Teses / dissertações sobre o tema "Glutaminase – métabolisme"
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Murcy, Florent. "Le rôle de la glutaminolyse hépatique dans l'athérosclérose". Electronic Thesis or Diss., Université Côte d'Azur, 2022. http://www.theses.fr/2022COAZ6022.
Texto completo da fonteCardiovascular diseases are the leading cause of death worldwide with 17 million deaths each year and represent a major public health challenge. Despite existing therapies aimed at restoring lipid homeostasis, the prevalence of these diseases keeps increasing and new targets must be find. Recently, new factors have been identified as potential actors in the development of atherosclerotic plaques. Among them, glutamine, a conditionally essential amino acid, and its metabolism have been linked to the incidence of cardiovascular disease and inflammation. Two major enzymes are involved in controlling the flow of this amino acid within our body. Glutaminase 2 (GLS2) metabolizes glutamine into glutamate and the reverse reaction is mediated by glutamine synthetase (GS). During our study, we first studied the effect of their inhibition in a mouse model of atherosclerosis with adeno-associated virus (AAV) injection or methionine sulfoximine. While GS inhibition has a little impact on lesion development, GLS2 deficiency leads to an increase in atherosclerotic plaque size. At the same time, plasma glutamine is increased. There was no major change in classical cardiovascular risk factors or even inflammation. By performing analyzes of the transcriptional profile of the liver and aortas of GLS2 KO animals, we noticed that many genes involved in the remodeling of the extracellular matrix and in the cell/matrix interaction were deregulated. Dedicated stainings of the plaques corroborated the RNA sequencing and identified regulation of key matrix-modulating enzymes supporting the hypothesis of a weakening of the extracellular matrix. Especially, we found an increase in the activity of transglutaminase 2 (TGM2), one of the pivotal regulator of matrix integrity. We next investigated the therapeutic opportunity by overexpressing hepatic GLS2. In our mouse model overexpressing the enzyme, we observed a decrease in atherosclerotic plaque size as well as a decrease in plasma glutamine. GLS2 seems to be a new player in the prevention of atherosclerosis not only by maintaining cell homeostasis but also by guaranteeing the environment integrity in which they evolve. It would be interesting to explore this new target at a time when therapies seem to be running out of steam
Nekooie, Marnany Nioosha. "The Intersection of Metabolism and Neural Crest Cell Development". Electronic Thesis or Diss., Paris 12, 2022. http://www.theses.fr/2022PA120066.
Texto completo da fonteMetabolism as a keystone of stem cells' fate not only supplies demands for energy and precursor molecules but also has roles in chromatin remodeling. In vertebrate embryos, neural crest (NC) cells constitute a remarkable population of embryonic progenitors, which upon delamination from dorsal neural tube, extensive migration and differentiation give rise to both neural/neuronal and mesenchymal derivatives. The developmental potential of NC cells necessitates epigenetic remodeling and environmental cues. Accordingly, the intersection of metabolism and NC plasticity will provide critical insights into the regulation of NC cell identity and development. Thus, I intended to figure out the metabolism role in the developmental aspect of one sub-population of NC cells, trunk type. The first part of my study resulted in a general view of the metabolic impacts on all developmental NC steps. I evidenced that glucose oxidation is a pivotalmetabolic profile governing NC delamination, adhesion, migration, proliferation, maintenance of stemness, and widespread differentiation. Given the incidence of G1/S transition upon EMT in trunk NC cells, the inhibition of pentose phosphate pathway (PPP) was unable to influence the NC delamination, suggesting a metabolic adaptation to maintain developmental steps and survival. Hence, In the next step, I sought to appreciate how metabolic pathways integrate into the NC delamination. The rewiring of glycolysis pathway under PPP suppression in delaminating stage provided support for multi metabolic pathways recruited by NC progenitors in response to the metabolic stress. My study also elucidated the metabolic reprograming from PPP to glucose oxidation in trunk NC cells, aligned with delaminating to migratory transition of these cells. Additionally, besides glucose, glutamine had a prominent role in pluripotent acquisition anddelamination of NC progenitors that triggers the nuclear localization of glutaminase (GLS) upon EMT step. Therefore, the nuclear GLS localization of pre-migratory NC cells in delaminating stage suggests the gene regulatory function for GLS. Altogether, my results indicated the intersection of metabolism and NC reprograming from pluripotent step to the NC commitment, defined respectively by promoted PPP and nuclear localization of GLS to glucose-based OXPHOSphenotype with cytoplasmic GLS localization. Moreover, the possible interaction between GLS and B-catenin fostered the new concept about the contribution of GLS to Wnt signaling, holding promise for understanding the etiology of many neurocristopathies
Hasan, Bou Issa Lama. "Étude des dépendances génomiques dans le myélome multiple surexprimant MYC". Electronic Thesis or Diss., Université de Lille (2022-....), 2024. http://www.theses.fr/2024ULILS011.
Texto completo da fonteMultiple myeloma (MM) is a hematological malignancy that accounts for around 13% of hematological cancers and is characterized by the uncontrolled proliferation of malignant plasma cells in the bone marrow. MM progresses from precursor stages, known as monoclonal gammopathy of undetermined significance (MGUS) and smoldering multiple myeloma (SMM), to the symptomatic form, MM. It is an incurable malignancy in which heterogeneity and clonal evolution allow treatment escape and disease progression. MYC alterations play an essential role in this progression. However, MYC is not therapeutically targetable due to its nuclear localization and the protein's short half-life.To overcome this, we hypothesized that the proliferative advantage induced by MYC overexpression creates genomic dependencies on other signalling pathways that become essential for cell survival. To test this hypothesis, we applied a novel approach by leveraging large-scale loss of function screen (Achilles) and 1869 small molecules screen to identify MYC-induced genomic vulnerabilities. When identified, these vulnerabilities offer an opportunity to selectively target cancer cells harbouring this overexpression and spare normal cells.Our analyses demonstrate the dependence of MYC overexpressing cells on glutamine metabolism, in particular on the GLS1 (glutaminase). We validated and functionally delineated this dependence in vitro using different approaches.Our small molecule screen highlighted that NAD synthesis inhibitors had a preferential effect on the proliferation of MYC overexpressing cells. Considering that glutamine and NAD have closely interlinked metabolic networks, we investigated the possibility of a potential synergistic effect between GLS1 and NAMPT inhibitors. We demonstrated the effectiveness of this new synergistic combination to target MYC-driven MM cells in vitro and in vivo.These results establish a solid methodological basis that can be used to develop new therapeutic approaches to address unmet therapeutic needs to target MYC in MM
Rumbach, Lucien. "Valproate de sodium et métabolisme de l'ammoniaque". Université Louis Pasteur (Strasbourg) (1971-2008), 1989. http://www.theses.fr/1989STR1BH16.
Texto completo da fonteJacque, Nathalie. "Étude du métabolisme de la glutamine dans les leucémies aiguës myéloïdes". Thesis, Sorbonne Paris Cité, 2015. http://www.theses.fr/2015USPCB221/document.
