Academic literature on the topic 'Metabolome modification'
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Journal articles on the topic "Metabolome modification"
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Rieusset, Laura, Marjolaine Rey, Florence Wisniewski-Dyé, Claire Prigent-Combaret, and Gilles Comte. "Wheat Metabolite Interferences on Fluorescent Pseudomonas Physiology Modify Wheat Metabolome through an Ecological Feedback." Metabolites 12, no. 3 (March 9, 2022): 236. http://dx.doi.org/10.3390/metabo12030236.
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Plant roots exude a wide variety of secondary metabolites able to attract and/or control a large diversity of microbial species. In return, among the root microbiota, some bacteria can promote plant development. Among these, Pseudomonas are known to produce a wide diversity of secondary metabolites that could have biological activity on the host plant and other soil microorganisms. We previously showed that wheat can interfere with Pseudomonas secondary metabolism production through its root metabolites. Interestingly, production of Pseudomonas bioactive metabolites, such as phloroglucinol, phenazines, pyrrolnitrin, or acyl homoserine lactones, are modified in the presence of wheat root extracts. A new cross metabolomic approach was then performed to evaluate if wheat metabolic interferences on Pseudomonas secondary metabolites production have consequences on wheat metabolome itself. Two different Pseudomonas strains were conditioned by wheat root extracts from two genotypes, leading to modification of bacterial secondary metabolites production. Bacterial cells were then inoculated on each wheat genotypes. Then, wheat root metabolomes were analyzed by untargeted metabolomic, and metabolites from the Adular genotype were characterized by molecular network. This allows us to evaluate if wheat differently recognizes the bacterial cells that have already been into contact with plants and highlights bioactive metabolites involved in wheat—Pseudomonas interaction.
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Zhang, Zhonghui, Feng Zhang, Yuan Deng, Lisong Sun, Mengdi Mao, Ridong Chen, Qi Qiang, et al. "Integrated Metabolomics and Transcriptomics Analyses Reveal the Metabolic Differences and Molecular Basis of Nutritional Quality in Landraces and Cultivated Rice." Metabolites 12, no. 5 (April 22, 2022): 384. http://dx.doi.org/10.3390/metabo12050384.
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Rice (Oryza sativa L.) is one of the most globally important crops, nutritionally and economically. Therefore, analyzing the genetic basis of its nutritional quality is a paramount prerequisite for cultivating new varieties with increased nutritional health. To systematically compare the nutritional quality differences between landraces and cultivated rice, and to mine key genes that determine the specific nutritional traits of landraces, a seed metabolome database of 985 nutritional metabolites covering amino acids, flavonoids, anthocyanins, and vitamins by a widely targeted metabolomic approach with 114 rice varieties (35 landraces and 79 cultivars) was established. To further reveal the molecular mechanism of the metabolic differences in landrace and cultivated rice seeds, four cultivars and six landrace seeds were selected for transcriptome and metabolome analysis during germination, respectively. The integrated analysis compared the metabolic profiles and transcriptomes of different types of rice, identifying 358 differentially accumulated metabolites (DAMs) and 1982 differentially expressed genes (DEGs), establishing a metabolite–gene correlation network. A PCA revealed anthocyanins, flavonoids, and lipids as the central differential nutritional metabolites between landraces and cultivated rice. The metabolite–gene correlation network was used to screen out 20 candidate genes postulated to be involved in the structural modification of anthocyanins. Five glycosyltransferases were verified to catalyze the glycosylation of anthocyanins by in vitro enzyme activity experiments. At the same time, the different mechanisms of the anthocyanin synthesis pathway and structural diversity in landrace and cultivated rice were systematically analyzed, providing new insights for the improvement and utilization of the nutritional quality of rice landrace varieties.
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Brindle, Kevin M. "Metabolomics: Pandora's Box or Aladdin's Cave?" Biochemist 25, no. 1 (February 1, 2003): 15–17. http://dx.doi.org/10.1042/bio02501015.
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Functional genomics, the elucidation of gene function from studies of the effects of gene modification on cellular phenotype, has prompted the development of massively parallel and increasingly comprehensive screening tools for assessing the expression of mRNAs (transcriptomics) and proteins (proteomics). For a more complete description of the effects of changes in genotype or physiological conditions on cellular phenotype, we also need to define the status of a third class of biomolecules in the cell, the small-molecule metabolites. Study of the latter has been termed metabolomics and the metabolite complement the metabolome.
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Creek, Darren J., Brunda Nijagal, Dong-Hyun Kim, Federico Rojas, Keith R. Matthews, and Michael P. Barrett. "Metabolomics Guides Rational Development of a Simplified Cell Culture Medium for Drug Screening against Trypanosoma brucei." Antimicrobial Agents and Chemotherapy 57, no. 6 (April 9, 2013): 2768–79. http://dx.doi.org/10.1128/aac.00044-13.
