Academic literature on the topic 'Lipid metabolism[Fatty acid synthesis]'
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Journal articles on the topic "Lipid metabolism[Fatty acid synthesis]"
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Kim, Hyun Uk. "Lipid Metabolism in Plants." Plants 9, no. 7 (July 9, 2020): 871. http://dx.doi.org/10.3390/plants9070871.
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In plants, lipids function in a variety of ways. Lipids are a major component of biological membranes and are used as a compact energy source for seed germination. Fatty acids, the major lipids in plants, are synthesized in plastid and assembled by glycerolipids or triacylglycerols in endoplasmic reticulum. The metabolism of fatty acids and triacylglycerols is well studied in most Arabidopsis model plants by forward and reverse genetics methods. However, research on the diverse functions of lipids in plants, including various crops, has yet to be completed. The papers of this Special Issue cover the core of the field of plant lipid research on the role of galactolipids in the chloroplast biogenesis from etioplasts and the role of acyltransferases and transcription factors involved in fatty acid and triacylglycerol synthesis. This information will contribute to the expansion of plant lipid research.
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Nichols, Frank, and Baliram Maraj. "Relationship between Hydroxy Fatty Acids and Prostaglandin E2 in Gingival Tissue." Infection and Immunity 66, no. 12 (December 1, 1998): 5805–11. http://dx.doi.org/10.1128/iai.66.12.5805-5811.1998.
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ABSTRACT Bacterial hydroxy fatty acids and alpha-hydroxy fatty acids have been demonstrated in complex lipid extracts of subgingival plaque and gingival tissue. However, little is known about the relationship between these hydroxy fatty acids in plaque and gingival tissues or the significance of these complex lipids in promoting inflammatory periodontal disease. The present study determined the percentages of ester-linked and amide-linked hydroxy fatty acids in complex lipids recovered from plaque and gingival tissue samples and the relationship between bacterial hydroxy fatty acids and alpha-hydroxy fatty acids in the lipid extracts. To evaluate a potential role for these hydroxy fatty acids in inflammatory periodontal disease, gingival tissue samples were examined for a relationship between prostaglandin E2 (PGE2) and hydroxy fatty acids recovered in gingival lipid. This investigation demonstrated that alpha-hydroxy fatty acids are only ester linked in plaque lipids but are largely amide linked in gingival tissue lipids. Furthermore, the level of alpha-hydroxy fatty acid in gingival lipid is directly related to the level of the bacterial hydroxy fatty acid 3-OHiso-branched C17:0 (3-OH iC17:0) in the same lipid extract. However, the relationship between hydroxy fatty acids in gingival lipids does not parallel the fatty acid relationship observed in plaque lipids. Finally, alpha-hydroxy fatty acid levels in gingival tissue lipids correlate directly with the recovery of PGE2 in the same tissue samples. These results demonstrate that alpha-hydroxy fatty acid levels in gingival lipids are directly related to both 3-OH iC17:0 bacterial lipid levels and PGE2 levels. These results indicate that in periodontal tissues there are unusual host-parasite interactions involving penetration of bacterial lipid in association with an altered gingival lipid metabolism and prostaglandin synthesis.
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Poitelon, Yannick, Ashley M. Kopec, and Sophie Belin. "Myelin Fat Facts: An Overview of Lipids and Fatty Acid Metabolism." Cells 9, no. 4 (March 27, 2020): 812. http://dx.doi.org/10.3390/cells9040812.
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Myelin is critical for the proper function of the nervous system and one of the most complex cell–cell interactions of the body. Myelination allows for the rapid conduction of action potentials along axonal fibers and provides physical and trophic support to neurons. Myelin contains a high content of lipids, and the formation of the myelin sheath requires high levels of fatty acid and lipid synthesis, together with uptake of extracellular fatty acids. Recent studies have further advanced our understanding of the metabolism and functions of myelin fatty acids and lipids. In this review, we present an overview of the basic biology of myelin lipids and recent insights on the regulation of fatty acid metabolism and functions in myelinating cells. In addition, this review may serve to provide a foundation for future research characterizing the role of fatty acids and lipids in myelin biology and metabolic disorders affecting the central and peripheral nervous system.
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Valença, Isabel, Ana Rita Ferreira, Marcelo Correia, Sandra Kühl, Carlo van Roermund, Hans R. Waterham, Valdemar Máximo, Markus Islinger, and Daniela Ribeiro. "Prostate Cancer Proliferation Is Affected by the Subcellular Localization of MCT2 and Accompanied by Significant Peroxisomal Alterations." Cancers 12, no. 11 (October 27, 2020): 3152. http://dx.doi.org/10.3390/cancers12113152.
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Reprogramming of lipid metabolism directly contributes to malignant transformation and progression. The increased uptake of circulating lipids, the transfer of fatty acids from stromal adipocytes to cancer cells, the de novo fatty acid synthesis, and the fatty acid oxidation support the central role of lipids in many cancers, including prostate cancer (PCa). Fatty acid β-oxidation is the dominant bioenergetic pathway in PCa and recent evidence suggests that PCa takes advantage of the peroxisome transport machinery to target monocarboxylate transporter 2 (MCT2) to peroxisomes in order to increase β-oxidation rates and maintain the redox balance. Here we show evidence suggesting that PCa streamlines peroxisome metabolism by upregulating distinct pathways involved in lipid metabolism. Moreover, we show that MCT2 is required for PCa cell proliferation and, importantly, that its specific localization at the peroxisomal membranes is essential for this role. Our results highlight the importance of peroxisomes in PCa development and uncover different cellular mechanisms that may be further explored as possible targets for PCa therapy.
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Abulnaja, Khalid O., and John L. Harwood. "Effect of a Safener Towards Thiocarbamates on Plant Lipid Metabolism." Zeitschrift für Naturforschung C 46, no. 9-10 (October 1, 1991): 931–33. http://dx.doi.org/10.1515/znc-1991-9-1035.
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Abstract It has been found that various thiocarbamate herbicides, known to alter surface wax and cutin synthesis, inhibit the elongation of fatty acids. We have proposed this as a mode of action of such compounds. Because it is believed that the sulphoxide metabolites of thiocarbamates are the active intermediates, we have examined the action of 1-aminobenzotriazole (an inhibitor of sulphoxide formation) on the inhibition of very long-chain fatty acid biosynthesis. In all tissues tested, aminobenzotriazole was able to block the specific inhibitory effect of thiocarbamates on fatty acid elongation. These results add further support to our proposal that fatty acid elongation is a sensitive target site for thiocarbamate herbicides in plants.
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Cheng, Xiang, Feng Geng, Yaogang Zhong, Zhihua Tian, Meixia Pan, Chunming Cheng, Craig Horbinski, Xiaokui Mo, Xianlin Han, and Deliang Guo. "CBMT-29. PROMOTING FATTY ACID STORAGE BY DIACYLGLYCEROL-ACYLTRANSFERASE 1 PROTECTS GLIOBLASTOMA AGAINST OXIDATIVE STRESS AND MAINTAINS LIPID HOMEOSTASIS FOR RAPID TUMOR GROWTH." Neuro-Oncology 21, Supplement_6 (November 2019): vi39. http://dx.doi.org/10.1093/neuonc/noz175.151.