Texto completo da fonteCancer cells survival is dependent on high energetic and biosynthetic activity, and glutamine is involved in many metabolic processes necessary for this adaptation. In acute myeloid leukemia (AML), growth and proliferation are promoted by activation of several signaling pathways, including mTORC1. Essential amino acids, in particular leucine, are required for mTORC1 activation. Glutamine enters into the cell via the SLC1A5 transporter and then allows the input of leucine via the bidirectional SLC7A5 transporter. Therefore, the intracellular glutamine concentration is a limiting step in the activation of mTORC1 by leucine. We studied the effects of glutamine deprivation in AML using different tools (medium without glutamine, shRNA against the SLC1A5 glutamine transporter and the drug L-asparaginase, which has an extracellular glutaminase activity) and observed mTORC1 and protein synthesis inhibition. SLC1A5 transporter knockdown inhibits tumor growth in a xenotransplantation model. L-asparaginase inhibits mTORC1 and induces apoptosis in proportion to its glutaminase activity and independently of asparagine concentration. Glutamine privation induces the expression of glutamine synthase and autophagy, and these two processes are involved in the resistance to glutamine privation in some leukemic cell lines. However, apoptosis induced by glutamine privation is not related to the inhibition of mTORC1, since it is not modified in the presence of a constitutively active mutant of mTOR. We next focused on the oxidative phosphorylation, another glutamine dependent pathway in many cancers. The initial step of the intracellular catabolism of glutamine is the conversion of glutamine to glutamate by enzymes called glutaminases. Different glutaminases isoforms exist that are encoded by the GLS1 and GLS2 genes. Glutamate is then converted to α-ketoglutarate, an essential TCA cycle intermediate. In AML cell lines, we observed that glutamine privation inhibits mitochondrial oxidative phosphorylation. The protein glutaminase C (GAC), an isoform of GLS1, is constantly expressed in AML but also in normal CD34 + hematopoietic progenitors. The knockdown of GLS1 by inducible shRNA or by the CB-839 compound reduced oxidative phosphorylation, leading to proliferation inhibition and apoptosis induction in leukemia cells. Genetic invalidation of GLS1 inhibits tumor formation and improves survival of mice in a xenograft model. Conversely, the targeting of GLS1 has no cytotoxic or cytostatic effects on normal hematopoietic progenitors. These anti-leukemic effects are inhibited by the addition of α-ketoglutarate, and those induced by the CB-839 are suppressed in the presence of an ectopically expressed GACK320A hyperactive mutant, confirming the essential role of maintaining an active TCA cycle in AML cells. Finally, we showed that glutaminolysis inhibition induces the intrinsic mitochondrial pathway of apoptosis and acts synergistically with the specific inhibition of BCL-2 by ABT-199. These results demonstrate that specific targeting of glutaminolysis is another way to exploit glutamine addiction in AML and that an active TCA cycle in essential for AML cell survival
Polat, Ibrahim Halil. "Rôle fonctionnel des pentoses phosphates et glutamine dans le métabolisme des cellules cancéreuses". Thesis, Université Grenoble Alpes (ComUE), 2016. http://www.theses.fr/2016GREAS031/document.
Texto completo da fonteMoreover, we characterized the metabolic adaptations that breast cancer cells undergo in the deprivation of glutamine or when mitochondria are defected. We conducted metabolic flux analysis using metabolomics and fluxomics approaches and we employed Systems Biology approaches in order to estimate a global view of flux alterations in different culture conditions. We observed an increased pyruvate cycle with glutamine deprivation, thus indicating that targeting the enzymes of this pathway such as malic enzyme could be a promising approach combined with inhibition of glutaminase enzyme. On the other hand, we observed that mimicking hypoxia by oligomycin treatment redirected breast cancer cells to increase reductive carboxylation. Considering that hypoxia is a common condition in the tumor environment, targeting reductive carboxylation mechanism could be a novel strategy to fight against cancer. Collectively, all the results provided in this thesis demosntrate the importance of metabolism in cancer cell proliferation and survival. This work also highlights the importance of Systems Biology approaches to comprehend the molecular mechanisms underlying complex multifactorial diseases in order to point out new potential therapeutic targets
Baverel, Gabriel. "Métabolisme de l'alanine et de l'aspartate dans le cortex rénal du cobaye". Lyon 1, 1985. http://www.theses.fr/1985LYO19060.
Texto completo da fonteMaurin, Claire. "Régulation de la glutamine synthétase chez le cocolithophoridé Emiliania Huxleyi". Brest, 1997. http://www.theses.fr/1997BRES2008.
Texto completo da fonteVercoutère, Barbara. "Voies et régulations du métabolisme hépatique de la glutamine chez des souris normales et déficientes en récepteur à l'hormone thyroïdienne par invalidation de gènes : aspects cellulaires et moléculaires". Lyon 1, 2002. http://www.theses.fr/2002LYO10202.
Texto completo da fonteBodineau, Clément. "Biochemical characterization of mTORC1 regulation by glutamine metabolism". Thesis, Bordeaux, 2020. http://www.theses.fr/2020BORD0163.
Texto completo da fonteGlutamine is the most abundant amino acid in the blood of mammals and its metabolism is particularly important for tumour cell proliferation. Cancer cells metabolize glutamine mostly through glutaminolysis, a metabolic process catabolized by glutaminase (GLS) and glutamate dehydrogenase (GDH) that activates mTORC1 signalling. Together with AMPK, the mTORC1 pathway is a key regulator of cell growth and proliferation. The unbalanced activation of mTORC1 by glutaminolysis during amino-acid starvation leads to a non-canonical apoptotic cell death known as “glutamoptosis”. In this thesis project, we identified that the reactivation of AMPK prevented both mTORC1 activation and cell death during glutamoptosis both in vitro and in vivo; suggesting an active role of AMPK during this process. Surprisingly, the connection between glutamine and AMPK, mediated by ATP, did not involve the necessary participation of glutaminolysis. Rather, we demonstrated the crucial role of the asparagine synthetase (ASNS) and the GABA shunt for the production of ATP during glutamine sufficiency, necessary for the metabolic control of the AMPK/mTORC1 axis. Indeed, the complete inhibition of mTORC1 required both the inhibition of GLS and the ASNS. Hence, we propose a model by which glutamine metabolism regulates mTORC1 pathway through two independent branches involving glutaminolysis and ASNS/GABA shunt that should be considered for potential targeted therapies against cancer
Martin, Guy. "Métabolisme hépatique et rénal de la glutamine et de l'alanine chez le rat : étude par RMN 13C du métabolisme rénal de l'aspartate chez le cobaye". Lyon 1, 1987. http://www.theses.fr/1987LYO10045.
Texto completo da fonteVittorelli, Anne. "Caractérisation des tranches de rein humain coupées avec précision : viabilité, métabolisme, réactivité pharmaco-toxicologie, cryoconservation". Lyon 1, 2003. http://www.theses.fr/2003LYO10252.