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ABSTRACTIn vitroculture methods underpin many experimental approaches to biology and drug discovery. The modification of established cell culture methods to make them more biologically relevant or to optimize growth is traditionally a laborious task. Emerging metabolomic technology enables the rapid evaluation of intra- and extracellular metabolites and can be applied to the rational development of cell culture media. In this study, untargeted semiquantitative and targeted quantitative metabolomic analyses of fresh and spent media revealed the major nutritional requirements for the growth of bloodstream formTrypanosoma brucei. The standard culture medium (HMI11) contained unnecessarily high concentrations of 32 nutrients that were subsequently removed to make the concentrations more closely resemble those normally found in blood. Our new medium, Creek's minimal medium (CMM), supportsin vitrogrowth equivalent to that in HMI11 and causes no significant perturbation of metabolite levels for 94% of the detected metabolome (<3-fold change; α = 0.05). Importantly, improved sensitivity was observed for drug activity studies in whole-cell phenotypic screenings and in the metabolomic mode of action assays. Four-hundred-fold 50% inhibitory concentration decreases were observed for pentamidine and methotrexate, suggesting inhibition of activity by nutrients present in HMI11. CMM is suitable for routine cell culture and offers important advantages for metabolomic studies and drug activity screening.
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Saunier, Amélie, Stéphane Greff, James D. Blande, Caroline Lecareux, Virginie Baldy, Catherine Fernandez, and Elena Ormeño. "Amplified Drought and Seasonal Cycle Modulate Quercus pubescens Leaf Metabolome." Metabolites 12, no. 4 (March 30, 2022): 307. http://dx.doi.org/10.3390/metabo12040307.
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The intensification of summer drought expected with climate change can induce metabolism modifications in plants to face such constraints. In this experiment, we used both a targeted approach focused on flavonoids, as well as an untargeted approach, to study a broader fraction of the leaf metabolome of Quercus pubescens exposed to amplified drought. A forest site equipped with a rainfall exclusion device allowed reduction of natural rainfall by ~30% over the tree canopy. Leaves of natural drought (ND) and amplified drought (AD) plots were collected over three seasonal cycles (spring, summer, and autumn) in 2013 (the second year of rain exclusion), 2014, and 2015. As expected, Q. pubescens metabolome followed a seasonal course. In the summer of 2015, the leaf metabolome presented a shifted and early autumnal pattern because of harsher conditions during this year. Despite low metabolic modification at the global scale, our results demonstrated that 75% of Quercus metabolites were upregulated in springs when trees were exposed to AD, whereas 60 to 73% of metabolites (93% in summer 2015), such as kaempferols and quercetins, were downregulated in summers/autumns. Juglanin, a kaempferol pentoside, as well as rhododendrin derivatives, were upregulated throughout the year, suggesting an antioxidant ability of these metabolites. Those changes in terms of phenology and leaf chemistry could, in the end, affect the ecosystem functioning.
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Balonov, Ilja, Max Kurlbaum, Ann-Cathrin Koschker, Christine Stier, Martin Fassnacht, and Ulrich Dischinger. "Changes in Plasma Metabolomic Profile Following Bariatric Surgery, Lifestyle Intervention or Diet Restriction—Insights from Human and Rat Studies." International Journal of Molecular Sciences 24, no. 3 (January 25, 2023): 2354. http://dx.doi.org/10.3390/ijms24032354.
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Although bariatric surgery is known to change the metabolome, it is unclear if this is specific for the intervention or a consequence of the induced bodyweight loss. As the weight loss after Roux-en-Y Gastric Bypass (RYGB) can hardly be mimicked with an evenly effective diet in humans, translational research efforts might be helpful. A group of 188 plasma metabolites of 46 patients from the randomized controlled Würzburg Adipositas Study (WAS) and from RYGB-treated rats (n = 6) as well as body-weight-matched controls (n = 7) were measured using liquid chromatography tandem mass spectrometry. WAS participants were randomized into intensive lifestyle modification (LS, n = 24) or RYGB (OP, n = 22). In patients in the WAS cohort, only bariatric surgery achieved a sustained weight loss (BMI −34.3% (OP) vs. −1.2% (LS), p ≤ 0.01). An explicit shift in the metabolomic profile was found in 57 metabolites in the human cohort and in 62 metabolites in the rodent model. Significantly higher levels of sphingolipids and lecithins were detected in both surgical groups but not in the conservatively treated human and animal groups. RYGB leads to a characteristic metabolomic profile, which differs distinctly from that following non-surgical intervention. Analysis of the human and rat data revealed that RYGB induces specific changes in the metabolome independent of weight loss.
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Včelařová, Ludmila, Vladimír Skalický, Ivo Chamrád, René Lenobel, Martin F. Kubeš, Aleš Pěnčík, and Ondřej Novák. "Auxin Metabolome Profiling in the Arabidopsis Endoplasmic Reticulum Using an Optimised Organelle Isolation Protocol." International Journal of Molecular Sciences 22, no. 17 (August 29, 2021): 9370. http://dx.doi.org/10.3390/ijms22179370.
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The endoplasmic reticulum (ER) is an extensive network of intracellular membranes. Its major functions include proteosynthesis, protein folding, post-transcriptional modification and sorting of proteins within the cell, and lipid anabolism. Moreover, several studies have suggested that it may be involved in regulating intracellular auxin homeostasis in plants by modulating its metabolism. Therefore, to study auxin metabolome in the ER, it is necessary to obtain a highly enriched (ideally, pure) ER fraction. Isolation of the ER is challenging because its biochemical properties are very similar to those of other cellular endomembranes. Most published protocols for ER isolation use density gradient ultracentrifugation, despite its suboptimal resolving power. Here we present an optimised protocol for ER isolation from Arabidopsis thaliana seedlings for the subsequent mass spectrometric determination of ER-specific auxin metabolite profiles. Auxin metabolite analysis revealed highly elevated levels of active auxin form (IAA) within the ER compared to whole plants. Moreover, samples prepared using our optimised isolation ER protocol are amenable to analysis using various “omics” technologies including analyses of both macromolecular and low molecular weight compounds from the same sample.
