: diacylglycerol acyltransferases (PDATs) and cholinephosphotransferases, responsible for the removal of unusual fatty acids from phosphatidylcholine (PC) in microsomal preparations from developing oil seeds. The metabolism of sn-2-[14C]acyl-PC was monitored in microsomal preparations from various oilseeds having either medium-chain, acetylenic, epoxy or hydroxy fatty acids as their major fatty acids in the oil. The results indicate that PDAT plays a major role in removing ricinoleic acid and vernolic acid from phospholipids in Ricinus communis and Crepis palaestina seeds, respectively. However, vernolic, crepenynic and capric acids are primarily removed from phospholipids by phospholipases in Euphorbia lagascae, Crepis rubra and elm seeds, respectively. Further, we show that significant PDAT activity is also present in vegetative tissues of Arabidopsis thaliana.
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Ly, Dang Thi Phuong, Pham Minh Quan, Trinh Thi Thu Huong, Valeria P. Grigorchuk, Pham Quoc Long, Luu Van Huyen, and Andrey B. Imbs. "INVESTIGATION ON CONTENT OF FATTY ACIDS, PHOSPHOLIPIDS, AND PHOSPHOLIPID MOLECULAR SPECIES COMPOSITION OF THE VIETNAMESE CORAL Bebryce sp." Tạp chí Khoa học và Công nghệ Biển 18, no. 2 (June 30, 2018): 178–86. http://dx.doi.org/10.15625/1859-3097/18/2/12971.
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In the fatty acid composition of total lipid of the soft coral Bebryce sp., the concentration of unsaturated fatty acid predominates. The composition of saturated fatty acids is very diverse, including all saturated fatty acids from C14 to C26. The unsaturated fatty acids with high concentration are C20: 4n-6, 20:5n-3, 22:6n-3, 24:5n-6, 26:3n-6, 26:2n-6, 26:2n-7, 28:3n-6. In the fatty acids composition of the studied coral, there is presence of characterized fatty acids for the existence of sponges C25-C28 (demospongic fatty acids) with total content 29,86%. Most of the Bebryce coral species do not have zooxanthellae, therefore, in the fatty acids composition, either it is lack or contains only a small amount of markers fatty acids for zooxanthellae such as 18:5n-3, 18:4n-3, 18:3n-6, 20:4n-3. In the phospholipid content of the soft coral Bebryce sp., there is presence of characterized classes for Cnidarian animals such as phosphatidylethanolamine (PE), phosphatidylchonline (PC), phosphatidylserine (PS), phosphatidylinositol (PI), phosphonolipid is ceramide aminoethylphosphonate (CAEP). PC account for the highest concentration (37,20% of total phospholipid). The molecular species of phospholipid classes of Bebryce sp. for the first time were investigated. In the results, there we 60 phospholipid molecular species identified in 5 classes. The molecular species with high content in the classes were PE 20:4/18:1e, PE 20:4/19:1, PC 20:4/18:0e, PC 20:4/16:0e, PS 24:5/18:0e, PI 24:5/18:0, CAEP18:2base/16:0 and CAEP 18:1base/16:0.
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Rubin, B. B., G. Chang, S. Liauw, A. Young, A. Romaschin, and P. M. Walker. "Phospholipid peroxidation deacylation and remodeling in postischemic skeletal muscle." American Journal of Physiology-Heart and Circulatory Physiology 263, no. 6 (December 1, 1992): H1695—H1702. http://dx.doi.org/10.1152/ajpheart.1992.263.6.h1695.
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Reperfusion of ischemic skeletal muscle is associated with white blood cell (WBC) sequestration and hydroperoxy-conjugated diene (HCF) formation, a marker of free radical-mediated phospholipid peroxidation. The purpose of this study was to define the kinetics of phospholipid fatty acyl peroxidation, deacylation, and remodeling in postischemic skeletal muscle during prolonged reperfusion in vivo, and to determine whether reperfusion with WBC and plasma-depleted blood would attenuate postischemic phospholipid peroxidation and myocyte necrosis. The isolated, paired, canine gracilis muscle model was used. After 5 h of ischemia, muscles underwent unaltered reperfusion or initial reperfusion with WBC-deficient blood cells resuspended in hydroxyethyl starch, followed by return to normal circulation (modified reperfusion). The concentration of native fatty acids and HCDs of linoleic acid extracted from muscle phospholipids was quantified by gas chromatography and positively identified by mass spectrometry. Ischemia and reperfusion resulted in phospholipid deacylation and a selective increase in phospholipid stearic acid content, but had no effect on total phospholipid phosphorus. Modified reperfusion decreased 1) early HCD formation (54%) and 2) postischemic skeletal muscle necrosis (49%). These data suggest that reperfusion results in phospholipid deacylation and remodeling, and that the initial oxidant stress during reperfusion may be a significant determinant of ultimate muscle necrosis.