Texto completo da fonteLapouble, Eve. "Métabolisme cérébral et épilepsie : études de deux analogues structuraux du glutamate chez la souris". Orléans, 2002. http://www.theses.fr/2002ORLE2030.
Texto completo da fonteOizel, Kristell. "Métabolisme et sensibilité à la mort cellulaire dans le glioblastome". Nantes, 2015. https://archive.bu.univ-nantes.fr/pollux/show/show?id=a1401556-8497-464e-bdda-d0068fe3297e.
Texto completo da fonteTumor cells undergo metabolic adaptations allowing them to sustain a high proliferative rate and to resist to cell death signals, especially increasing aerobic glycolysis and glutaminolysis. Glioblastoma multiforme (GBM), the most common brain tumor in adults, is characterized by a strong resistance to therapeutic treatments and the presence of cancer stem cells. This PhD project investigated the link between metabolism and cell death sensitivity in GBM. First, we studied the impact of isocitrate dehydrogenase (IDH) mutation recently identified in GBM patients. We show that mutated IDH induces a reduced sensitivity to etoposide-induced cell death mediated through a mitochondrial NADH pool reduction. Second, we aimed to determine if glutaminolysis inhibition could modulate cell death response in GBM tumor model. We show that epigallocatechin gallate (EGCG), an inhibitor of glutamate dehydrogenase (GDH), can sensitize GBM cell lines to cell death. Furthermore, in primary cultures models, EGCG sensitize the GBM mesenchymal subtype to cell death. This cellular model derived directly from patients tumors allows to keep the initial tumor heterogeneity, in particular the presence of cancer stem cells. These results show a direct link between metabolism and cell death resistance and open new therapeutic strategies. Thus EGCG could be a good candidate as an adjuvant in current GBM therapy in the context of personalized treatment
Lévy, Pierre. "Hepatitis C virus-induced reprogramming of glutamine metabolism". Thesis, Lyon 1, 2014. http://www.theses.fr/2014LYO10328.
Texto completo da fonteChronic infection with hepatitis C virus (HCV) is one of the main etiologies of hepatocellular carcinoma (HCC). However, mechanisms of HCV-related tumorigenesis are ill-defined. Recent literature data suggest that HCV infection may reprogram glucose metabolism in a cancerlike fashion. The Warburg effect, or aerobic glycolysis, is a hallmark of cancer. Activation of this pathway allows tumor cells to sustain high rates of energy production and provide sufficient biosynthetic precursors for proliferation. Likewise, the induction of similar metabolic alterations may favor HCV multiplication through the rapid production of nucleotides, amino acids and lipids. To complement aerobic glycolysis, tumor cells become frequently dependent on glutamine. The partial oxidation of glutamine through the glutaminolytic pathway can fuel their energy metabolism and several anabolic pathways. However, the role of glutamine metabolism in HCV life cycle has not been documented so far. I focused my PhD research project on the characterization of metabolic alterations triggered by HCV. In particular, I evaluated the occurrence of distinctive features of tumor cell metabolism in HCVinfected cells, with a specific attention on glutamine utilization. In the HCVcc cell culture model, I report the induction of a metabolic reprogramming towards higher rates of glutaminolysis upon HCV infection. HCV-induced transcriptional activation of MYC, along with several glutamine transporters and glutaminase, is likely to be responsible for this metabolic shift. Interestingly, increases in transcript levels of these factors in liver biopsies of patients with chronic hepatitis C suggest that this metabolic reprogramming may be relevant in vivo. Moreover, these metabolic changes may expose new drug targets against HCV as suggested by the inhibition of the virus replication upon suppression of glutaminolysis via different strategies. Altogether, these findings uncover a potential link between chronic hepatitis C and HCC through the installation of a favorable metabolic environment for tumor development
Obrist, Florine. "Les vulnérabilités métaboliques des cancers résistants au cisplatine". Thesis, Université Paris-Saclay (ComUE), 2017. http://www.theses.fr/2017SACLS571/document.
Texto completo da fonteCisplatin is the most widely used chemotherapeutic agent, and resistance of neoplastic cells against this cytoxicant pose a major problem in clinical oncology. Here, we explored potential metabolic vulnerabilities of cisplatin-resistant non-small cell lung cancer and ovarian cancer cell lines. Cisplatin resistant clones were more sensitive to killing by nutrient deprivation in vitro and in vivo than their parental cisplatin-sensitive controls. The susceptibility of cisplatin-resistant cells to starvation could be explained by a particularly strong dependence on glutamine. Glutamine depletion was sufficient to restore cisplatin responses of initially cisplatin-resistant clones, and glutamine supplementation rescued cisplatin resistant clones from starvation-induced death. Mass spectrometric metabolomics and specific interventions on glutamine metabolism revealed that, in cisplatin-resistant cells, glutamine is mostly required for nucleotide biosynthesis rather than for anaplerotic, bioenergetic or redox reactions. As a result, cisplatin-resistant cancers became exquisitely sensitive to treatment with antimetabolites that target nucleoside metabolism
Nguyen, Tra ly. "Biochemical and cellular characterization of the interplay between glutamine metabolism, mTOR and Notch1 signaling in cancer therapy". Thesis, Bordeaux, 2018. http://www.theses.fr/2018BORD0053.
Texto completo da fonteTumorigenesis is a multistep process, consisting of genetic alterations that drive the malignant transformation of normal human cells. During this transformation, different oncogenic pathways are upregulated. mTORC1 and Notch1 signaling are well-known oncogenic pathways which play a central role in the regulation of cell growth and metabolism. Anti-mTORC1 and Notch1 therapies are approved as cancer treatments for several types of tumor but there are still developed resistances and relapse diseases. Thus, the main aim of this work is to study the inhibition of mTORC1 and Notch1 signaling pathway in cancer cells in order to design new therapeutic anti-cancer strategies. In the first place, we reported new class of mTORC1 inhibitors which has cytotoxicity specifically towards cancer cells. We demonstrated that ICSN3250, an analogue of the cytotoxic marine alkaloid halitulin, inhibited mTORC1 and induced cell death. The molecular mechanism of this inhibition is based on the displacement of the lipid phosphatidic acid, an activator of mTORC1 complex, from the FRB domain of mTOR protein. At the second stage, we have studied the connection between glutamine metabolism and Notch1 signaling in T-cell acute lymphoblastic leukemia (TALL). Metabolic changes in cancer cells are advantageous for rapid cell proliferation and tumor growth. We have generated Notch1-driven T-ALL cells and analyzed the consequences of Notch1 activation on glutamine metabolism. Indeed, under glutamine withdrawal, Notch1 upregulation induced apoptotic cell death by disrupting the accumulation of glutamine synthetase, a glutamine producing-enzyme. Overall, this thesis work allowed to describe new strategies to target mTORC1 and Notch1 pathways in cancer, which need future investigations to study their efficacy in therapies
Ferreira, Matias Maria. "Targeting the metabolic environment to modulate T cell effector function". Thesis, Montpellier, 2019. http://www.theses.fr/2019MONTT020.