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Desmet, Sandrien, Kris Morreel, and Rebecca Dauwe. "Origin and Function of Structural Diversity in the Plant Specialized Metabolome." Plants 10, no. 11 (November 6, 2021): 2393. http://dx.doi.org/10.3390/plants10112393.
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The plant specialized metabolome consists of a multitude of structurally and functionally diverse metabolites, variable from species to species. The specialized metabolites play roles in the response to environmental changes and abiotic or biotic stresses, as well as in plant growth and development. At its basis, the specialized metabolism is built of four major pathways, each starting from a few distinct primary metabolism precursors, and leading to distinct basic carbon skeleton core structures: polyketides and fatty acid derivatives, terpenoids, alkaloids, and phenolics. Structural diversity in specialized metabolism, however, expands exponentially with each subsequent modification. We review here the major sources of structural variety and question if a specific role can be attributed to each distinct structure. We focus on the influences that various core structures and modifications have on flavonoid antioxidant activity and on the diversity generated by oxidative coupling reactions. We suggest that many oxidative coupling products, triggered by initial radical scavenging, may not have a function in se, but could potentially be enzymatically recycled to effective antioxidants. We further discuss the wide structural variety created by multiple decorations (glycosylations, acylations, prenylations), the formation of high-molecular weight conjugates and polyesters, and the plasticity of the specialized metabolism. We draw attention to the need for untargeted methods to identify the complex, multiply decorated and conjugated compounds, in order to study the functioning of the plant specialized metabolome.
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Wu, Si, Jun Zhang, Feifei Li, Wei Du, Xin Zhou, Mian Wan, Yi Fan, et al. "One-Carbon Metabolism Links Nutrition Intake to Embryonic Development via Epigenetic Mechanisms." Stem Cells International 2019 (March 10, 2019): 1–8. http://dx.doi.org/10.1155/2019/3894101.
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Beyond energy production, nutrient metabolism plays a crucial role in stem cell lineage determination. Changes in metabolism based on nutrient availability and dietary habits impact stem cell identity. Evidence suggests a strong link between metabolism and epigenetic mechanisms occurring during embryonic development and later life of offspring. Metabolism regulates epigenetic mechanisms such as modifications of DNA, histones, and microRNAs. In turn, these epigenetic mechanisms regulate metabolic pathways to modify the metabolome. One-carbon metabolism (OCM) is a crucial metabolic process involving transfer of the methyl groups leading to regulation of multiple cellular activities. OCM cycles and its related micronutrients are ubiquitously present in stem cells and feed into the epigenetic mechanisms. In this review, we briefly introduce the OCM process and involved micronutrients and discuss OCM-associated epigenetic modifications, including DNA methylation, histone modification, and microRNAs. We further consider the underlying OCM-mediated link between nutrition and epigenetic modifications in embryonic development.
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Tong, Tong, Si Chen, Lianrong Wang, You Tang, Jae Yong Ryu, Susu Jiang, Xiaolin Wu, et al. "Occurrence, evolution, and functions of DNA phosphorothioate epigenetics in bacteria." Proceedings of the National Academy of Sciences 115, no. 13 (March 12, 2018): E2988—E2996. http://dx.doi.org/10.1073/pnas.1721916115.
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The chemical diversity of physiological DNA modifications has expanded with the identification of phosphorothioate (PT) modification in which the nonbridging oxygen in the sugar-phosphate backbone of DNA is replaced by sulfur. Together with DndFGH as cognate restriction enzymes, DNA PT modification, which is catalyzed by the DndABCDE proteins, functions as a bacterial restriction-modification (R-M) system that protects cells against invading foreign DNA. However, the occurrence of dnd systems across a large number of bacterial genomes and their functions other than R-M are poorly understood. Here, a genomic survey revealed the prevalence of bacterial dnd systems: 1,349 bacterial dnd systems were observed to occur sporadically across diverse phylogenetic groups, and nearly half of these occur in the form of a solitary dndBCDE gene cluster that lacks the dndFGH restriction counterparts. A phylogenetic analysis of 734 complete PT R-M pairs revealed the coevolution of M and R components, despite the observation that several PT R-M pairs appeared to be assembled from M and R parts acquired from distantly related organisms. Concurrent epigenomic analysis, transcriptome analysis, and metabolome characterization showed that a solitary PT modification contributed to the overall cellular redox state, the loss of which perturbed the cellular redox balance and induced Pseudomonas fluorescens to reconfigure its metabolism to fend off oxidative stress. An in vitro transcriptional assay revealed altered transcriptional efficiency in the presence of PT DNA modification, implicating its function in epigenetic regulation. These data suggest the versatility of PT in addition to its involvement in R-M protection.
Dissertations / Theses on the topic "Metabolome modification"
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BREUILLE, DENIS. "Modifications du metabolisme proteique induites par le sepsis et mediateurs impliques." Clermont-Ferrand 2, 1993. http://www.theses.fr/1993CLF20576.