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Abstract Fatty acids are essential building blocks and energy substrates of lipids in cells. They constitute the major structural components of membrane lipids, i.e., glycerophospholipids and sphingolipids, and also serve as an important energy resource. Whereas excess fatty acids or dysregulation of fatty acid metabolism causes lipotoxicity, leading to severe cell damage. We previously identified that lipid metabolism is dramatically altered in glioblastoma (GBM), especially fatty acid synthesis, which is greatly elevated in various types of cancers. However, how tumor cells prevent excessive fatty acids accumulation from inducing lipotoxicity has rarely been studied. We recently identified that GBM greatly upregulates diacylglycerol-acyltransferase 1 (DGAT1) to direct excess fatty acids into triglycerides and lipid droplets to prevent oxidative stress. Inhibiting DGAT1 disrupts lipid homeostasis and shifts excessive fatty acids moving into mitochondria for oxidation, resulting in a high level of reactive oxygen species (ROS), mitochondrial damage, cytochrome c release and apoptosis. Inhibiting carnitine palmitoyltransferase to reduce fatty acids shuttling into mitochondria significantly decreases ROS and rescues cell death caused by DGAT1 inhibition. Xenograft models show that genetic or pharmacological inhibition of DGAT1 blocks lipid droplet formation, induces tumor cell apoptosis and markedly suppresses GBM tumor growth. Together, our study demonstrates that DGAT1 upregulation protects GBM from oxidative damage and maintains lipid homeostasis by facilitating excess fatty acids storage. Our data further show that targeting DGAT1 specifically induces lipotoxicity in tumor cells, while sparing normal brain, which is a very promising therapeutic strategy antagonizing GBM and has a high potential to shift current paradigm in treating GBM.
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Wu, Jiayue, Linlin Peng, Shubin Dong, Xiaofei Xia, and Liangcheng Zhao. "Transcriptome analysis of Chelidonium majus elaiosomes and seeds provide insights into fatty acid biosynthesis." PeerJ 7 (May 3, 2019): e6871. http://dx.doi.org/10.7717/peerj.6871.
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Background Elaiosomes are specialized fleshy and edible seed appendages dispersed by ants. Lipids are the primary components of elaiosomes. Chelidonium majus is a well-known plant, the seeds of which are dispersed by ants. Previous studies have identified the presence of primary fatty acids in its elaiosomes and seeds. However, the molecular mechanisms underlying fatty acid biosynthesis in elaiosomes remain unknown. Methods In order to gain a comprehensive transcriptional profile of the elaiosomes and seeds of C. majus, and understand the expression patterns of genes associated with fatty acid biosynthesis, four different developmental stages, including the flower-bud (Ch01), flowering (Ch02), young seed (Ch03), and mature seed (Ch04) stages, were chosen to perform whole-transcriptome profiling through the RNA-seq technology (Illumina NGS sequencing). Results A total of 63,064 unigenes were generated from 12 libraries. Of these, 7,323, 258, and 11,540 unigenes were annotated with 25 Cluster of Orthologous Groups, 43 Gene Ontology terms, and 373 Kyoto Encyclopedia of Genes and Genomes pathways, respectively. In addition, 322 genes were involved in lipid transport and metabolism, and 508 genes were involved in the lipid metabolism pathways. A total of 41 significantly differentially expressed genes (DEGs) involved in the lipid metabolism pathways were identified, most of which were upregulated in Ch03 compared to Ch02, indicating that fatty acid biosynthesis primarily occurs during the flowering to the young seed stages. Of the DEGs, acyl-ACP thioesterases, acyl carrier protein desaturase (DESA1), and malonyl CoA-ACP transacylase were involved in palmitic acid synthesis; stearoyl-CoA desaturase and DESA1 were involved in oleic acid synthesis, and acyl-lipid omega-6 desaturase was involved in linoleic acid synthesis.
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Moibi, J. A., R. J. Christopherson, and E. K. Okine. "In vivo and in vitro lipogenesis and aspects of metabolism in ovines: Effect of environmental temperature and dietary lipid supplementation." Canadian Journal of Animal Science 80, no. 1 (March 1, 2000): 59–67. http://dx.doi.org/10.4141/a99-049.
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Twenty-four wether lambs were randomly allocated to six treatments to investigate the effect of temperature and dietary lipid supplements on fatty acid synthesis and metabolic activity in sheep. The treatments consisted of four groups exposed to either cold (0 °C) or warm temperature (+23 °C) and given ad libitum access to either a control barley-based diet or with lipid supplementation. Two other groups were placed on the dietary regimen at 0 °C, but pair-fed to intake of animals in the +23 °C environment. At 5 wk, fatty acid synthesis was measured by [1-14C]acetate incorporation into tissue lipids. Cold exposure and dietary lipid supplementation had no effect (P > 0.05) on in vivo fatty acid synthesis rates in either longissimus dorsi or the liver. In both subcutaneous and mesenteric adipose tissue depots, the rate of acetate incorporation into tissue lipid was not significantly affected by cold exposure. In the perirenal fat depot, cold exposure increased (P < 0.05) the rate of fatty acid synthesis, while lipid supplementation decreased (P < 0.05) the rate in all tissue adipose depots. In vitro, mesenteric and perirenal adipose tissues from cold pair-fed animals had higher (P < 0.05) rates of fatty acid synthesis compared to tissues from animals in the warm environment. However, there was no effect of dietary lipid supplementation in these two fat depots. Metabolic heat production, and energy and nitrogen excretion by animals were increased (P < 0.05) by cold exposure while lipid supplementation had the opposite effect (P < 0.05). The relationship between average daily gain and feed intake was linear at both warm and cold environments, but with higher (P < 0.05) average daily gain at all levels of intake in the cold compared to the warm environment. Results indicate that both environment and diet regulate metabolic activity in sheep. However, there were differences in lipogenic response by tissues to the treatments. Key words: Environmental temperature, dietary lipid, fatty acid synthesis, metabolic rate, sheep
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Cazzolli, R., D. L. Craig, T. J. Biden, and C. Schmitz-Peiffer. "Inhibition of glycogen synthesis by fatty acid in C2C12 muscle cells is independent of PKC-α, -ε, and -θ." American Journal of Physiology-Endocrinology and Metabolism 282, no. 6 (June 1, 2002): E1204—E1213. http://dx.doi.org/10.1152/ajpendo.00487.2001.
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We have previously shown that glycogen synthesis is reduced in lipid-treated C2C12 skeletal muscle myotubes and that this is independent of changes in glucose uptake. Here, we tested whether mitochondrial metabolism of these lipids is necessary for this inhibition and whether the activation of specific protein kinase C (PKC) isoforms is involved. C2C12 myotubes were pretreated with fatty acids and subsequently stimulated with insulin for the determination of glycogen synthesis. The carnitine palmitoyltransferase-1 inhibitor etomoxir, an inhibitor of β-oxidation of acyl-CoA, did not protect against the inhibition of glycogen synthesis caused by the unsaturated fatty acid oleate. In addition, although oleate caused translocation, indicating activation, of individual PKC isoforms, inhibition of PKC by pharmacological agents or adenovirus-mediated overexpression of dominant negative PKC-α, -ε, or -θ mutants was unable to prevent the inhibitory effects of oleate on glycogen synthesis. We conclude that neither mitochondrial lipid metabolism nor activation of PKC-α, -ε, or -θ plays a role in the direct inhibition of glycogen synthesis by unsaturated fatty acids.
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Li, Tiangang, and John Y. L. Chiang. "Regulation of Bile Acid and Cholesterol Metabolism by PPARs." PPAR Research 2009 (2009): 1–15. http://dx.doi.org/10.1155/2009/501739.