Texto completo da fonteT cells are stimulated upon interaction with their cognate antigen. While much research has focused on the role of antigen presenting cells (APC) and cytokines as important components of the T cell microenvironment, recent data highlight the importance of the metabolic environment in sustaining the energetic and biosynthetic demands that are induced upon antigen stimulation. The subsequent metabolic reprogramming of the T cell is conditioned by the nutrient composition and oxygen levels. Notably, this environment can be altered by pathological conditions such as tumors and data from our group, as well as others, have shown that the competition of T cells and tumor cells for limiting amounts of nutrients has a negative impact on T cells, inhibiting their anti-tumor effector functions. This effect is due, at least in part, to the distinct metabolic profiles of T lymphocyte subsets; T effector cells (including Th1 cells) are highly glycolytic while suppressive Foxp3+ regulatory T cells (Tregs) display a mixed metabolism with increased levels of lipid oxidation. It is therefore important to determine how changes in the metabolic programming of anti-tumor T cells impacts on their persistence and function. Indeed, in the context of my PhD research, I found that high levels of the glucose transporter Glut1 was associated with a significantly increased level of IFNγ secretion by both CD4 and CD8 T cells. Furthermore, there was a bias of CD8 over CD4 lymphocytes in the Glut1-hi T cell subset. These data point to the importance of metabolic alterations in the fate and effector function of T lymphocytes and during my PhD, I focused on elucidating the metabolic parameters that regulate effector and regulatory T cells, with the goal of improving the efficacy of anti-tumor T cells. In this context, I contributed to initial studies from our group, revealing a critical role for extracellular nutrient availability in terminal CD4+ T cell differentiation. Activation of naïve CD4+ T cells under conditions of glutamine deprivation caused them to differentiate into induced Treg (iTreg). Moreover, the skewing of glutamine-deprived naive CD4+ T cells to a Foxp3+ fate occurred even under Th1-polarizing conditions, blocking terminal Th1 differentiation. Under glutamine-deprived conditions, we found that alpha-ketoglutarate (αKG), a glutamine-derived metabolite, rescued Th1 differentiation. I then evaluated the impact of aKG under glutamine-replete conditions in the Th1/iTreg differentiation processes. My studies showed that, under Th1-polarizing conditions, aKG markedly enhanced naïve CD4+ T cell differentiation into Th1 cells and increased IFNg secretion. Moreover, under Treg-polarizing conditions, αKG decreased Foxp3 expression and increased the secretion of inflammatory cytokines such as IFNg, GM-CSF and IL-17. Notably, the aKG-mediated alteration in T cell differentiation was associated with an augmented oxidative phosphorylation (OXPHOS), and inhibiting the citric acid cycle and the mitochondrial complex II with malonate, an inhibitor of succinate dehydrogenase (SDH), alleviated the αKG-mediated block in Treg differentiation. Impressively, these aKG-mediated changes in the Th1/Treg balance were maintained in vivo, promoting a Th1-like profile in T cells expressing an anti-tumor chimeric antigen receptor (CAR) in tumor-bearing mice. Thus, our data show that low intracellular aKG content, caused by limited external glutamine availability, imposes a Treg phenotype while high aKG levels shift the balance towards a Th1 phenotype.Altogether, the data generated during my PhD will promote the development of metabolic strategies aimed at modulating T cell function and foster the design of nutrient transporter-based approaches that can be used to select T lymphocytes with enhanced anti-tumor effector properties
Coëffier, Moïse. "Influence de la glutamine sur la réponse inflammatoire et le métabolisme protéique au niveau de l'intestin humain". Paris 7, 2002. http://www.theses.fr/2002PA077054.
Texto completo da fonteVincent, Nadine. "Action de la glycine sur le métabolisme de la glutamine et sur l'uréogénèse dans les hépatocytes isolés de rat". Lyon 1, 1990. http://www.theses.fr/1990LYO1T087.
Texto completo da fonteLeleu, Olivier. "Étude du métabolisme azoté du colza : régulation de l'activité nitrate réductase en fonction du développement et des sources azotées". Lille 1, 2000. https://pepite-depot.univ-lille.fr/RESTREINT/Th_Num/2000/50376-2000-306.pdf.
Texto completo da fonteLe, Bacquer Olivier. "Effets trophiques de la glutamine : études in vivo chez le nouveau-né prématuré et in vitro sur un modèle d'entérocytes humains en culture". Nantes, 2002. http://www.theses.fr/2002NANT18VS.
Texto completo da fonteAnimal and human studies suggest that glutamine supply may enhance whole body protein synthesis stimulation and improve gut trophicity during critical illness. The mechanisms of these effects remain unclear. This work combines an in vivo study in very-low-birth-weight infants with two in vitro studies using the Caco-2 cell line as a model of human enterocytes in culture. Our results show that 1) in parenterally fed preterm, a 24h glutamine supplementation decreases whole body protein synthesis, but may have an acute protein-sparing effect, as it suppresses protein breakdown and oxidation; 2) we also demonstrate that glutamine deprivation impairs protein synthesis in a model of enterocytes. Finally, 3) apical nutrient deprivation, a model of fasting, impairs protein synthesis, depletes glutathione pool, and increases transepithelial permeability. Most of these parameters are restored by glutamine supplementation, probably through glutamine utilization as a source of energy. Taken together, these findings suggest that glutamine may improve protein accretion in preterm infants through an anti-catabolic effect, and regulate gut barrier function by stimulating intestinal protein synthesis
Martin, Francis. "Contribution à l'étude du métabolisme primaire de symbiotes ectomycorhiziens". Paris 11, 1986. http://www.theses.fr/1986PA112219.
Texto completo da fonteThe primary metabolism of ectomycorrhizal fungi and beech (Fagus Sylvatica) octomycorrhlzas has been studied. Natural abundance nuclear magnetic resonance spectroscopy (NMR) has been used to study the carbon (carbohydrates, fatty acids) and phosphorus (polyphosphates) storage compounds in intact mycelia from the ectomycorrhizal fungi. Particular attention has been paid to the biochemical pathways leading to the catabolism of glucose and the biosynthesis of carbohydrates and amino acids. In the ectomycorrhizal ascomycete Cenococcum geophilum, mannitol is not only a storage carbon compound but is also involved in the production of NADPH via the mannitol cycle. A large part of the carbon of glucose was used to form trehalose after cycling through this cycle. Pyruvate, arising from glycolysis and the pentose phosphate shunt, enters the Krebs cycle through both carboxylase and pyruvate dehydrogenase activities. The Krebs cycle, acetate metabolism and the fixation furnish high intracellular pools of glutamine, glutamate, alanine, x-aminobutyrate and arginine. Gluconeogenesis was operative during acetate utilization and led to the formation of mannitol and trehalose. The differences observed between the metabolism of acetate and glucose are discussed. Ammonium assimilation was followed in N-starved and N-rich mycelia of Cenococcum geophilum. From the composition of free amino acid pools, 15N labelling patterns and effects of enzyme inhibitors, NH4+ assimilation appears to proceed via the glutamate dehydrogenase pathway. The NADPH-glutamate dehydrogenase was therefore purified to homogeneity and its catalytic and physicochemical properties determined. The biosynthesis of glutamine is rapid and is presumably used by the mycelium to store nitrogen and to avoid ammonium toxification. Another feature of the N metabolism is the significant formation of alanine. X-aminobutyrate and arginine. Ammonium assimilation and amino acid biosynthesis have been followed in ectomycorrhizal roots of Fagus sylvatica. The absorption of ammonium ions was associated with a rapid synthesis of free amino acids. The 15N 1abe11ing patterns suggest that nitrogen assimilation occurs via the glutamine synthetase/glutamate synthase pathway, and that glutamate dehydrogenase plays little, if any, part in this process. Alternative m0031s for the nitrogen assimilation pathways ln fungal and host tissues are presented
Dugelay, Sylvie. "Caractérisation du métabolisme de l'alanine dans le cortex rénal de lapin : étude par spectroscopie RMN". Lyon 1, 1992. http://www.theses.fr/1992LYO1T134.