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Ce travail concerne l'etude des modifications du metabolisme proteique lors du sepsis. La premiere partie correspond a la mise au point d'un modele animal de sepsis reproduisant chez le rat l'etat hypercatabolique prolonge observe chez le patient septique. Les animaux sont fortement anorexiques et presentent une perte de poids tres marquee pendant 2 a 3 jours, puis moins aigue jusqu'au sixieme - huitieme jour postinfectieux suivie d'une reprise lente. L'atrophie musculaire atteint 40% du contenu proteique initial et semble identique pour des muscles de differents types metaboliques. La deuxieme partie du travail est une description des modifications des vitesses de synthese des proteines de l'organisme et des principaux organes. Les animaux infectes presentent une vitesse de synthese des proteines du corps entier augmentee de 28% par rapport a des temoins pair-fed. Le foie participe fortement a cette augmentation puisque la quantite de proteines synthetisee a son niveau represente 31% de celle de l'organisme entier au lieu de 15% chez un animal sain. A l'inverse, la quantite de proteines synthetisees dans les muscles est diminuee de 30% chez les animaux infectes par rapport a leur temoins pair-fed. D'autres organes semblent presenter une activation de leur synthese proteique dans la mesure ou la vitesse fractionnaire de synthese des proteines du corps entier sans foie est augmentee malgre la diminution observee dans les muscles. La faible augmentation observee dans le tube digestif ne semble pas pouvoir contrebalancer la diminution due aux muscles. La derniere partie du travail est une etude de la mediation de ces perturbations. L'administration de pentoxifylline 30 minutes avant l'infection inhibe tres fortement la secretion du facteur necrosant des tumeurs (tnf), limite l'anorexie, les pertes de poids, l'atrophie musculaire et la diminution des vitesses de synthese des proteines musculaires. Par contre, la reaction inflammatoire hepatique caracterisee par l'augmentation des vitesses de synthese proteique du foie n'est pas modifiee. Ceci indique une implication directe des cytokines et probablement du tnf dans les perturbations du metabolisme proteique induites par le sepsis.
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MANSOOR, VINCENT ODILE. "Les modifications du metabolisme proteique lors de la reponse de phase aigue." Clermont-Ferrand 1, 1998. http://www.theses.fr/1998CLF1MM10.
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SANWALD, PATRICIA. "Metabolisme et modifications des capacites metaboliques : exemple du dolasetron, un antagoniste des recepteurs 5-ht3." Strasbourg 1, 1994. http://www.theses.fr/1994STR15045.
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BRAVARD, ANNE. "Modifications du metabolisme antioxydant en relation avec les anomalies chromosomiques dans les cellules transformees et tumorales." Paris 7, 1993. http://www.theses.fr/1993PA077025.
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Les relations entre les modifications d'activite des principales enzymes antioxydantes et les anomalies des segments chromosomiques portant les genes codant pour ces enzymes, ont ete etudiees dans les fibroblastes humains et les chondrocytes de lapin transformes par sv40, ainsi que dans les melanomes humains. De bonnes correlations existent entre les activites de la superoxyde dismutase 1, de la superoxyde dismutase 2 (sod2), de la glucose-6-phosphate dehydrogenase et le nombre de chromosomes portant leurs genes respectifs. Cependant, la deregulation de l'activite sod2 dans les fibroblastes humains transformes par sv40 et dans les melanomes ferait egalement intervenir un represseur non identifie. Les activites des autres enzymes antioxydantes ne sont pas liees aux anomalies chromosomiques; en particulier celle de la glutathion reductase et de la glutathion peroxydase (gpx) qui semblent plutot etre regulees par l'activite d'autres enzymes du meme metabolisme. La baisse de l'ensemble des activites antioxydantes dans les clones de fibroblastes humains au cours de leur transformation par sv40 renforce l'hypothese d'un role des modifications du metabolisme antioxydant dans la transformation cellulaire. Les alterations des activites sod2 et gpx seraient particulierement importantes car elles se maintiennent dans les lignees etablies de fibroblastes humains transformes par sv40 et sont egalement presentes dans les chondrocytes de lapin transformes par sv40. Ces modifications pourraient etre en rapport avec les anomalies mitochondriales mises en evidence dans les deux modeles. Finalement, la baisse de l'activite sod2 pourrait favoriser la proliferation des fibroblastes transformes par sv40 et des melanomes humains
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Ebrard, Sylvie. "Modifications métaboliques et de la composition corporelle chez les diabétiques de type 2 après mise sous insuline." Montpellier 1, 2000. http://www.theses.fr/2000MON11149.
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BARDOT, VALERIE. "Modifications du metabolisme des purines et des pyrimidines dans les tumeurs humaines, relation avec les desequilibres chromosomiques." Paris 7, 1994. http://www.theses.fr/1994PA077200.