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BRUCE, Jennifer S., and Andrew M. SALTER. "Metabolic fate of oleic acid, palmitic acid and stearic acid in cultured hamster hepatocytes." Biochemical Journal 316, no. 3 (June 15, 1996): 847–52. http://dx.doi.org/10.1042/bj3160847.
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Unlike other saturated fatty acids, dietary stearic acid does not appear to raise plasma cholesterol. The reason for this remains to be established, although it appears that it must be related to inherent differences in the metabolism of the fatty acid. In the present study, we have looked at the metabolism of palmitic acid and stearic acid, in comparison with oleic acid, by cultured hamster hepatocytes. Stearic acid was taken up more slowly and was poorly incorporated into both cellular and secreted triacylglycerol. Despite this, stearic acid stimulated the synthesis and secretion of triacylglycerol to the same extent as the other fatty acids. Incorporation into cellular phospholipid was lower for oleic acid than for palmitic acid and stearic acid. Desaturation of stearic acid, to monounsaturated fatty acid, was found to be greater than that of palmitic acid. Oleic acid produced from stearic acid was incorporated into both triacylglycerol and phospholipid, representing 13% and 6% respectively of the total after a 4 h incubation. Significant proportions of all of the fatty acids were oxidized, primarily to form ketone bodies, but by 8 h more oleic acid had been oxidized compared with palmitic acid and stearic acid.
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Fokina, N. N., T. R. Ruokolainen, I. N. Bakhmet, and N. N. Nemova. "Lipid composition in response to temperature changes in blue mussels Mytilus edulis L. from the White Sea." Journal of the Marine Biological Association of the United Kingdom 95, no. 8 (April 17, 2015): 1629–34. http://dx.doi.org/10.1017/s0025315415000326.
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Alterations of membrane lipid composition (cholesterol, phospholipids and their fatty acids) in response to various temperature changes were studied in blue mussels Mytilus edulis L. from the White Sea. Lipid composition changes after acute temperature stress, especially a temperature drop, included a significant reduction of the membrane phospholipid content directly (1 h) after return to the initial temperature, which was presumably a consequence of a non-specific stress reaction in the mussels. A longer recovery period (24 h) as well as long-term temperature acclimation (14 days) induced changes in gill fatty acid composition (for instance, a rise in phospholipid unsaturated fatty acids under low temperature impact), indicating ‘homeoviscous adaptation’ to maintain the membranes in response to temperature fluctuations. Moreover, the gill cholesterol level in mussels varied especially at long-term temperature exposure.
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Lalande, R., B. Gagnon, R. A. Chapman, and G. M. Barnett. "Soil microbial populations, activity, and community structure in continuous corn or forage systems under organic or inorganic fertilization in eastern Canada." Canadian Journal of Soil Science 85, no. 1 (February 1, 2005): 27–38. http://dx.doi.org/10.4141/s04-043.
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Succession of soil microbial communities proceeds interdependently with crop development under the control of edaphic, agricultural, and climatic conditions. Soil microbial community composition and activity were characterized in two managed cropping systems (continuous corn or mixed forage) receiving liquid hog manure (LHM) or inorganic fertilization (IF) since 1989. Microbial community composition was determined from patterns of phospholipid fatty acids (PLFA). Soil microbial biomass C, enzymatic activity, and total phospholipids were greater under forage than under continuous corn. Principal component analysis (PCA) revealed a high degree of variation in PLFA composition and microbial community structure due to treatments and time of sampling. The first two PCA axes explained 80 to 90% of the variability on all sampling dates. Two main groups were created along the first component, the first comprising all forage treatments and a second with LHM-treated continuous corn. The IF and control-treated continuous corn were differentiated from all others on the second component. All groups were characterized by specific microbial communities. The most significant shift in specific groups of fatty acids was caused by LHM addition to continuous corn, especially due to the relative abundance of the fungal fatty acid 18:29,12. Our findings indicated that the addition of organic materials, rich in available C and N, induced development of diverse microbial populations, which can be successfully monitored by phospholipid fatty acid prof iles. Key words: Microbial community, phospholipid fatty acid profiles, hog manure, corn, forage
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Carpenter-Boggs, Lynne, Ann C. Kennedy, and John P. Reganold. "Use of Phospholipid Fatty Acids and Carbon Source Utilization Patterns To Track Microbial Community Succession in Developing Compost." Applied and Environmental Microbiology 64, no. 10 (October 1, 1998): 4062–64. http://dx.doi.org/10.1128/aem.64.10.4062-4064.1998.