Texto completo da fonteMichoudet, Christian. "Métabolisme du glucose dans le cortex rénal du cobaye : apport de la spectroscopie RMN". Lyon 1, 1987. http://www.theses.fr/1987LYO10003.
Texto completo da fonteLavoinne, Alain. "Influence de l'adénosine, de l'éthionine et de la glutamine sur le métabolisme glucidique de l'hépatocyte isolé de rat". Rouen, 1986. http://www.theses.fr/1986ROUES012.
Texto completo da fonteMoison, Michaël. "Rôle des glutamine synthétases cytosoliques et des asparagine synthétases dans le métabolisme azoté chez Arabidopsis thaliana et Brassica napus". Thesis, Paris 11, 2014. http://www.theses.fr/2014PA112394/document.
Texto completo da fonteWinter oilseed rape (Brassica napus) is grown for its oil-rich seeds and for proteins, used in animal feed cake. It requires high nitrogen inputs due to the low efficiency of nitrogen utilization that characterizes this species. A large proportion of absorbed nitrogen is indeed returned to the soil when leaves fall. Improving nitrogen remobilization to promote seed filling is then required to improve yield and limit fertilizer use. Asparagine and glutamine are important amino acids for phloem translocation. This thesis focuses on the two multigenic families in charge of asparagine and glutamine synthesis: cytosolic glutamine synthetase (GLN1) and asparagine synthetase (ASN). Studies were performed on the two Brassicaceae, rapeseed and Arabidopsis thaliana. The GLN1 gene expressions were investigated in Arabidopsis by a combination of molecular biology and cytology. The five GLN1 genes are differentially expressed in Arabidopsis depending on ageing and nitrogen availability. The identified BnaGLN1 genes in Brassica napus also showed age and nitrogen dependent expressions. Interestingly, expression profiles were similar between homologous genes in Arabidopsis and rapeseed, suggesting that homologous genes share similar function in the two species. The role of Arabidopsis GLN1 genes for nitrogen remobilization to the seeds was monitored using ¹⁵N tracing experiments on individual mutants. The GLN1 genes play a role in the remobilization of nitrogen from the rosette leaves to the reproductive organs. However, their effect is weak and non-specific of one GS1 isoform. ASN genes also presented specific expression profiles depending on organs, age and nitrogen availability. The ¹⁵N tracing revealed that ASN1 and ASN2 are both involved in nitrogen remobilization from the rosette to the seeds. Our studies provide a basis for future translational approaches to improve oilseed rape
Biran, Marc. "Application de la résonance magnétique nucléaire à l'étude du métabolisme hépatique : métabolisme du glutamate et de la glutamine dans le foie perfusé de rat, développements méthodologiques pour la SRM clinique". Bordeaux 2, 1994. http://www.theses.fr/1994BOR28279.
Texto completo da fonteThe first part of this work concerns the study of the metabolic compartmentation of glutamate and glutamine in the isolated and perfused rat liver. The results are obtained by using 13C enriched substrates, coupled with nuclear magnetic resonance detection. Thus, we have shown the existence of two glutamate pools, one in the periportal zone and the second in the perivenous zone. The quantification of these pools can be peformed by 13C specific enrichments determination. In the same way, biochemical assays on cellular extracts and excreted perfusate have specified the role of glutamate, glutamine and urea in the ammonium ions detoxification phenomenon in the liver. The second part of this work contributes to technological and methodological developments in the clinical use of magnetic resonance spectroscopy (MRS). Large radiofrequency coils have been elaborated to observe different nuclei : a 31P/IH coil (2T). In the same way, 2 dimension spectroscopic imaging sequences have been developed. Perfectly, localized 31P MRS spectra were performed. The comparison of investigation results on healthy volunteers and patients with various pathologies have shown significant differences. 13C MRS spectra with proton decoupling, were performed on volunteers (aftter power deposition and tissu heating calculation). 13C human liver spectra were performed at 2T for the first time by using spectroscopic imaging sequence
Vilmont, Marie. "Etude du métabolisme du glutathion dans l'érythrocyte sain et infesté par "Plasmodium falciparum" : application à la recherche d'antimalariques". Paris 5, 1990. http://www.theses.fr/1990PA05P622.
Texto completo da fonteFouto, Matias Jorge Eduardo. "Adaptation intestinale expérimentale après résection étendue du grêle ; étude "in vitro" du métabolisme entérocytaire de la glutamine par la méthode de la chambre de Ussing/ Jorge Eduardo Fouto Matias". Montpellier 1, 1994. http://www.theses.fr/1994MON1T014.
Texto completo da fonteTirado, Torres Juan Luis. "Contribution à l'étude des activités glutamine synthétase et glutamate déshydrogénase comme marqueurs du métabolisme azoté chez la feuille de soja". Montpellier 2, 1987. http://www.theses.fr/1987MON20109.
Texto completo da fonteKhayath, Naji. "Etude de l'adaptation de schistosoma mansoni à son environnement nutritif : rôles de la glutanime dans le métabolisme énergétique du sporocyste et analyse de la diversification de la famille des récepteurs de l'insuline chez le parasite". Lille 2, 2006. http://www.theses.fr/2006LIL2S026.
Texto completo da fonteThevenon, Sylvie. "Caractéristiques de métabolisme du 13C-glucose dans des tranches de foie de rats coupées avec précision : effet de l'insuline et de la glutamine". Lyon 1, 2004. http://www.theses.fr/2004LYO10159.
Texto completo da fonteWe characterized glucose metabolism and its regulation in rat precision cut liver slices incubated 24 or 48 hours with increasing 13C-glucose concentration with or without insulin and/or glutamine. Enzymatic methods and carbon-13 spectroscopy NMR showed that oxidation in Krebs cycle as well as the synthesis of glucose, glycogen and triglycerides increased with 13C-glucose concentration. Under certain conditions, glucose uptake, pentose phosphate pathway and glycogen and triglycerides synthesis were sensitive to insulin. In absence of insulin, the glutamine (10 mM) stimulated glycogen synthesis but didn't modify the triglyceride synthesis or ketogenesis from glucose. No effects were found in presence of insulin. We conclude that rat liver slices are a good model for the qualitative and quantitative studies of the liver glucose metabolism and its hormonal regulation
Quillard, Muriel. "Glutamine et régulation du métabolisme hépatique : modulation de l'expression du gène de l'argininosuccinate synthétase et du gène de la phosphoénolpyruvate carboxykinase". Rouen, 1997. http://www.theses.fr/1997ROUES062.