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Afin de preciser la signification des anomalies chromosomiques observees dans les cancers humains, l'hypothese d'une correlation avec les deregulations metaboliques a ete emise. L'analyse cytogenetique des cancers colorectaux a permis de distinguer deux types de cancers et les desequilibres chromosomiques observes dans ces tumeurs suggerent des modifications du metabolisme des pyrimidines. Une bonne correlation a pu etre mise en evidence, d'une part entre les activites thymidine kinase et thymidylate synthase et le nombre de chromosomes portant les genes respectifs, et d'autre part entre ces activites enzymatiques et le type cytogenetique de ces tumeurs, en particulier apres transplantation sur souris athymiques. Pour confirmer cette hypothese, d'autres tumeurs humaines ont ete etudiees, plus particulierement d'origine neuroectodermique comme les gliomes et les melanomes, pour lesquelles les desequilibres chromosomiques suggerent plutot des alterations du metabolisme des purines. Les activites de plusieurs enzymes impliquees dans ce metabolisme ont donc ete mesurees en relation avec les desequilibres chromosomiques observes dans ces tumeurs. Les gliomes et les melanomes sont caracterises par une baisse globale du metabolisme des purines, affectant la voie de recuperation et le catabolisme, comme le suggeraient les pertes chromosomiques frequemment observees dans ces tumeurs. De plus, les gliomes et les melanomes qui ont a la fois une origine embryonnaire et un profil cytogenetique proches, presentent egalement pour les purines, un profil metabolique comparable. Enfin, les neuroblastomes humains sont des tumeurs egalement d'origine neuroectodermique, qui peuvent se repartir en deux groupes en fonction des donnees cliniques et cytogenetiques. Nos resultats ont montre que ces deux groupes de tumeurs, caracterises par des profils chromosomiques distincts, presentaient deux profils metaboliques differents pour les purines et les pyrimidines. L'ensemble de ces travaux montre qu'il existe bien une relation entre le profil de desequilibres chromosomiques et le profil de deviations metaboliques dans ces tumeurs humaines. Toutefois, les alterations chromosomiques n'expliquent pas les modifications d'activites des enzymes impliquees dans le metabolisme des purines, par un effet de dosage genique. Nos resultats mettent egalement en evidence dans les gliomes, que les modifications metaboliques precedent l'apparition des anomalies chromosomiques et semblent en relation avec la progression tumorale, suggerant leur role determinant dans le processus de cancerogenese, en particulier a des stades precoces
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Golly, Francis. "Metabolisme des phospholipides dans les neurones de poulet en culture primaire : modifications induites par la cdp-choline." Université Louis Pasteur (Strasbourg) (1971-2008), 1986. http://www.theses.fr/1986STR13149.
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Lors de lesions nerveuses par retrait de co::(2), l'etude du metabolisme des lipides a montre qu'un traitement a la cdp-choline ne modifie pas la distribution et la synthese des phospholipides et des acides gras mais provoque par contre une diminution de la liberation d'acides gras. La cdp-choline diminue l'activite phospholiposique a1 au niveau des membranes et protege donc celles-ci de la degradation
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EBNER, SYLVIE. "Regulation hormonale du metabolisme du glucose dans les adipocytes bruns isoles de rat : modification au cours de la lactation." Paris 6, 1989. http://www.theses.fr/1989PA066166.
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Le glucose est un substrat important du tissu adipeux brun. En presence d'insuline, l'adipocyte brun se comporte comme un adipocyte blanc stockant les acides gras formes a partir de glucose, sous forme de triglycerides dans des gouttelettes lipidiques. L'addition de noradrenaline modifie la repartition du glucose dans les differentes voies du metabolisme. En effet, en absence de noradrenaline le glucose est essentiellement dirige vers la synthese des acides gras, mais en presence de noradrenaline, on observe une redirection de l'utilisation principale du glucose de la lipogenese vers l'oxidation. Lors de la periode de lactation, il y a une diminution de l'utilisation de glucose par les tissus peripheriques, permettant d'orienter preferentiellement le glucose vers la glande mammaire. In vivo, il a ete montre qu'il y avait une resistance a l'insuline au niveau du tissu adipeux brun des rattes allaitantes. Cette insulino-resistance se situe a un niveau post-recepteur, en effet ni la liaison de l'insuline, ni l'activite kinase du recepteur ne sont alterees pendant la lactation. Par contre, on observe in vitro dans les adipocytes bruns isoles de rattes allaitantes une resistance a l'insuline au niveau de la lipogenese et de l'oxydation. Notre travail permet d'envisager lors de la periode de lactation un defaut au niveau de la liberation d'un mediateur membranaire qui activerait la pyruvate deshydrogenase
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Corio-Costet, Marie-France. "Modification par le fenpropimorphe du profil sterolique de plantes et effet sur le metabolisme steroidien d'un insecte phytophage (locusta migratoria)." Université Louis Pasteur (Strasbourg) (1971-2008), 1986. http://www.theses.fr/1986STR13155.
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Nous avons adopte une strategie, consistant en la modification qualitative et quantitative de la composition sterolique de plantes. Pour cefaire, nous avons traite des plantes a l'aide d'inhibiteurs de la biosynthese des sterols, possedant essentiellement deux cibles: la cycloeucalenol-obtusifoliol isomerase et la delta-huit-delta-sept-sterol isomerase. En agissant de la sorte, en bloquant diverses etapes de la biosynthese des phytosterols, nous accumulons de nouveaux sterols, en l'occurence des cyclopropylsterols. La molecule utilisee pour induire de telles modifications, est un fongicide systemique: le fenpropimorphe. Nous avons etudie le comportement de cette molecule en tant qu'inhibiteur chez des cellules animales (fibroblastes de souris) et chez des cellules vegetales (mais et ble)
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Lefèvre, Guillaume. "Modifications du métabolisme des lipides de la lipopéroxydation et des fonctions granulocytaires dans les états septiques graves." Paris 11, 1995. http://www.theses.fr/1995PA114834.