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Bile acids are amphipathic molecules synthesized from cholesterol in the liver. Bile acid synthesis is a major pathway for hepatic cholesterol catabolism. Bile acid synthesis generates bile flow which is important for biliary secretion of free cholesterol, endogenous metabolites, and xenobiotics. Bile acids are biological detergents that facilitate intestinal absorption of lipids and fat-soluble vitamins. Recent studies suggest that bile acids are important metabolic regulators of lipid, glucose, and energy homeostasis. Agonists of peroxisome proliferator-activated receptors (PPARα, PPARγ, PPARδ) regulate lipoprotein metabolism, fatty acid oxidation, glucose homeostasis and inflammation, and therefore are used as anti-diabetic drugs for treatment of dyslipidemia and insulin insistence. Recent studies have shown that activation of PPARαalters bile acid synthesis, conjugation, and transport, and also cholesterol synthesis, absorption and reverse cholesterol transport. This review will focus on the roles of PPARs in the regulation of pathways in bile acid and cholesterol homeostasis, and the therapeutic implications of using PPAR agonists for the treatment of metabolic syndrome.
Dissertations / Theses on the topic "Lipid metabolism[Fatty acid synthesis]"
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Souza, Paulo Fernando Araujo de. "The effects of dietary fat on the metabolism of the lactating rat." Thesis, University of Oxford, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.276817.
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Stahl, Richard J. (Richard John). "Fatty acid and glycerolipid biosynthesis in pea root plastids." Thesis, McGill University, 1990. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=22389.
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Fatty acid biosynthesis from (1-$ sp{14}$C) acetate was optimized in plastids isolated from primary root tips of 7-day-old germinating pea seeds. Fatty acid synthesis was maximum at 82.3 nmol/hr/mg protein in the presence of 200$ mu$M acetate, 0.5mM each of NADH, NADPH and CoA, 6mM each of ATP and MgCl$ sb2$, 1mM each of MnCl$ sb2$ and glycerol-3-phosphate (G3P), 15mM KHCO$ sb3$, and 0.1M Bis tris propane, pH 8.0 incubated at 35C. At the standard incubation temperature of 25C, fatty acid synthesis was linear for up to 6 hours with 80 to 120 $ mu$g/ml plastid protein. ATP and CoA were absolute requirements, whereas divalent cations, potassium bicarbonate and reduced nucelotides all improved activity by 2 to 10 fold. Mg$ sp{2+}$ and NADH were the preferred cation and nucleotide, respectively. G3P and dihydroxyacetone phosphate had little effect, and dithiothreitol and detergents generally inhibited incorporation of $ sp{14}$C-acetate into fatty acid.Glycerolipid synthesis was obtained from $ sp{14}$C-acetate, (U-$ sp{14}$C) G3P and (U-$ sp{14}$C) glycerol at relative rates of 3.7:1.0:0.1, respectively. (Abstract shortened by UMI.)
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Qi, Qungang. "The role of glycolytic metabolism in fatty acid and glycerolipid biosynthesis in pea root plastids." Thesis, McGill University, 1995. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=39980.
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The interaction between the glycolytic metabolism and fatty acid and glycerolipid biosynthesis in pea root (Pisum sativum L.) plastids was assessed in this study. When various glycolytic intermediates were used to substitute for the APT requirement for fatty acid synthesis from acetate, phosphoenolpyruvate, 2-phosphoglycerate, fructose-6-phosphate and glucose-6-phosphate each gave 48, 17, 23 and 17%, respectively, of the ATP-control activity. Similarly, in the absence of exogenously supplied ATP, the optimized triose-phosphate shuttle, which consists of 2 mM dihydroxyacetone phosphate, 2 mM oxaloacetic acid and 4 mM inorganic phosphate, gave up to 44% the ATP-control activity in promoting fatty acid synthesis from acetate. These results suggest that 3-phosphoglycerate kinase and pyruvate kinase in these plastids can function in intraplastidic ATP production through substrate level phosphorylation. However, in all cases, exogenously supplied ATP gave the greatest rates of fatty acid and glycerolipid synthesis. Radiolabeled pyruvate, glucose, glucose-6-phosphate, and malate in comparison to acetate were all variously utilized for fatty acid and glycerolipid biosynthesis by the root plastid. At the highest concentrations tested (3-5 mM), the rates of incorporation of pyruvate, glucose-6-phosphate and acetate into fatty acids were 183, 154, 125 nd 99 nmol $ rm cdot h sp{-1} cdot mg sp{-1}$, respectively. Malate was the least effective precursor, giving less than 55 nmol $ rm cdot h sp{-1} cdot mg sp{-1}$. Acetate incorporation was approximately 55% dependent on exogenously supplied reduced nuclotides (NADPH and NADH), whereas the utilization of the remaining precursors was only approximately 10-20% dependent on NAD(P)H. These results indicate that the entire pathway of carbon flow from glycolysis, including pyruvate dehydrogenase (PDHase), to fatty acids is operating in pea root plastids. Further, the intraplastidic glycolytic pathway plays an important role in provi
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Behrman, Roger L. "The effects of dietary fat and age on adipose tissue composition and fatty acid synthesis levels in strain A/ST mice." Virtual Press, 1990. http://liblink.bsu.edu/uhtbin/catkey/722436.
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Differences in fatty acid distributions in adipose tissue and fatty acid synthetase levels in the liver were determined in Strain A/ST mice of different ages and diets. Since fatty acids have been found to be influential in many disease processes such as heart disease and cancer, which become more prevalent with increasing age, it is important to understand the processes of fat metabolism and changes that occur during the life-stage of senescence. Fatty acid distributions were determined by gas liquid chromatography and fatty acid synthetase (FAS) activities by spectrophotometry.The data from FAS analyses indicated that the mice fed the highfat palmitic acid and low-fat corn oil diets were similar to previous research. The mice fed the stearic acid diets had FAS activity that was affected in a very different manner than other high-fat diets.The results of this study also indicated that aging does not significantly effect the distribution of fatty acids in the adipose tissue of experimental mice. Weight gain in the middle age mice appears to be the result of an increase in all types of fatty acids and not just increased storage of one or a few types.Department of Biology
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Park, Young kyoung. "Metabolic engineering of the yeast Yarrowia lipolytica for the production of even- and odd-chain fatty acids." Thesis, université Paris-Saclay, 2020. http://www.theses.fr/2020UPASB010.