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ABSTRACT Carbon source utilization and phospholipid fatty acid analyses were used to track the rapidly changing microbial community in composting dairy waste. Microbial abilities to utilize common plant sugars increased during composting. Community phospholipid profiles changed significantly over time. Phospholipids suggested the presence of more thermophiles and fewer bacteria with continued compost development.
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Jolly, Christopher A., Eric J. Murphy, and Friedhelm Schroeder. "Differential influence of rat liver fatty acid binding protein isoforms on phospholipid fatty acid composition: phosphatidic acid biosynthesis and phospholipid fatty acid remodeling." Biochimica et Biophysica Acta (BBA) - Lipids and Lipid Metabolism 1390, no. 3 (February 1998): 258–68. http://dx.doi.org/10.1016/s0005-2760(97)00186-0.
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Helge, Jørn W., Ben J. Wu, Mette Willer, Jens R. Daugaard, Leonard H. Storlien, and Bente Kiens. "Training affects muscle phospholipid fatty acid composition in humans." Journal of Applied Physiology 90, no. 2 (February 1, 2001): 670–77. http://dx.doi.org/10.1152/jappl.2001.90.2.670.
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Training improves insulin sensitivity, which in turn may affect performance by modulation of fuel availability. Insulin action, in turn, has been linked to specific patterns of muscle structural lipids in skeletal muscle. This study investigated whether regular exercise training exerts an effect on the muscle membrane phospholipid fatty acid composition in humans. Seven male subjects performed endurance training of the knee extensors of one leg for 4 wk. The other leg served as a control. Before, after 4 days, and after 4 wk, muscle biopsies were obtained from the vastus lateralis. After 4 wk, the phospholipid fatty acid contents of oleic acid 18:1(n-9) and docosahexaenoic acid 22:6(n-3) were significantly higher in the trained (10.9 ± 0.5% and 3.2 ± 0.4% of total fatty acids, respectively) than the untrained leg (8.8 ± 0.5% and 2.6 ± 0.4%, P < 0.05). The ratio between n-6 and n-3 fatty acids was significantly lower in the trained (11.1 ± 0.9) than the untrained leg (13.1 ± 1.2, P < 0.05). In contrast, training did not affect muscle triacylglycerol fatty acid composition. Citrate synthase activity was increased by 17% in the trained compared with the untrained leg ( P < 0.05). In this model, diet plays a minimal role, as the influence of dietary intake is similar on both legs. Regular exercise training per se influences the phospholipid fatty acid composition of muscle membranes but has no effect on the composition of fatty acids stored in triacylglycerols within the muscle.
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Reithuber, Elisabeth, Priyanka Nannapaneni, Olena Rzhepishevska, Anders E. G. Lindgren, Oleksandr Ilchenko, Staffan Normark, Fredrik Almqvist, Birgitta Henriques-Normark, and Peter Mellroth. "The Bactericidal Fatty Acid Mimetic 2CCA-1 Selectively Targets Pneumococcal Extracellular Polyunsaturated Fatty Acid Metabolism." mBio 11, no. 6 (December 15, 2020): e03027-20. http://dx.doi.org/10.1128/mbio.03027-20.
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ABSTRACTStreptococcus pneumoniae, a major cause of pneumonia, sepsis, and meningitis worldwide, has the nasopharynges of small children as its main ecological niche. Depletion of pneumococci from this niche would reduce the disease burden and could be achieved using small molecules with narrow-spectrum antibacterial activity. We identified the alkylated dicyclohexyl carboxylic acid 2CCA-1 as a potent inducer of autolysin-mediated lysis of S. pneumoniae, while having low activity against Staphylococcus aureus. 2CCA-1-resistant strains were found to have inactivating mutations in fakB3, known to be required for uptake of host polyunsaturated fatty acids, as well as through inactivation of the transcriptional regulator gene fabT, vital for endogenous, de novo fatty acid synthesis regulation. Structure activity relationship exploration revealed that, besides the central dicyclohexyl group, the fatty acid-like structural features of 2CCA-1 were essential for its activity. The lysis-inducing activity of 2CCA-1 was considerably more potent than that of free fatty acids and required growing bacteria, suggesting that 2CCA-1 needs to be metabolized to exert its antimicrobial activity. Total lipid analysis of 2CCA-1 treated bacteria identified unique masses that were modeled to 2CCA-1 containing lysophosphatidic and phosphatidic acid in wild-type but not in fakB3 mutant bacteria. This suggests that 2CCA-1 is metabolized as a fatty acid via FakB3 and utilized as a phospholipid building block, leading to accumulation of toxic phospholipid species. Analysis of FabT-mediated fakB3 expression elucidates how the pneumococcus could ensure membrane homeostasis and concurrent economic use of host-derived fatty acids.IMPORTANCE Fatty acid biosynthesis is an attractive antibiotic target, as it affects the supply of membrane phospholipid building blocks. In Streptococcus pneumoniae, it is not sufficient to target only the endogenous fatty acid synthesis machinery, as uptake of host fatty acids may bypass this inhibition. Here, we describe a small-molecule compound, 2CCA-1, with potent bactericidal activity that upon interactions with the fatty acid binding protein FakB3, which is present in a limited number of Gram-positive species, becomes metabolized and incorporated as a toxic phospholipid species. Resistance to 2CCA-1 developed specifically in fakB3 and the regulatory gene fabT. These mutants reveal a regulatory connection between the extracellular polyunsaturated fatty acid metabolism and endogenous fatty acid synthesis in S. pneumoniae, which could ensure balance between efficient scavenging of host polyunsaturated fatty acids and membrane homeostasis. The data might be useful in the identification of narrow-spectrum treatment strategies to selectively target members of the Lactobacillales such as S. pneumoniae.