Texto completo da fonteOburoglu, Leal. "Metabolic fueling of hematopoietic stem cell differentiation to the erythroid lineage". Thesis, Montpellier 2, 2014. http://www.theses.fr/2014MON20122.
Texto completo da fonteHematopoietic stem cells (HSCs) possess two fundamental characteristics; self-renewal capacity and the ability to give rise to all blood cell lineages. Before their commitment to a specific lineage, these cells are maintained in a quiescent state in the bone marrow. Asymmetric division is essential for the maintenance of the stem cell compartment while symmetric division results in HSC differentiation. The hypoxic environment of the bone marrow is conducive to anaerobic glycolysis and fatty acid oxidation, preserving stem cell quiescence and asymmetric division, respectively. However, it is not known whether the commitment of an HSC to a lymphoid, myeloid or erythroid lineage fate, is regulated by a metabolic switch. Indeed, while much research has shown a critical role for cytokines and cell-cell contacts in the commitment of HSCs to distinct hematopoietic lineages, the possibility that nutrient entry and metabolism may contribute to this process was not considered until very recently. Cell differentiation is associated with proliferation resulting in increased metabolic requirements that can be met by energy sources such as glucose, fatty acids, lactate, or glutamine, amongst others. While glucose and glutamine are both precursors for the production of ATP, lipids and nucleotides, their relative contributions to metabolic pathways driving HSC lineage commitment have not been evaluated. Interestingly, we and others previously found that the Glut1 glucose transporter is highly upregulated only during the final mitoses of HSC-driven erythroid differentiation, suggesting that other nutrients may regulate early stages of erythroid lineage commitment. During my PhD, I was interested in determining whether nutrient availability and utilization regulate HSC differentiation to the erythroid lineage. Interestingly, I found that the ASCT2 glutamine transporter is expressed at high levels on HSCs. Downregulation of ASCT2 or blocking glutamine metabolism abrogated erythroid differentiation of HSCs and diverted erythropoietin-signaled HSCs towards a myeloid fate. Under conditions where glutamine utilization was blocked, erythroid differentiation was not restored by directly replenishing the tricarboxylic acid cycle but rather, was dependent on de novo nucleotide biosynthesis. Surprisingly, 2-deoxyglucose, a glucose analogue that inhibits glycolysis, enhanced erythropoiesis. Glutamine and glucose catabolism also differentially modulated erythropoiesis in vivo, under stress conditions. To better elucidate the mechanism(s) via which glutamine supports the erythroid lineage specification of HSCs, we evaluated the metabolic pathways fueled by glutamine. Carbon/nitrogen-labeled glutamine tracing experiments showed that the rate-limiting step in EPO-induced erythroid differentiation is glutamine-dependent de novo nucleotide biosynthesis while glutamine entry into the TCA cycle (anaplerosis) is not required. Furthermore, the accelerated erythroid differentiation in the presence of 2-DG was associated with a striking increase in pentose phosphates, precursors of nucleotides. Notably, the shunting of glucose into the pentose phosphate pathway (PPP), rather than glycolysis, was essential for erythropoiesis. In conclusion, my research shows that the coordinated redirection of glucose and glutamine into the production of nucleotides is the sine qua non condition for the erythroid differentiation of HSCs
Leblond, Jonathan. "Etude de la protéolyse intestinale au cours d’une inflammation expérimentale et modulation nutritionnelle par la glutamine". Rouen, 2007. http://www.theses.fr/2007ROUES011.
Texto completo da fonteDuring inflammatory states and stress situations, needs in nitrogen and energy increase,especially in tissues with fast renewal like intestinal mucosa. Protein metabolism could be modified with increase of protein degradation, proteolysis, which could play critical role in the maintenance of the intestinal integrity. There are three main pathways pf proteolysis : lysosomal pathway, calcium dependent pathway and proteasome pathway. In gut, data on proteolysis in physiological and pathological conditions remain limited. To describe intestinal proteolysis modulation during inflammatory state, we have used two experimental models. With an in vitro model, cells of HCT-8 epithelial cell line, we have demonstrated that only proteasome pathway was affected by inflammatory conditions with enhanced antigen presentations. During pharmaco-nutritional modulation by glutamine, production of the IL-8pro-inflammatory cytokine was decreased. Glutamine acts through a reduction of IkBα degradation by proteasome. During induced experimental enterocolitis in rat by methotrexate, proteasome pathway was significantly inhibited than lysosomal pathway was stimulated. Such activation may participate to observed mucosal damages. In comparison of food intake restriction, methotrexate treatments induced more important decrease of protein synthesis with enhanced activities for lysosomal and calcium dependent pathways. Perspectives are to modulate these modifications of proteolysis by specific pharmaco-nutrients
Bedell, Jean-philippe. "Purification, caractérisation et régulation de la glutamine synthétase racinaire chez le Douglas (Pseudotsuga menziesii) : étude de son activité dans les mycorhizes Douglas-Laccaria bicolor". Nancy 1, 1996. http://docnum.univ-lorraine.fr/public/SCD_T_1996_0279_BEDELL.pdf.
Texto completo da fonteSene, Ndiaga. "Implication du métabolisme azoté dans la relation plante-insecte : étude des fluctuations des enzymes glutamine synthétase (GS) et glutamate déshydrogénase (GDH) chez le couple Solanum tuberosum-Myzus persicae". Amiens, 2009. http://www.theses.fr/2009AMIE0119.
Texto completo da fonteMyzus persicae which is one of the potato cultures devastators, feeds exclusively on plants phloem compartment. The phloem is the main route for the long-distance transport of photoassimilates and its sap is rich in sugars, particularly, in sucrose. The elaborated phloem sap is also composed of numerous free amino acids, and the relative concentrations of those are strongly unbalanced, which concerns, in particular, a small proportion of essential amino acids. At first, we have shown an increase in the enzymatic activities of the glutamine synthetase (GS) and the glutamate dehydrogenase (GDH) during the plant development, which has been confirmed by the western-blots and immunohistochemical study. The latter has shown the almost exclusive presence of the GS1 and GDH proteins in phloem companion cells. A study of these enzymes status on the scale of the plant and during plant development has shown a real effect of M. Persicae infection on the GS and GDH, which are two key enzymes probably involved in amino acids synthesis and in the control of fine reorientation of carbon and nitrogenous metabolisms. The induction of these enzymes appears only on the local level as compared to the observed changes of metabolites which are affected on both local and systematic levels. All changes inducted by the aphids suggest that the aphids are able to modify the nutritional composition of phloem in order to gain in qualitative and quantitive increase in amino acids. Our observations have also shown that the change in nitrogenous metabolism, inducted by transgenesis or mutagenesis, has a clear effect on the alimentary habits of the studied aphids
Benhmammouch, Saloua. "Régulations intrinsèques et extrinsèques du métabolisme de la glutamine sur les fonctions effectrices des macrophages et conséquences sur le développement des plaques d'athéromes". Electronic Thesis or Diss., Université Côte d'Azur, 2023. http://www.theses.fr/2023COAZ6033.