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Les huiles microbiennes sont considérées comme des alternatives prometteuses aux combustibles fossiles qui suscitent de plus en plus de préoccupations environnementales et énergétiques. Les acides gras à chaîne impaires (AGI), un type de lipide inhabituel, sont des composés d’intérêt ayant diverses applications biotechnologiques. L’objectif de cette thèse est de développer Yarrowia lipolytica comme souche plateforme, par l’ingénierie métabolique, pour la production d’AGI.Pour développer Y. lipolytca, l'identification et la caractérisation d’une nouvelle série de promoteurs érythritol-hybrides-inductible (pEYK1, pEYD1, et dérivés) ont été réalisées. La série de promoteurs hybrides a montré des forces variables, l'induction à base d'érythritol a augmenté de 2,2 à 32,3 fois dans la souche WT et de 2,9 à 896,1 fois dans la souche eyk1Δ. Ces promoteurs amélioreront la capacité de moduler l'expression de gènes chez Y. lipolytica.Pour la production d’AGI, la tolérance au propionate a été étudiée. Deux gènes, RTS1 et MFS1, améliorant la résistance au propionate ont été identifiés par le criblage d’une banque d’ADN génomique. Par des stratégies d’ingénierie métabolique, comme l’inhibition de la voie compétitive, l’augmentation les pools de précurseurs, et l’amélioration de l’accumulation de lipides totale, la production d'AGI a été augmentée de 0,14 g/L à 1,87 g/L. La production de novo des AGI sans supplémentation de propionate a également été explorée. Par surexpression des gènes dans la voie de synthèse de la thréonine, la production d’AGI été augmentée de 12 fois par rapport à la souche sauvage (0,36 versus 0,03 g/L).En résumé, des souches de Y. lipolytica ont été développées pour produire efficacement des AGI, principalement l’acide heptadécénoïque. Ce travail ouvre la voie à la production microbienne d'AGI et de ses dérivés à plus grande échelleMicrobial oils are regarded as promising alternatives to fossil fuels with growing environmental and energy concerns. Odd-chain fatty acids (OCFAs), a type of unusual lipids, are value-added compounds with various biotechnological applications. The objective of the thesis was to develop Yarrowia lipolytica as a platform strain for the production of OCFAs by metabolic engineering.For developing Y. lipolytica, the identification and characterization of a new series of erythritol-hybrid-inducible promoters (pEYK1, pEYD1, and derivatives) were explored. The hybrid promoter series showed variable strengths, erythritol-based induction increased 2.2 to 32.3 times in the WT strain and 2.9 to 896.1 times in the eyk1Δ strain, which will improve the modulation of gene expression for metabolic engineering of Y. lipolytica.For OCFA production, tolerance to propionate was studied. Two genes, RTS1 and MFS1, were identified as propionate-tolerant genes by screening a genomic DNA library. Through metabolic engineering strategies, such as inhibiting competitive pathways, increasing precursor pools, and enhancement of total lipid accumulation, OCFA production was increased from 0.14 g/L to 1.87 g/L. De novo production of OCFAs without propionate supplementation was also explored by overexpression of the threonine synthesis pathway. OCFAs production was increased by 12-times; 0.36 versus 0.03 g/L for WT.In summary, Y. lipolytica strains were developed to produce high-amount of OCFAs, mainly heptadecenoic acid. This work paves the way for the microbial production of OCFAs and their derivatives at the industrial scale
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Masterson, Christine. "Carnitine and fatty acid metabolism in higher plants." Thesis, University of Newcastle Upon Tyne, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.254030.
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Zampelas, Antonios. "Effect of dietary fatty acid structure and composition on postprandial lipid metabolism." Thesis, University of Surrey, 1993. http://epubs.surrey.ac.uk/770401/.
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In this thesis effects of dietary fatty acid composition and of positional distribution of fatty acids in dietary TAG, on postprandial lipid and hormone responses, were investigated. A6 week fish oil supplementation period (2.7 g n-3 fatty acids per day) decreased fasting TAG and increased TC (p<0.05) and LDL-C (p<0.05) levels in normal subjects. Postprandial plasma TAG responses to a test meal were also significantly reduced following the fish oil supplementation period (area under the response curves, p<0.001). Apolipoproteins A-I and B responses did not alter in response to chronic fish oil supplementation. Type II diabetics responded differently to normal subjects to fish oil supplementation. Fasting lipid and apolipoprotein levels were not significantly altered, and the postprandial TAG response to a test meal showed a trend towards higher values following the fish oil supplementation period. In the study of effects of dietary TAG structure on postprandial lipid apolipoprotein (A-I, B), hormone (insulin, GIP) and glucose responses, no effect of test meals differing in the positional distribution of palmitic acid at the sn-2 or the sn-3 positions of the TAG molecule were seen. In a study of acute effects of dietary fatty acid composition in healthy male subjects, a fish oil test meal (40 g fish oil concentrate), significantly reduced plasma TAG postprandial responses compared with a mixed oil meal (containing 40 g of a mixture of oils high in SFA and mimicking the current U. K. dietary fat intake), p<0.05. Post-heparin LPL activity was also significantly increased 12 hours following the fish oil test meal (p<0.01). A 40 g corn oil test meal did not have any significant effect on postprandial lipid, hormone (insulin and GIP), and retinyl palmitate levels (the latter was administered with each test meal-700 I. U. /kg of body weight) compared with the other two test meals. A feeding study, using a rat model, showed that following two weeks of a fish oil diet (5%, w/w) the postprandial incorporation of [U-t4C]glucose into hepatic total lipids and TAG measured in vitro, was significantly reduced compared with rates measured in animals on a mixed oil diet (p<0.05). In the presence of the two anabolic hormones, insulin and GIP, in vitro rates of hepatic cholesterogenesis increased (p<0.05), and these effects of hormones were independent of the type of the diet fed. In addition, plasma TAG levels were significantly lower in the fish oil group compared with levels in the mixed oil and corn oil dietary groups (p<0.05), and plasma insulin levels were significantly higher in the mixed oil dietary group than in the other two groups (p<0.001).
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Erol, Erdal. "Heart- and liver-type fatty acid binding proteins in lipid and glucose metabolism." Diss., Texas A&M University, 2004. http://hdl.handle.net/1969.1/1148.
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Heart-type Fatty Acid-Binding Protein (H-FABP) is required for high rates of skeletal muscle long chain fatty acid (LCFA) oxidation and esterification. Here we assessed whether H-FABP affects soleus muscle glucose uptake when measured in vitro in the absence of LCFA. Wild type and H-FABP null mice were fed a standard chow or high fat diet before muscle isolation. With the chow, the mutation increased insulin-dependent deoxyglucose uptake by 141% (P<0.01) at 0.02 mU/ml of insulin, but did not cause a significant effect at 2 mU/ml insulin; skeletal muscle triglyceride and long chain acyl-CoA (LCACoA) levels remained normal. With the fat diet, the mutation increased insulin-dependent deoxyglucose uptake by 190% (P<0.01) at 2 mU/ml insulin, thus partially preventing insulin resistance, and completely prevented the threefold (P<0.001) diet-induced increase of muscle triglyceride levels; however, muscle LCACoA levels showed little or no reduction. With both diets, the mutation reduced the basal (insulinindependent) soleus muscle deoxyglucose uptake by 28% (P<0.05). These results establish a close relationship of FABP-dependent lipid pools with insulin sensitivity, and indicate the existence of a non-acute, antagonistic, and H-FABP-dependent fatty acid regulation of basal and insulin-dependent muscle glucose uptake.
Liver fatty acid binding protein (L-FABP) has been proposed to limit the availability of chain LCFA for oxidation and for peroxisome proliferator-activated receptor (PPAR-alpha), a fatty acid binding transcription factor that determines the capacity of hepatic fatty acid oxidation. Here, we used L-FABP null mice to test this hypothesis. Under fasting conditions, this mutation reduced β-hydroxybutyrate (BHB) plasma levels as well as BHB release and palmitic acid oxidation by isolated hepatocytes. However, the capacity for ketogenesis was not reduced: BHB plasma levels were restored by octanoate injection; BHB production and palmitic acid oxidation were normal in liver homogenates; and hepatic expression of key PPAR-alpha target (MCAD, mitochondrial HMG CoA synthase, ACO, CYP4A3) and other (CPT1, LCAD) genes of mitochondrial and extramitochondrial LCFA oxidation and ketogenesis remained at wild-type levels. These results suggest that under fasting conditions, hepatic L-FABP contributes to hepatic LCFA oxidation and ketogenesis by a nontranscriptional mechanism.