Full textBook chapters on the topic "Metabolome modification"
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Nassar, Ala F. "Improving Drug Design: Considerations for the Structural Modification Process." In Biotransformation and Metabolite Elucidation of Xenobiotics, 163–216. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2010. http://dx.doi.org/10.1002/9780470890387.ch4.
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Memelink, Johan, Jan W. Kijne, Robert van der Heijden, and Rob Verpoorte. "Genetic Modification of Plant Secondary Metabolite Pathways Using Transcriptional Regulators." In Plant Cells, 103–25. Berlin, Heidelberg: Springer Berlin Heidelberg, 2001. http://dx.doi.org/10.1007/3-540-45302-4_4.
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Boekelheide, Kim, Julia Eveleth, M. Diana Neely, and Tracy M. Sioussat. "Microtubule Assembly is Altered Following Covalent Modification by the n-Hexane Metabolite 2,5-Hexanedione." In Advances in Experimental Medicine and Biology, 433–42. Boston, MA: Springer New York, 1991. http://dx.doi.org/10.1007/978-1-4684-5877-0_59.
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Ravichandiran, Nerethika, Muneesh Kumar Barman, Sai Tejaswi Lavuri, Manjita Srivastava, Shalini Sakthivel, Meenakshi Singh, Kailash Chand, Subash C. Sonkar, and Prudhvilal Bhukya. "Precision Medicine in Cancer." In Handbook of Research on Advancements in Cancer Therapeutics, 433–66. IGI Global, 2021. http://dx.doi.org/10.4018/978-1-7998-6530-8.ch015.
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Cancer is the one of the deadliest diseases and takes the lives of millions of people every year across the world. Due to disease heterogeneity and multi-factorial reasons, traditional treatment such as radiation therapy, immunotherapy, or chemotherapy are effective only among a small population of the patients. Tumors can have different fundamental genetic causes and protein expressions that differ from one patient to another. This variability among individual lends itself to the field of precision and personalized medicine. Following the completion of human genome sequencing, significant progress has been observed in the characterization of human epigenome, proteome, and metabolome. Pharmacogenetics and pharmacogenomics use this sequence to study the genetic causes of individual variations in drug response and the simultaneous impact of change in genome that decide the patient's response to drug respectively. On summation, identify the subpopulation of patient and provide them tailored therapy thus increasing the effectiveness of treatment. All these evolved the field of precision or personalized medicine that plays a crucial role in cancer prevention, prognosis, diagnosis, and therapeutics. These tailored therapies are characterized by increased efficiency and reduced toxicity. Not all cancers have genetic variability; some are also influenced by polymorphism of gene encoding enzymes that play an important role in pharmacokinetics of drug. The discoveries of cancer predisposition genes allow diagnosis of a patient at risk of cancer development and let them make the decision on précised individual risk modification characteristic. The use of CYP2D6 genotyping for breast cancer, mutation in KRAS in colorectal cancer, genomic variation in EGFR in small lung cancer, melanoma are some of the examples of importance of cancer predisposition genes. In recent times, distinct molecular subtypes of cancers have been identified with requirement of different treatment for each subtype. Precision medicine shifts the trend from reaction to prevention and forestalls disease progression.
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"Modification of Metabolite Flow Through Metabolic Pathways." In Enzyme Regulation in Metabolic Pathways, 67–73. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2017. http://dx.doi.org/10.1002/9781119155423.ch6.
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Zocchi, Giovanni. "Kinematics of Enzyme Action." In Molecular Machines, 81–121. Princeton University Press, 2018. http://dx.doi.org/10.23943/princeton/9780691173863.003.0003.
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Enzymes are catalysts as well as the molecular machines that generate and maintain the nonequilibrium state of the cell. There are roughly two main mechanisms by which enzymes provide the control function for the network of chemical reactions in the cell. One is the presence or absence of the enzyme, controlled by gene expression. The other is allosteric control: the modulation of the activity of an individual enzyme caused by binding of a specific ligand, often a small metabolite, or else caused by so-called post-translational modifications. This chapter addresses what could be variously called the quasi-equilibrium aspects, or steady state, or kinematics, of enzyme operation, and what one learns from time-independent perturbations of this steady state. Topics discussed include Michaelis–Menten kinetics, the method of the DNA springs, force and elastic energy in the enzyme–DNA chimeras, injection of elastic energy vs. activity modulation, and connection to nonlinear dynamics.
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Hoa, Vu Quynh, Tran Thi Minh Hang, and Vu Hai Yen. "Metabolomic profile modification and enhanced disease resistance derived from alien genes introgression in plants." In Biocontrol Agents and Secondary Metabolites, 225–37. Elsevier, 2021. http://dx.doi.org/10.1016/b978-0-12-822919-4.00009-0.
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Eryılmaz Pehlivan, Fadime. "Diet-Epigenome Interactions: Epi-Drugs Modulating the Epigenetic Machinery During Cancer Prevention." In Epigenetics - “A Parallel Universe” in the Study of Cancer Biology [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.95374.