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Price, Edwin R., and Christopher G. Guglielmo. "The effect of muscle phospholipid fatty acid composition on exercise performance: a direct test in the migratory white-throated sparrow (Zonotrichia albicollis)." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 297, no. 3 (September 2009): R775—R782. http://dx.doi.org/10.1152/ajpregu.00150.2009.
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Dietary polyunsaturated fatty acids (PUFA) can have various effects on animal physiology through their roles as energy, structural, regulatory, and signaling molecules. Of recent interest has been the incorporation of dietary PUFA into muscle membranes as phospholipids, thereby potentially affecting exercise performance by mechanisms such as altered mitochondrial proton leak and membrane-bound protein activity. We first studied the effects of a high-ω6 PUFA diet vs. a high-ω3 PUFA diet on peak metabolic rate (PMR) in white-throated sparrows, and additionally measured mRNA expression of fatty acid transporters and the activity of major oxidative enzymes. Our experiment, thus, allowed a test of the “natural doping” hypothesis. With a simple diet manipulation, the two groups of sparrows diverged significantly in both muscle phospholipid composition and adipose triacylglycerol composition. The high-ω6 sparrows achieved higher PMR without a change in enzyme activity or transporter expression. We then fed sparrows the 2 diets, followed by a food restriction (Hω3RI and Hω6RI treatments). When their adipose stores were exhausted, we fed both groups a common diet of intermediate fatty acid composition. This protocol resulted in the Hω6RI and Hω3RI groups diverging significantly in muscle phospholipid composition, but they had substantially similar adipose stores. PMR did not differ between the Hω6RI and Hω3RI groups. We conclude that muscle phospholipids do not play a major role in affecting exercise performance. The fatty acid composition of stored triacylglycerol may instead affect exercise via the preferential use of particular fatty acids by muscles.
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Beavis, Janine, John L. Harwood, Gerald A. Coles, and John D. Williams. "Synthesis of Phospholipids by Human Peritoneal Mesothelial Cells." Peritoneal Dialysis International: Journal of the International Society for Peritoneal Dialysis 14, no. 4 (October 1994): 348–55. http://dx.doi.org/10.1177/089686089401400407.
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Objective To assess the capacity of cultured human peritoneal mesothelial cells to synthesize choline-containing phospholipids. The study compares the phospholipids secreted from cultured cells with those which we, and others, have identified in the dialysate of patients treated by continuous ambulatory peritoneal dialysis (CAPD). Patients CAPD effluent was collected from 8 patients who had been receiving CAPD treatment for at least 11 months and who had normal ultrafiltration. Cell Cultures Using human omental tissue, homogeneous cultures of mesothelial cells were established. Methods Synthesis of phospholipids by mesothelial cells was assessed following incubation with [methyl14C] choline chloride-a precursor capable of being in corporated into phosphatidylcholine (PtdCho) and sphingomyelin. Lipids from CAPD effluent, cultured cells, and cell medium were extracted in chloroform/methanol. Phospholipids were separated and identified by thin layer chromatography. Synthesis and secretion of PtdCho and other choline-containing lipids by the mesothelial cells were determined by β scintillation counting of the appropriate bands, while the fatty acid composition of the phospholipids was ascertained by gas liquid chromatography. Results Synthesis and secretion of PtdCho by mesothelial cells were observed during a 96-hour period. When maintained in medium replete with essential fatty acids, the fatty acid composition of the PtdCho synthesized by cultured mesothelial cells closely resembled that isolated from the peritoneal cavity. Conclusion The demonstration of phospholipid secretion from mesothelial cells, with a fatty acid composition similar to the phospholipids isolated from peritoneal dialysate, lends added support to the hypothesis that the mesothelial cells are the source of the peritoneal phospholipids. As such they offer a useful experimental system in which to study peritoneal phospholipid synthesis.