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Jenkins, Benjamin John. "The role of alpha oxidation in lipid metabolism." Thesis, University of Cambridge, 2018. https://www.repository.cam.ac.uk/handle/1810/278025.
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Recent findings have shown an inverse association between the circulating levels of pentadecanoic acid (C15:0) and heptadecanoic acid (C17:0) with the risk of pathological development in type 2 diabetes, cardio vascular disease and neurological disorders. From previously published research, it has been said that both these odd chain fatty acids are biomarkers of their dietary intake and are significantly correlated to dietary ruminant fat intake. However, there are profound studies that show the contrary where they do not display this biomarker correlation. Additionally, several astute studies have suggested or shown odd chain fatty acid endogenous biosynthesis, most often suggested via alpha oxidation; the cleavage of a single carbon unit from a fatty acid chain within the peroxisomes. To better understand the correlations and interactions between these two fatty acids with pathological development, the origin of these odd chain fatty acids needed to be determined, along with confirming their association with the disease aetiology. To minimise animal & human experimentation we made use of existing sample sets made available through institutional collaborations, which produced both animal and human interventional study samples suitable for odd chain fatty acid investigations. These sample collaborations allowed us to comprehensively investigate all plausible contributory sources of these odd chain fatty acids; including from the intestinal microbiota, from dietary contributions, and derived from novel endogenous biosynthesis. The investigations included two intestinal germ-free studies, two ruminant fat diet studies, two dietary fat studies and an ethanol intake study. Endogenous biosynthesis was assessed through: a stearic acid infusion, phytol supplementation, and an Hacl1 knockout mouse model. A human dietary intervention study was used to translate the results. Finally, a study comparing circulating baseline C15:0 and C17:0 levels with the development of glucose intolerance. We found that the circulating C15:0 and C17:0 levels were not significantly influenced by the presence or absence of intestinal microbiota. The circulating C15:0 levels were significantly and linearly increased when the C15:0 dietary composition increased; however, there was no significant correlation in the circulating C17:0 levels with intake. Circulating levels of C15:0 were affected by the dietary composition and factors affecting the dietary intake, e.g. total fat intake and ethanol, whereas circulating C17:0 levels were found to be independent of these variables. In our studies, the circulating C15:0 levels were not significantly affected by any expected variations in alpha oxidation caused by pathway substrate inhibition or gene knockout. However, C17:0 was significantly related, demonstrating it is substantially endogenously biosynthesised. Furthermore, we found that the circulating C15:0 levels, when independent of any dietary variations, did not correlate with the progression of glucose intolerance when induced, but the circulating C17:0 levels did significantly relate and linearly correlated with the development of glucose intolerance. To summarise, the circulating C15:0 and C17:0 levels were independently derived; the C15:0 levels substantially correlated with its dietary intake, whilst the C17:0 levels proved to be separately derived from its endogenous biosynthesis via alpha oxidation of stearic acid. C15:0 was found to be minimally endogenously biosynthesised via a single cycle of beta oxidation of C17:0 in the peroxisomes, however, this did not significantly contribute to the circulating levels of C15:0. Additionally, only the baseline levels of C17:0 significantly correlated with the development of glucose intolerance. These findings highlight the considerable differences between both of these odd chain fatty acids that were once thought to be homogeneous and similarly derived. On the contrary, they display profound dietary, metabolic, and pathological differences.
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Johnson, Philip E. "Interaction of subcellular compartments during lipid synthesis in oilseed rape (Brassica napus L.)." Thesis, University of East Anglia, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.302211.
Full textBooks on the topic "Lipid metabolism[Fatty acid synthesis]"
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Gluckman, Sir Peter, Mark Hanson, Chong Yap Seng, and Anne Bardsley. Vitamin B7 (biotin) in pregnancy and breastfeeding. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780198722700.003.0011.
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Biotin is a water-soluble B vitamin (vitamin B7) which acts as a coenzyme to carboxylases and has roles in gluconeogenesis, fatty acid synthesis, and amino acid catabolism. Reduced activity of biotin-dependent enzymes (acetyl-CoA carboxylase I and II, and propionyl-CoA carboxylase) alters lipid metabolism and may impair synthesis of polyunsaturated fatty acids and prostaglandins; in addition, biotin has effects on gene expression by binding covalently to histones. Deficiency can be caused by prolonged consumption of egg whites, which contain the biotin-binding protein avidin. Smoking accelerates the degradation of biotin, which can result in marginal biotin deficiency. The effects of deficiency include disruption of immune function and lipid metabolism, with some evidence of teratogenicity in animals. Dietary deficiency is unlikely, although high consumption of egg whites should be avoided in pregnancy.
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Glatz, Jan F. C., and A. T. M. Jansen. Cellular Lipid Binding Proteins. Springer London, Limited, 2012.
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Cellular Lipid Binding Proteins. Springer, 2011.
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C, Glatz Jan F., ed. Cellular lipid binding proteins. Dordrecht: Kluwer Academic Pub., 2002.
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Kim, Min Sun. Effect of vitamin B-6 status on fatty acid and lipid metabolism in women. 1997.
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Kim, Min Sun. Effect of vitamin B-6 status on fatty acid and lipid metabolism in women. 1997.
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Koljak, Reet. Novel fatty acid dioxygenases from the corals plexaura homomalla and gersemia fruticosa. Tallin Technical University, 2001.
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Fatty Acid and Lipotoxicity in Obesity and Diabetes (Novartis Foundation Symposia). Wiley, 2008.
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Iversen, Leslie. Endocannabinoids. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780190846848.003.0004.
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The endocannabinoids are part of a large family of lipid signaling molecules derived from arachidonic acid, including the prostaglandins and leukotrienes, which are important mediators of inflammation. Far less is known about the newer members of the endocannabinoid group, and it remains unclear whether they all play important functional roles. This chapter reviews the multiple members of this family and their biosynthesis and inactivation. Physiological functions, including retrograde synaptic signaling, control of energy metabolism, regulation of pain sensitivity, and cardiovascular control, are discussed. In addition, the chapter reports the synthesis of novel agonists, antagonists, and compounds inhibiting endocannabinoid inactivation as novel medicines.
Book chapters on the topic "Lipid metabolism[Fatty acid synthesis]"
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Barrett, Philippa B., and John L. Harwood. "Thiocarbamate Action on very Long Chain Fatty Acid Synthesis in Plants." In Plant Lipid Metabolism, 115–17. Dordrecht: Springer Netherlands, 1995. http://dx.doi.org/10.1007/978-94-015-8394-7_33.
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Slabaugh, Mary, Jeff Leonard, Gordon Huestis, Jim Crane, and Steve Knapp. "Genetic and Biochemical Studies of Medium Chain Fatty Acid Synthesis in Cuphea." In Plant Lipid Metabolism, 499–502. Dordrecht: Springer Netherlands, 1995. http://dx.doi.org/10.1007/978-94-015-8394-7_137.
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Tate, Patricia L., Charles Ainsworth, Gary Kodiert, and Albert Abbott. "The Phylogenetic Relationships of the Species within the Section Arachis Utilizing a Fatty Acid Synthesis Gene." In Plant Lipid Metabolism, 30–32. Dordrecht: Springer Netherlands, 1995. http://dx.doi.org/10.1007/978-94-015-8394-7_8.
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Pollard, Michael R., and Sheo S. Singh. "Fatty Acid Synthesis in Developing Oilseeds." In The Metabolism, Structure, and Function of Plant Lipids, 455–63. Boston, MA: Springer New York, 1987. http://dx.doi.org/10.1007/978-1-4684-5263-1_84.