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The roles of diet and environment on health have been known since ancient times. Cancer is both a genetic and an epigenetic disease and a complex interplay mechanism of genetic and environmental factors composed of multiple stages in which gene expression, protein and metabolite function operate synchronically. Disruption of epigenetic processes results in life-threatening diseases, in particular, cancer. Epigenetics involves altered gene expression without any change of nucleotide sequences, such as DNA methylation, histone modifications and non-coding RNAs in the regulation of genome. According to current studies, cancer is preventable with appropriate or balanced food and nutrition, in some cases. Nutrient intake is an environmental factor, and dietary components play an importent role in both cancer development and prevention. Due to epigenetic events induce changes in DNA and thus influencing over all gene expression in response to the food components, bioactive compounds and phytochemicals as potent antioxidants and cancer preventive agents have important roles in human diet. Several dietray components can alter cancer cell behavior and cancer risk by influencing key pathways and steps in carcinogenesis, including signaling, apoptosis, differentiation, or inflammation. To date, multiple biologically active food components are strongly suggested to have protective potential against cancer formation, such as methyl-group donors, fatty acids, phytochemicals, flavonoids, isothiocyanates, etc. Diet considered as a source of either carcinogens that are present in certain foods or acting in a protective manner such as vitamins, antioxidants, detoxifying substances, chelating agents etc. Thus, dietary phytochemicals as epigenetic modifiers in cancer and effects of dietary phytochemicals on gene expression and signaling pathways have been widely studied in cancer. In this chapter, current knowledge on interactions between cancer metabolism, epigenetic gene regulation, and how both processes are affected by dietary components are summerized. A comprehensive overview of natural compounds with epigenetic activity on tumorogenesis mechanisms by which natural compounds alter the cancer epigenome is provided. Studies made in epigenetics and cancer research demonstrated that genetic and epigenetic mechanisms are not separate events in cancer; they influence each other during carcinogenesis, highlighting plant-derived anticancer compounds with epigenetic mechanisms of action, and potential use in epigenetic therapy. Recent investigations involving epigenetic modulations suggest that diet rich in phytochemicals not only reduce the risk of developing cancer, but also affect the treatment outcome.
Conference papers on the topic "Metabolome modification"
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Christie, D. J., H. Diaz-Arauzo, and J. M. Cook. "REACTIONS OF DRUG-DEPENDENT ANTIBODIES WITH METABOLITES OF QUININE (Qn) AND QUINIDINE (Qd)." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644578.
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In many cases of drug-induced immunologic thrombocytopenia (DITP), a metabolite, rather than the native drug, is suspected of provoking the destructive drug-dependent antibodies (DDAB) responsible for this severe hemorrhagic disorder. However, this has not previously been investigated for Qn- and Qd-DDAB. We report evidence that the native drugs, and not their metabolites, are the provocative agents in Qn and Qd DITP. Reactions of Qn- and Qd-DDAB with platelets were studied with the native drugs and four of their metabolites: the N-oxide and 10,11-diol derivatives (quinuclidine ring modifications), the des-methyl derivatives (aromatic quinoline ring modification), and 2'-quininone and 2'-quinidinone (2'-oxo derivatives) (also quinoline ring modifications on Qn and Qd, respectively). Five antibodies were studied:two Group 1 DDAB (specific for compounds with native configuration at asymmetric carbon positions), two Group 2 DDAB (similar to Group 1 DDAB but also known to require the methoxy group on the quinuclidine ring for full activity), and one Group 3 DDAB (reactive with the native drug, its stereoisomer, and several nonmetabolic analogs of both compounds) . Using a complement-dependent 51Cr-lysis assay, the reactions of all DDAB with platelets and the four metabolites were similar to 100-fold weaker when compared to reactions obtained with the native drug, with these exceptions:Group 2 DDAB failed to react with the desmethyl and 2'-oxo metabolites and the Group 3 DDAB failed to react with 2'-oxo Qd. This observation shows that the activity of certain DDAB is critically dependent on the native quinoline ring structure. Importantly, none of the DDAB reacted more strongly with any of the metabolites tested when compared with reactions in the presence of the native drug. These findings indicate that DDAB react with platelets preferentially in the presence of the unaltered Qn and Qd molecules and suggest that, while the role of metabolites cannot be entirely ruled out, the native structure of the drug molecule is sufficient to stimulate production of the antibodies responsible for DITP.
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Suttie, W. J., A. Cheung, and M. G. Wood. "ENZYMOLOGY OF THE VITAMIN K-DEPENDENT CARBOXYLASE: CURRENT STATUS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643991.