Texto completo da fonteCardiometabolic diseases are a major global health problem, affecting millions of people worldwide. The World Health Organization (WHO) estimates that cardiovascular diseases, such as atherosclerosis, cause more than 17 million deaths per year due to their complications.We already know that immune response nature taking place in the atherosclerotic plaque is a central factor in the development of the pathology. A large part of this immune response is supported by macrophages which will actively participate in the establishment and development of the plaque. Excessive macrophage activation can lead to an uncontrolled inflammatory response and accelerate the progression of atherosclerotic plaques. Macrophages activation is supported by their metabolism, which is dependent on the cellular microenvironment. This rising area of research is called immunometabolism. However, the mechanisms underlying this metabolic control of macrophages are not fully elucidated.We were interested in glutamine as a source of energy for macrophages. We focused on its metabolism within myeloid cells, which is supported by 2 enzymes: glutaminase 1 (GLS1) allowing the synthesis of glutamate from glutamine and glutamine synthetase (GS) which produces glutamine from of glutamate. We modulated these enzymes within macrophages either by a genetic knock-out of GLS in myeloid cells or by inhibiting GS thanks to a pharmacological approach.Our results highlighted a lower activity of GLS1 glutaminase in atherosclerotic plaque macrophages from mouse model of atherosclerosis that is not compensated by the other GLS2 isoform. Systemic perturbation of glutamine metabolism in mice with defective hepatic glutaminolysis did not exacerbate the development of atherosclerosis meditated by specific deficiency of GLS1 in macrophages. Altogether, these findings reveal that GLS1-dependent macrophage glutaminolysis is the culprit of the cell intrinsic reparative and resolutive functions of macrophages in atherosclerotic plaques. Unexpectedly, we observed that pharmacological inhibition of glutamine synthetase (GS) by MSO acted as a metabolic rheostat from macrophage effector functions depending on the environmental milieu. However, this metabolic rheostat is partially lost upon GLS1 deficiency further supporting the original hypothesis that glutamine is a dominant nutrient utilized by macrophage to perform their effector functions. High-throughput transcriptional profiling next identified that among several Solute Carrier (SLC) membrane transporters, SLC7A7 was most likely one of the dominant glutamine importers that sustained glutamine influx in macrophages to support GLS1-dependent glutaminolysis. These results shed light on novel glutamine metabolism players allowing atherosclerosis plaque macrophages metabolic reprograming
Abely, Michel. "Métabolisme de la glutamine et transports de l'eau et des électrolytes dans l'épithélium intestinal du lapin : effets de la toxine du choléra, de la déshydratation et de la malnutrition". Paris 7, 2002. http://www.theses.fr/2002PA077001.
Texto completo da fonteKlysz, Dorota. "Impact of lymphopenia-inducing regimens and energetic resources on the fate of adoptively transferred T cells". Thesis, Montpellier 2, 2014. http://www.theses.fr/2014MON20184/document.
Texto completo da fonteAnti-tumor therapies have improved significantly over the decade. However, the currently used treatments have important limitations, notably for metastatic cancers, and the development of new approaches is therefore a high priority. Adoptive T cell therapy (ACT) represents an innovative strategy that has shown much promise. This therapy is based on the infusion of tumor-specific T cells, which have been manipulated and expanded ex vivo, into patients who have been rendered lymphopenic by chemotherapy and/or irradiation. It is interesting to note that while lymphodepletion is attained by the vast majority of conditioning regimens, the effects of these protocols on the host environment and potentially, on the destiny of adoptively-transferred T cells had not been elucidated prior to the studies which we initiated. Using a murine model, we found that the fate of adoptively-transferred T cells differs markedly in mice rendered lymphopenic by sub-lethal irradiation as compared to a busulfan/cyclophosphamide (Bu/Cy) chemotherapy regimen. Irradiation-mediated lymphopenia resulted in a skewed IL-7-dependent proliferation of donor CD8+ T cells, whereas Bu/Cy treatment led to an increased IL-7-independent, rapid CD4+ T cell proliferation. These alterations in T cell proliferation were associated with striking changes in the host microenvironment. More specifically, we demonstrated that the proportion and localization of different dendritic cell (DC) subsets in lymphoid organs were differentially affected by the type of conditioning. Furthermore, we found that these DC controlled the rapid donor CD4+ T cell division detected in Bu/Cy-treated mice as depletion of CD11c+ DC inhibited this proliferation. Altogether, our studies demonstrate that lymphopenic regimens generate distinct host environments which modulate the fate of adoptively-transferred T cells. Durind my PhD, we also investigated an original and novel aspect of the microenvironement by studying the potential role of nutrients as metabolic regulators of T cell effector function. Glutamine is the most abundant amino acid in the plasma and contributes to the bioenergetic and biosynthetic requirements of proliferating T cells. Here, we demonstrated that activation of CD4+ T cells under glutamine-deprived conditions results in a delayed mTOR activation with reduced early ATP production and decreased proliferation. Moreover, these conditions resulted in the conversion of naïve CD4+ T cells into Foxp3+ regulatory T cells (Tregs). This de novo Treg differentiation occurred even under Th1-polarizing conditions and was TGFβ-dependent. Interestingly, glutamine deprivation did not inhibit Th2 differentiation. Importantly, these converted Foxp3+ T cells showed enhanced in vivo persistence and were highly suppressive, completely protecting Rag-deficient mice from the development of autoimmune inflammatory bowel disease as efficiently as natural-occuring Tregs. Thus, our data reveal the external metabolic environment to be a key regulator of a CD4 T lymphocyte's differentiation. Altogether, the data generated during my PhD provide new insights into the identification of parameters that can potentially alter the survival and reactivity of adoptively-transferred T cells
Bhatnagar, Lakshmi. "Contribution a l'étude du métabolisme du soufre et de l'azote chez deux archaebactéries méthanogènes". Paris 7, 1985. http://www.theses.fr/1985PA077102.
Texto completo da fontePortais, Jean-Charles. "Etude par spectroscopie de RMN du carbone-13 du métabolisme intermédiaire de cellules gliales normales et tumorales". Bordeaux 2, 1993. http://www.theses.fr/1993BOR28269.
Texto completo da fonteBrun, Annick. "Contribution à l'étude de la glutamine synthétase et de la glutamate déshydrogénase à NADP chez le champignon ectomycorhizien laccaria laccata : purification, propriétés physico-chimiques et localisation dans les ectomycorhizes de Douglas". Nancy 1, 1992. http://www.theses.fr/1992NAN10169.