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Rawsthorne, Stephen, and Fan Kang. "Synthesis of Starch and Fatty Acids By Plastids Isolated from Developing Embryos of Oilseed Rape." In Plant Lipid Metabolism, 479–81. Dordrecht: Springer Netherlands, 1995. http://dx.doi.org/10.1007/978-94-015-8394-7_131.
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Harwood, John L. "Medium and Long-chain Fatty Acid Synthesis." In The Metabolism, Structure, and Function of Plant Lipids, 465–72. Boston, MA: Springer New York, 1987. http://dx.doi.org/10.1007/978-1-4684-5263-1_85.
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Morand, Olivier, and Marie-Stéphane Aigrot. "A Model for Studying Membrane Fatty Acid Transport : Acyl-Coenzyme a Synthesis in Human Erythrocyte Ghosts." In Enzymes of Lipid Metabolism II, 437–49. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-5212-9_57.
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Yamada, Mitsuhiro, Misako Kato, Ikuo Nishida, Kazuo Kawano, Akihiko Kawaguchi, and Tomoko Ehara. "Modulation of Fatty Acid Synthesis in Plants by Thiolactomycin." In The Metabolism, Structure, and Function of Plant Lipids, 447–54. Boston, MA: Springer New York, 1987. http://dx.doi.org/10.1007/978-1-4684-5263-1_83.
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Hoang, Giang, Kiet Nguyen, and Anne Le. "Metabolic Intersection of Cancer and Cardiovascular Diseases: Opportunities for Cancer Therapy." In The Heterogeneity of Cancer Metabolism, 249–63. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-65768-0_18.
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AbstractAccording to data from the World Health Organization, cardiovascular diseases and cancer are the two leading causes of mortality in the world [1]. Despite the immense effort to study these diseases and the constant innovation in treatment modalities, the number of deaths associated with cardiovascular diseases and cancer is predicted to increase in the coming decades [1]. From 2008 to 2030, due to population growth and population aging in many parts of the world, the number of deaths caused by cancer globally is projected to increase by 45%, corresponding to an annual increase of around four million people [1]. For cardiovascular diseases, this number is six million people [1]. In the United States, treatments for these two diseases are among the most costly and result in a disproportionate impact on low- and middleincome people. As the fight against these fatal diseases continues, it is crucial that we continue our investigation and broaden our understanding of cancer and cardiovascular diseases to innovate our prognostic and treatment approaches. Even though cardiovascular diseases and cancer are usually studied independently [2–12], there are some striking overlaps between their metabolic behaviors and therapeutic targets, suggesting the potential application of cardiovascular disease treatments for cancer therapy. More specifically, both cancer and many cardiovascular diseases have an upregulated glutaminolysis pathway, resulting in low glutamine and high glutamate circulating levels. Similar treatment modalities, such as glutaminase (GLS) inhibition and glutamine supplementation, have been identified to target glutamine metabolism in both cancer and some cardiovascular diseases. Studies have also found similarities in lipid metabolism, specifically fatty acid oxidation (FAO) and synthesis. Pharmacological inhibition of FAO and fatty acid synthesis have proven effective against many cancer types as well as specific cardiovascular conditions. Many of these treatments have been tested in clinical trials, and some have been medically prescribed to patients to treat certain diseases, such as angina pectoris [13, 14]. Other metabolic pathways, such as tryptophan catabolism and pyruvate metabolism, were also dysregulated in both diseases, making them promising treatment targets. Understanding the overlapping traits exhibited by both cancer metabolism and cardiovascular disease metabolism can give us a more holistic view of how important metabolic dysregulation is in the progression of diseases. Using established links between these illnesses, researchers can take advantage of the discoveries from one field and potentially apply them to the other. In this chapter, we highlight some promising therapeutic discoveries that can support our fight against cancer, based on common metabolic traits displayed in both cancer and cardiovascular diseases.
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Liedvogel, Bodo. "Lipid Precursors in Plant Cells: The Problem of Acetyl CoA Generation for Plastid Fatty Acid Synthesis." In The Metabolism, Structure, and Function of Plant Lipids, 509–11. Boston, MA: Springer New York, 1987. http://dx.doi.org/10.1007/978-1-4684-5263-1_91.
Full textConference papers on the topic "Lipid metabolism[Fatty acid synthesis]"
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Al-Qeraiwi, Maha, Manar Al-Rashid, Nasser Rizk, Abdelrahman El Gamal, and Amena Fadl. "Hepatic Gene Expression Profile of Lipid Metabolism of Obese Mice after treatment with Anti-obesity Drug." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0214.
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Obesity is a global disorder with multifactorial causes. The liver plays a vital role in fat metabolism. Disorder of hepatic fat metabolism is associated with obesity and causes fatty liver. High fat diet intake (HFD) to mice causes the development of dietinduced obesity (DIO). The study aimed to detect the effects of anti-obesity drugs (sulforaphane; SFN and leptin) on hepatic gene expression of fat metabolism in mice that were fed HFD during an early time of DIO. Twenty wild types (WT) CD1 male mice aged ten weeks were fed a high fat diet. The mice were treated with vehicle; Veh (control group), and SFN, then each group is treated with leptin or saline. Four groups of treatment were: control group (vehicle + saline), Group 2 (vehicle + leptin), group 3 (SFN + saline), and group 4 (SFN + leptin). Body weight and food intake were monitored during the treatment period. Following the treatments of leptin 24 hour, fasting blood samples and liver tissue was collected, and Total RNA was extracted then used to assess the gene expression of 84 genes involved in hepatic fat metabolism using RT-PCR profiler array technique. Leptin treatment upregulated fatty acid betaoxidation (Acsbg2, Acsm4) and fatty acyl-CoA biosynthesis (Acot6, Acsl6), and downregulated is fatty acid transport (Slc27a2). SFN upregulated acylCoA hydrolase (Acot3) and long chain fatty acid activation for lipids synthesis and beta oxidation (Acsl1). Leptin + SFN upregulated fatty acid beta oxidation (Acad11, Acam) and acyl-CoA hydrolase (Acot3, Acot7), and downregulated fatty acid elongation (Acot2). As a result, treatment of both SFN and leptin has more profound effects on ameliorating pathways involved in hepatic lipogenesis and TG accumulation and lipid profile of TG and TC than other types of intervention. We conclude that early intervention of obesity pa could ameliorate the metabolic changes of fat metabolism in liver as observed in WT mice on HFD in response to anti-obesity treatment.
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Schick, Paul K., Barbara P. Schick, and Pat Webster. "THE EFFECT OF OMEGA 3 FATTY ACIDS ON MEGAKARYOCYTE ARACHIDONIC ACID METABOLISM." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642953.