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The vitamin K-dependent microsomal carboxylase converts glutamyl residues in precursor proteins to γ-carboxyglutamyl (Gla) residues in completed proteins. The enzyme activity is present in significant activities in most non-skeletal tissues but has been studied most extensively in rat and bovine liver. Early studies of the enzyme utilized bound precursors of vitamin K-dependent clotting factors as substrates for the enzyme and demonstrated that the enzyme requires the reduced form of vitamin K (vitamin KH2), O2, and CO2. Subsequent investigations have taken advantage of the observation that the enzyme will carboxylate low-molecular-weight peptide substrates with Glu-Glu sequences. Utilizing a substrate such as Phe-Leu-Glu-Glu-Leu, it has been possible to demonstrate that γ-C-H release from the Glu residue of a substrate is independent of CO2 concentration. The formation of vitamin K 2,3-epoxide can also be demonstrated in a crude microsomal system, and it can be shown that the formation of this metabolite can be stimulated by the presence of a peptide substrate of the carboxylase. These observations have led to the general hypothesis that the mechanism of action of the enzyme involves interaction of vitamin KH2 with O2 to form an oxygenated intermediate that can interact with a substrate Glu residue to abstract a γ-hydrogen and in the process he converted to vitamin K epoxide (KO). The current evidence suggests that, either directly or indirectly, removal of the γ-C-H results in the formation of a carbanion at the γ-position of the Glu residue which can interact with CO2 to form Gla. The Glu residue intermediate which is formed can be demonstrated to partition between accepting a proton in the media to reform Glu, or interacting with CO2 to form Gla. Current data do not distinguish between the direct formation of a carbanion coupled to proton removal, or the participation of a reduced intermediate. Recent studies have demonstrated that the enzyme will carry out a partial reaction, the formation of vitamin K epoxide, at a decreased rate in the absence of a Glu site substrate. Epoxide formation under these conditions has the same for O2 as the carboxylation reaction and is inhibited in the same manner as the carboxylation reaction. In the presence of saturating concentrations of a Glu site substrate and C02, the ratio of KO formed, γ-C-H released, and C02 formed is 1:1:1. However, KO formation can be uncoupled from and proceeds at a higher rate than γ-C-H bond cleavage and Gla formation at low Glu site substrate concentrations. At saturating concentrations of CO2, Gla formation is equivalent to γ-C-H bond cleavage, and this unity is not altered by variations in vitamin KH2 or peptide substrate concentrations. Natural compounds with vitamin K activity are 2-Me-l,4-naphthoquinones with a polyprenyl side chain at the 3-position. Studies of vitamin K analogs have demonstrated that a 2-Me group is essential for activity but that the group at the 3-position can vary significantly. Modification of the aromatic ring of the naphthoquinone nucleus by methyl group substitution can result in alterations of either the rate of the carboxylation reaction or the apparent affinity of the enzyme for the vitamin. Studies of a large number of peptide substrates have failed to reveal any unique primary amino acid sequence which is a signal for carboxylation. However, current evidence from a number of sources suggests that a basic amino acid rich "propeptide" region of the intracellular form of the vitamin K-dependent proteins is an essential recognition site for the enzyme. This region of the precursor is lost in subsequent processing, and the manner in which it directs this posttranslational event is not yet clarified. Supported by NIH grant AM-14881.
Reports on the topic "Metabolome modification"
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Brown Horowitz, Sigal, Eric L. Davis, and Axel Elling. Dissecting interactions between root-knot nematode effectors and lipid signaling involved in plant defense. United States Department of Agriculture, January 2014. http://dx.doi.org/10.32747/2014.7598167.bard.
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Root-knot nematodes, Meloidogynespp., are extremely destructive pathogens with a cosmopolitan distribution and a host range that affects most crops. Safety and environmental concerns related to the toxicity of nematicides along with a lack of natural resistance sources threaten most crops in Israel and the U.S. This emphasizes the need to identify genes and signal mechanisms that could provide novel nematode control tactics and resistance breeding targets. The sedentary root-knot nematode (RKN) Meloidogynespp. secrete effectors in a spatial and temporal manner to interfere with and mimic multiple physiological and morphological mechanisms, leading to modifications and reprogramming of the host cells' functions, resulted in construction and maintenance of nematodes' feeding sites. For successful parasitism, many effectors act as immunomodulators, aimed to manipulate and suppress immune defense signaling triggered upon nematode invasion. Plant development and defense rely mainly on hormone regulation. Herein, a metabolomic profiling of oxylipins and hormones composition of tomato roots were performed using LC-MS/MS, indicating a fluctuation in oxylipins profile in a compatible interaction. Moreover, further attention was given to uncover the implication of WRKYs transcription factors in regulating nematode development. In addition, in order to identify genes that might interact with the lipidomic defense pathway induced by oxylipins, a RNAseq was performed by exposing M. javanicasecond-stage juveniles to tomato protoplast, 9-HOT and 13-KOD oxylipins. This transcriptome generated a total of 4682 differentially expressed genes (DEGs). Being interested in effectors, we seek for DEGs carrying a predicted secretion signal peptide. Among the DEGs including signal peptide, several had homology with known effectors in other nematode species, other unknown potentially secreted proteins may have a role as root-knot nematodes' effectors which might interact with lipid signaling. The molecular interaction of LOX proteins with the Cyst nematode effectors illustrate the nematode strategy in manipulating plant lipid signals. The function of several other effectors in manipulating plant defense signals, as well as lipids signals, weakening cell walls, attenuating feeding site function and development are still being studied in depth for several novel effectors. As direct outcome of this project, the accumulating findings will be utilized to improve our understanding of the mechanisms governing critical life-cycle phases of the parasitic M. incognita RKN, thereby facilitating design of effective controls based on perturbation of nematode behavior—without producing harmful side effects. The knowledge from this study will promote genome editing strategies aimed at developing nematode resistance in tomato and other nematode-susceptible crop species in Israel and the United States.