Texto completo da fonteLecleire, Stéphane. "Modulation de l'inflammation intestinale et du métabolisme protéique par l'arginine et la glutamine : Etude chez le volontaire sain et au cours de la maladie de Crohn". Paris 7, 2008. http://www.theses.fr/2008PA077065.
Texto completo da fonteThe first study aimed to evaluate the effects of pharmacological doses of arginine on duodenal biopsies obtained in healthy volunteers, cultured with increasing doses of arginine and a control solution, in basal and experimental inflammation conditions. The effect of arginine on gut inflammation was assessed by the measure in the culture media of the main pro and anti-inflammatory cytokines by ELISA. Arginine had no effect on gut inflammation in these conditions. Arginine increased NO production in a dose-dependent manner in inflammatory conditions, and this production was correlated to IL-8 production. The second study aimed to evaluate the effects of arginine on gut protein synthesis and proteolysis. Duodenal biopsies obtained in healthy volunteers after enteral infusion of arginine or a control solution were analysed by GC-MS in order to determine the enrichment in stables isotopes in duodenal mucosa and in plasma with arginine and control solution. Moreover, proteolysis was analysed by RT-PCR of the three main proteolysis enzymes (ubiquitin, m-calpain, cathepsin). Arginine did not have any effect on gut protein synthesis or proteolysis in healthy volunteers. The third study was designed to assess the effects or arginine combined to glutamine on gut inflammation in patients with active Crohn's disease. Colonic biopsies were obtained and cultured in four different conditions including physiological and pharmacological doses of arginine and/or glutamine. Gut inflammation was evaluated by the dosage in different culture media of the main pro and anti-inflammatory cytokines by ELISA, and by the expression of p65 NF-kappaB, IkappaB, and p38 MARK by Western-blot. Arghigh/Glnhigh significantly decreased the production of TNFalpha, 1L-1beat, IL-8 and IL-6. Argˡ°ʷ/G\nhigh decreased IL-6 and IL-8 production, whereas Arghigh/Glnˡ°ʷ did not affect cytokine and NO production. Argˡ°ʷ/Gln and Arghigh/Glnhigh decreased NF-kappaB p65 subunit expression, whereas p38 MARK was only decreased by Arghigh/Glnhigh. Combined pharmacological doses of Arg and Gin decreased TNFalpha and the main pro-inflammatory cytokines release in active colonic CD biopsies via NF-kappaB and p38 MARK pathways. These results could be the basis of prospective studies evaluating thé effects of enteral supply of combined Arg and Gln during active CD.
Gouttebel, Marie-Claude. "Régénération intestinale après résections étendues de l'intestin grêle : étude expérimentale et clinique des syndromes de l'intestin court". Montpellier 2, 1990. http://www.theses.fr/1990MON20140.
Texto completo da fonteRival, Alain. "Cinétique de la nutrition minérale et métabolisme du carbone et de l'azote dans des suspensions cellulaires hétérotrophes et photomixotrophes : aspects physiologiques et biochimiques chez Abrus precatorius L. (Leguminosae)". Montpellier 2, 1989. http://www.theses.fr/1989MON20079.
Texto completo da fonteGonzález, Luz Estela de Bashan. "Ammonium metabolism coupled with indole-3-acetic acid in the microalgae Chlorella vulgaris when co-immobilized in alginate beads with the microalgae growth-promoting bacterium Azospirillum brasilense". Doctoral thesis, Université Laval, 2006. http://hdl.handle.net/20.500.11794/18340.
Texto completo da fonteAwada, Fatima. "Assesment of sorghum response to nitrogen availability". Thesis, Université Paris-Saclay (ComUE), 2016. http://www.theses.fr/2016SACLS312/document.
Texto completo da fonteSeven accessions of Sorghum bicolor were grown with low (N⁻) and optimal (N⁺) nitrate supply. Growth parameters (plant height and leaf numbers), physiological parameters (nitrate, protein, total N and total C contents) and the activity of glutamine synthetase (GS) were studied in leaves and roots of sorghum plants at three time points of early vegetative growth (2, 4 and, 6 weeks post emergence). Plant height and leaf number were higher with nitrate supply. Except for carbon, all studied parameters were sensitive to N availability and values were typically lower when nitrate supply was low. However, different genotypes displayed considerable variation in their response to N regimes. Variation among genotypes during early vegetative development was observed for plant height, but not for leaf number. Likewise, physiological parameters varied among accessions. A significant and strong correlation, N- and accession-dependent, was detected between plant height and nitrate content. Moreover, nitrate content and GS activity at early growth stages appeared to be good markers to discriminate between nitrate uptake and assimilation capacities of different accessions under both N conditions. In some sorghum accessions, protein and total N content were indicative of high nitrate reduction and assimilation even under N limitation. Chlorophyll content was also sensitive to N availability. Furthermore, expression studies of SbNRT1.1gene copies in leaves and roots of two accessions reflected variability in expression dependent on nitrogen condition, plant organ, plant age, and gene of interest. This study is helpful to characterize different aspects of the N metabolism in sorghum and may aid in the identification of sorghum genotypes with enhanced nitrogen use efficiency, a trait that is of key interest in one of the most important crop plants in arid and semi-arid regions
Mauve, Caroline. "Production et hydrolyse des amides : mécanismes chimiques, isotopie et applications : étude de la glutamine synthétase". Thesis, Paris 11, 2014. http://www.theses.fr/2014PA112397.
Texto completo da fonteNitrogen nutrition in bacteria and plants is currently an important topic, in particular to identify key points for metabolic improvements in N assimilation and more generally, to optimize fertilization and crop yield. In such a context, the amidation reaction catalyzed by glutamine synthetase (GS), which fixes ammonium (NH₄)⁺ into glutamine, is of crucial importance since it both represents the N entry in plants and the main step of N recycling (such as photorespiratory (NH₄)⁺. Here, we examined GS kinetics and chemical mechanism. Analytical methods (HPLC, NMR, GC-MS) have been set up so as to measure in vitro activities and isotopic abundance by isotope ratio mass spectrometry. These gave access to isotope effects (¹²C/¹³C, ¹⁴N/¹⁵N et H₂O/D₂O – solvent) during catalysis, with the GS from either E. coli or A. thaliana (GS1,2). Our results show that there no ¹²C/¹³C isotope effect but there is significant ¹⁴N/¹⁵N isotope fractionation of ca. 16‰. In addition, there is an inverse solvent isotope effect (reaction 1.5 to 2 times faster in D₂O). This suggests that forming the C----N bond (amidation) is partially rate-limiting (catalytic commitment of ca. 14% only) and the H-bond network in the active site is of substantial importance for the reaction rate. The occurrence of inverse ¹⁴N/¹⁵N isotope effects under certain circumstances as well as the drastic impact of changing the metal cofactor (Mg²⁺)) indicate that the amidation step can be reversible and that the coordination by the metal plays a key role in stabilizing reaction intermediates, by interfacing the solvent. In other words, in its natural solvent H₂O, the GS catalyses an intrinsically ‘difficult’ reaction (high energy barrier of amidation) made possible by both ATP cleavage and its exergonic nature