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Dietary omega 3 polyunsaturated fatty acids are thought to prevent atherosclerosis. It has been proposed that omega 3 fatty acids modify platelet arachidonic acid (20:4) metabolism and platelet function and thereby reduce the incidence of thrombosis. We have previously shown that megakaryocytes (MK), like platelets, contain large amounts of esterified 20:4. The study addresses the following questions: 1) Do omega 3 fatty acids have a primary action on 20:4 metabolism in MK rather than in platelets. 2) Do omega 3 marine oils, docosahexaenoic acid (22:6) and eicosapentaenoic acid (20:5), have a different effect on megakaryocyte 20:4 metabolism than does alpha linolenic acid (18:3), the major omega-3 fatty acid present in normal diets? 3) How do omega-3 fatty acids modify megakaryocyte 20:4 acid metabolism? MK and platelets were isolated from guinea pigs. Isolated cells were incubated with radiolabeled 20:4 acid and unlabeled 18:3, 20:5 or 22:6. Incubations were terminated by lipid extraction, lipid classes were separated by thin-layer chromatography and the incorporation of radiolabeled 20:4 into lipid species was measured by scintillation spectrometry.MK (106) can incorporate about 4 times more 20:4 than 109 platelets. We have previously shown that 20:4 is incorporated into all endogenous pools of 20:4 in MK while platelets appear to have a limited capacity to incorporate 20:4 into phosphatidyl-ethanolamine (PE). Marine oils, 22:6 and 20:5, had similar effects on the incorporation of radiolabeled 20:4 in MK. Both marine oils reduced the total uptake of 20:4 in megakaryocytes but the reduction occured primarily in PE and phosphatidylserine (PS) rather than in phosphatidylcholine (PC) and phosphatidylinositol (PI). Both 20:5 and 22:6 caused a 50% reduction in the incorporation of radiolabeled 20:4 into megakaryocyte PE and PS while only a 20% reduction into PC and PI. There was a striking difference in the effect of 18:3. Even though the incubation of megakaryocytes with 18:3 reduced the uptake of 20:4, the distribution of the incorporated 20:4 in phospholipids of megakaryocytes incubated with 18:3 was similar to that in controls. Thus, 18:3 did not have a selective effect on the incorporation of 20:4 into PE or PS. Whereas megakaryocyte 20:4 metabolism was significantly affected by omega-3 fatty acids, the incubation of guinea pig or human platelets with 22:6, 20:5 or 18:3 did not result in any alteration of the incorporation of 20:4 into platelet phospholipids.20:4 may be initially incorporated into megakaryocyte PC and subsequently transfered to PE and other phospholipids. Omega 3 marine oils, 20:5 and 22:6, appear to have a selective action on the incorporation or transfer of 20:4 into PE and PS. One mechanism for these observations would be an effect of marine oils on megakaryocyte acyltransferase and/or transacylases. Omega 3 linolenic acid appears to reduce the uptake of 20:4 but does not affect the transfer of 20:4 into PE and PS since there was no selective inhibition of uptake into PE or other megakaryocyte phospholipids. The observation that marine oils did not have any effect on 20:4 metabolism in platelets indicated that omega 3 polyunsaturated fatty acids primarily affect megakaryocytes. This phenomenon may result in the production of platelets with abnormal content and compartmentalization of arachidonic acid. The localization of 20:4 in different pools in these platelets could influence the availability of esterified 20:4 for the production of thromboxanes and other eicosanoids. Another implication of the study is that omega 3 fatty acids may have a greater effect on precursor cells than on differentiated cells and tissues and influence cellular maturation.
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Jafari, Naser, James Drury, Andrew J. Morris, Fredrick O. Onono, Payton D. Stevens, Tianyan Gao, Eun Y. Lee, Heidi L. Weiss, B. Mark Evers, and Yekaterina Zaytseva. "Abstract 1437: De novo fatty acid synthesis-driven sphingolipid metabolism promotes metastatic potential of colorectal cancer." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-1437.
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Lettiero, B., S. Kimbung, and S. Borgquist. "Abstract P6-02-04: Atorvastatin insensitivity is associated with increased lipid droplets accumulation and fatty acid metabolism in breast cancer cells." In Abstracts: 2016 San Antonio Breast Cancer Symposium; December 6-10, 2016; San Antonio, Texas. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.sabcs16-p6-02-04.
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Zantinge, Stephanie L., Katja Linher-Melville, Toran Sanli, and Gurmit Singh. "Abstract 5157: Prolactin plays a role in regulating fatty acid synthesis and metabolism in the prostate cancer cell line PC-3." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-5157.
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Kockmann, V., E. Véricel, M. Croset, and M. Lagarde. "IN VITRO AND IN VIVO EFFECT OF VITAMIN E ON NORMAL HUMAN PLATELETS. AGGREGATION AND ARACHIDONIC ACID (AA) METABOLISM." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644624.
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Oxygenated metabolism of AA through cyclooxygenase and lipoxygenase pathways involves peroxide species and vitamin E has been extensively studied as an agent that could reduce this lipid peroxidation. In the present study, effects of vitamin E has been investigated upon AA metabolism in normal human platelets with both in vivo and in vitro approaches. Using low doses of vitamin E either in vivo or in vitro, we have succeeded to almost double plasma and platelet a-tocopherol (determinated by HPLC). Despite such an enrichment platelet aggregation induced by agents involved in the AA cascade (collagen, arachidonate and U46619) was not affected. Similarly, the oxygenation of exogenous AA determined by HHT, HETE and TxB2 production was not modified. When the oxygenated products were measured after thrombin stimulation, some variations could be noted, although rarely significant. The tendency was a decrease after in vitro enrichment and an increase when enrichment occured in vivo. Basal oxygenated metabolism of AA in vivo was assessed by measuring 6-Keto-PGFla, 2,3-dinor-6-Keto-PGFla, TxB2 and 2,3-dinor-TxB2 in urine. All of them tended to increase after vitamin E intake, although not significantly. The oxygenation of eicosapentaenoic acid, which is markedly potentiated by AA through its hydroperoxide, 12 HPETE, was not altered after vitamin E treatment, confirming that vitamin E does not alter the specific peroxidation of polyunsaturated fatty acids in normal platelets. We conclude that vitamin E supplement does not affect the AA dependent aggregation neither the oxygenated metabolism of AA in normal human platelets. This does not exclude that it might be however useful in platelets that exhibit a relative deficiency in this vitamin (e.g. diabetes and aging) where it could slow down both AA peroxidation and aggregation.
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Broekman, M. J. "METABOLISM OF ARACHIDONATE RELEASED FROM THROMBIN-STIMULATED PLATELETS TO THROMBOXANE, 12-HYDROXYHEPTADECATRIENATE AND 12-HYDROXYEICOSATETRAENATE IS REGULATED BY ALBUMIN." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644623.
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Stimulation with high-dose thrombin of human platelets leads to release of arachidonate from phosphatidylethanolamine and phosphatidylcholine via a phosholipase A2 mechanism. Released arachidonate is subsequently reincorporated into cellular lipid, or oxygenated by cyclooxygenase or lipoxygenase of the cell which originally released the arachidonate, or of another cell in the local environment. Albumin is the major fatty acid-binding protein in plasma, where it is present at 600 uM. In addition, albumin binds and stabilizes labile eicosanoid intermediates. Albumin could therefore profoundly influence the pattern and time course of eicosanoid formation. The effects of added albumin (fatty acid-free) on accumulation of free arachidonate, measured by GLC, formation of 12-hydroxyhepta-decatrienoate (12HHT) and 12-hydroxyeicosatetraenoate (12HETE), measured by HPLC, were studied in washed platelets stimulated with thrombin (15 U/5×109 cells). Addition of 150 uM albumin increased free arachidonate accumulation from 3-5 nmol to 44 nmol 300 s following thrombin stimulation. In the presence of 150 uM albumin, aspirin-pretreatment did not further increase free arachidonate accumulation. Albumin dose-dependently inhibited arachidonate cyclooxygenation: 150 uM albumin reduced 12HHT formation by >55%, but arachidonate lipoxygenation (12HETE production) decreased by only 26%. Aspirin-treated platelets, in the absence of albumin, produced more than double the quantity of 12HETE of untreated platelets. Addition of 15 uM albumin to aspirin-treated platelets increased 12HETE production slightly, but higher levels of albumin (150 uM) led to a 60% decrease in 12HETE formation. This decrease was similar to the decrease in 12HHT induced by albumin in aspirin-free platelets. Albumin also increased the lag in onset of 12HETE formation caused by aspirin. These data demonstrate that eicosanoid production by thrombin-stimulated platelets is greatly down-regulated by comparatively very small quantities of albumin due to sequestration of released arachidonate.
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Agouni, Abdelali, Duck Y. Lee, Assaad A. Eid, Yves Gorin, and Kumar Sharma. "The Protective Role of Sestrin2 in High Fat Diet-Induced Nephropathy." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0134.
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Introduction: Obesity is a major risk factor for type-2 diabetes predisposing patients to diabetic nephropathy (DN), the leading cause of end-stage renal failure. Glomerular injury is a prominent pathological feature of DN. Sestrin2 (Sesn2) is a stress-induced protein, but its role in DN has not been investigated. Therefore, we have determined the impact of Sesn2 deletion in a mouse model of obesityinduced nephropathy. Materials and methods: We examined the effects of Sesn2-deficiency in a longterm (22 weeks) mouse model of high fat diet (HFD)-induced obesity on glomerular structure. The severity of renal injury and fibrosis in wild type (Sesn2+/+) mice (fed HFD or chow diets) was compared to that in Sesn2-deficient mice (Sesn2-/- ) fed HFD or chow diets. Animal work was carried out under an IACUC-approved protocol. Results: Data showed that Sesn2 ablation exacerbated HFD-induced glomerular fibrotic injury as evidenced by mesangial matrix hypertrophy and accumulation of both fibronectin and collagen IV. Western blot analysis revealed that HFD- or chow-fed Sesn2-/- mice exhibited higher protein expression of key lipogenic enzymes, fatty acid translocase CD36 (an indicator of lipid uptake), fatty acid synthase and ATP citrate lyase. Sesn2-deficiency in obese mice resulted in podocyte loss as indicated by reduced expression of synaptopodin. Glomerular lesions like those observed in HFD-fed wild-type mice were detected in Sesn2-/-mice fed a chow diet, indicating that the basal deletion of Sesn2 is deleterious by itself. Conclusions: We provide the first evidence that Sesn2 is renoprotective in obesity-induced nephropathy by diminishing lipid accumulation and blocking excessive lipid uptake and de novo lipid synthesis. Understanding the protective of Sesn2 should yield novel therapeutic interventions to effectively preserve glomerular function in obesity and diabetes.
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Norϕ, A., T. Smimonsen, K. Ytre-Arene, B. Lyngmo, and B. Svensson. "THE EFFECT OF TWO CHOLESTEROL-LOWERING AGENTS ON PLATELETS IN PATIENTS WITH HYPERCHOLESTEROLEMIA." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643801.
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Twenty-one subjects with type Ila hyperlipoproteinemia, receiving dietary treatment were given Synvinolin (MK-733), a HMG-CoA reductase inhibitor, 40 mg or Cholestyramin (Questran) 24 g daily for a period of 12 weeks.Serum lipids, platelet cholesterol, phospholipids and fatty acid composition and platelet function were measured before and after the intake of the two drugs.Both drugs reduced serum total cholesterol with approximately 50%. No significant changes were observed in platelet lipid concentrations or in the primary bleeding time. Collagen induced aggregation and thromboxane (TXA2) production were reduced, whereas thrombin induced aggregation and TXA2 production were unaffected. This study shows that both a cholesterol synthetase inhibitor and Cholestyramin reduce the total serum cholesterol concentration and also reduce platelet aggregation and thromboxane synthesis without changing the platelet cholesterol content or the cholesterol/phospholipid ratio. The effect on serum lipids and platelet function may indicate a beneficial effect of both drugs on arterial disease in patients with hypercholesterolemia.
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Murphy, S. "STORAGE OF PLATELETS FOR TRANSFUSION - CURRENT METHODS AND PROBLEMS TO BE SOLVED." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643999.
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In the 1970's, when platelet concentrates (PC) were stored in "first generation" plastic containers at 22°C, many showed a fall in pH.In vivo viability was well maintained as pH fell from the starting level, 7.1, to 6.2 but was progressively lost below thatlevel. pH after a storage interval correlated with the platelet count in the PC, the higher the count, the lower the pH after storage. Since 30-50% of PC might have pH below 6.2 after 3 days of storage, shelflife was severely limited.We now have "second generation" containers which allow storage for 7 days without significant fall in pH.Superior pH maintenance results from increased oxygen transport through the walls of the container thuspreventing platelet hypoxia within. Under all circumstances which we have examined, PC, pH correlates inversely with lactate concentration. The superiority of the "second generation" containers results from the lower rate of glycolysis within them due to the Pasteur effect. Like many cells, the platelet has a baseline rate of lactate production which is increased up to 8 times if oxidative metabolism is interrupted by hypoxia. For any container, there is an inverse relationship between PC pCL and platelet count since each platejlet |as a fixed oxygen demand. In "first generation" containers, the pO2 approached zero with platelet counts, 1.0-1.5 × 106 /mm3 , a range commonly seen in practice. At platelet counts above thatlevel, the platelets would have an increasing oxygendebt. The greater the oxygen debt is, the greater will be the rate of lactate production per platelet and, therefore, the rate of pH fall. An ideal "second generation" container will have oxygen permeability twice thgt 05 a "first generation" container such that platelets will begin to have an oxygen debt at platelet count, 2.4 × 106/mm3 , a level rarely seen in practice. In "second generation" containers, there is a continuing, linear production of lactate in spite of adequate oxygen supply. The major buffer in plasma for the hydrogen ion accompanying lactate production is bicarbonate. As lactate is produced, bicarbonate is consumed and pH remains stable until bicarbonate is completely depleted.Thereafter, pH falls precipitously.However, there is adequate bicarbonate in the 50 ml of plasma used as medium for the PC to buffer the baseline production of lactate for seven days.This is the major reason why storage for sevendays is now satisfactory.With knowledge of the oxygen transport capability of a container and measurement of pO2 within the container, we can calculate the rate of oxygen consumptionduring storage, 1.1 nmol/min/109 platelets. Knowing the rates of oxygen consumption and lactate production and the predicted rate of ATP synthesis from ADP for each type of metabolism we calculated that 85% ofATP regeneration is from oxidative metabolism. When we contrasted the rate of glucose consumption with the rate of lactate production, we were surprised that the slope of the regression line was exactly 0.5 suggesting that two moles of lactate were produced for each mole of glucose utilized and that there must be a prominent substrate for oxidative metabolism other than glucose. Recent work in our laboratory suggests fatty acid as such a substrate.There is much to be learned about storage in "secondgeneration" containers. At the onset of storage 70% of the platelets have a discoid appearance whereas after seven days only 30% do with most of the rest being spheres. Furthermore, 5-10% of cells are "leaf-shaped", elongated tubules, or ring forms. In addition, many studies have described reduced platelet function in vitro after storage. There is a 20-50% reduction in the maximal extent of aggregation with high ADP concentrations and the concentrations of single agonists which produce 50% of maximal response are increased after storage. However, we have been encouraged to find that the response to these agents was reduced much less when they were used a pairs. Finally, there is concern that trace bacterial contamination at the time of phlebotomy might allow enough proliferation to produce sepsis in recipients. Further research should improve our understanding inthese areas and the safety and efficacy of platelets after storage.