Relevant bibliographies by topics / Metabolic function

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Metabolic function'

Author: Grafiati
Published: 4 June 2021
Last updated: 14 February 2022

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Journal articles on the topic "Metabolic function"

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Morselli, Lisa L., Aurore Guyon, and Karine Spiegel. "Sleep and metabolic function." Pflügers Archiv - European Journal of Physiology 463, no. 1 (November 19, 2011): 139–60. http://dx.doi.org/10.1007/s00424-011-1053-z.

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Pandit, Abha, and Abhay Kumar Pandey. "Glycaemic regulation and metabolic syndrome: A reference to thyroid function state." Scholars Journal of Applied Medical Sciences 4, no. 6 (June 2016): 1906–8. http://dx.doi.org/10.21276/sjams.2016.4.6.7.

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Brockmöller, Jürgen, and Ivar Roots. "Assessment of Liver Metabolic Function." Clinical Pharmacokinetics 27, no. 3 (September 1994): 216–48. http://dx.doi.org/10.2165/00003088-199427030-00005.

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Gutch, Manish, Pankaj Agarwal, and MohitMohan Singh. "Thyroid function and metabolic syndrome." Thyroid Research and Practice 12, no. 3 (2015): 85. http://dx.doi.org/10.4103/0973-0354.157915.

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Zhang, Fengxue, Andrew J. Paterson, Ping Huang, Kai Wang, and Jeffrey E. Kudlow. "Metabolic Control of Proteasome Function." Physiology 22, no. 6 (December 2007): 373–79. http://dx.doi.org/10.1152/physiol.00026.2007.

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Proteasomes are major cellular proteases that are important for protein turnover and cell survival. Dysregulation of proteasome is related to many major human diseases. Regulation of the proteasome is beginning to be understood by the recent findings that proteasomes are modified and regulated by metabolic factors O-GlcNAcylation and PKA phosphorylation.
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Petit, P., M. M. Loubati�res-Mariani, S. Keppens, and M. J. Sheehan. "Purinergic receptors and metabolic function." Drug Development Research 39, no. 3-4 (November 1996): 413–25. http://dx.doi.org/10.1002/(sici)1098-2299(199611/12)39:3/4<413::aid-ddr23>3.0.co;2-0.

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Willis, R. "Metabolic control of heart function." Journal of Molecular and Cellular Cardiology 22, no. 9 (September 1990): x. http://dx.doi.org/10.1016/0022-2828(90)91073-g.

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Deeney, Jude T., Marc Prentki, and Barbara E. Corkey. "Metabolic control ofβ-cell function." Seminars in Cell & Developmental Biology 11, no. 4 (August 2000): 267–75. http://dx.doi.org/10.1006/scdb.2000.0175.

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Chugh, ShantiN, Kiran Chugh, Sandeep Goyal, and Vijay Shankar. "Thyroid function tests in metabolic syndrome." Indian Journal of Endocrinology and Metabolism 16, no. 6 (2012): 958. http://dx.doi.org/10.4103/2230-8210.102999.

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Pouryaghoub, Gholamreza, Ramin Mehrdad, and Mohammad Mehraban. "Metabolic Syndrome and Pulmonary Function Indices." Romanian Journal of Diabetes Nutrition and Metabolic Diseases 25, no. 3 (September 1, 2018): 261–69. http://dx.doi.org/10.2478/rjdnmd-2018-0030.

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Abstract Background and aims: Metabolic syndrome (MetS) is a collection of metabolic risk factors including increased waist circumference (WC), elevated blood pressure (BP), increased triglyceride (TG), decreased high density lipoprotein (HDL-C) and increased fasting blood sugar (FBS). We aimed to examine the relevance between the MetS and its components with reduced lung functions in adult men. Material and method: A total of 3899 adult men underwent screening examination between 2015-2016 in a cross-sectional survey. Results: The mean (± SD) age of our population was 37.25 (± 4.9) years. The overall prevalence of MetS was 7.6%. The total prevalence of reduced lung function in men with MetS was 13.8%. The most common type of reduced lung function was the restrictive pattern (7.1%). The forced expiratory volume of first second (FEV1) and forced vital capacity (FVC) values were significantly lower in men with MetS (both p<0.001). Also these values were significantly lower in diabetic men compared to non-diabetics and those with impaired fasting glucose (IFG). WC and HDL were the most potent predictors of reduced FEV1 and FVC. Conclusions: We obtained a positive independent association between MetS and reduced lung function in adult men which may be related mainly due to increased WC and decreased HDL.
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Dissertations / Theses on the topic "Metabolic function"

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Inskip, Jessica Ann. "Cardiovascular and metabolic function after thoracic spinal cord injury." Thesis, University of British Columbia, 2010. http://hdl.handle.net/2429/23500.

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Spinal cord injury (SCI) has the potential to disrupt autonomic pathways in the spinal cord leading to a range of autonomic dysfunctions. The cardiovascular (CV) and metabolic sequelae can restrict the lives of individuals with SCI and contribute to the deterioration of their cardiometabolic health. Here I investigated the whole-body CV and metabolic ramifications of experimental SCI in rats. Complete thoracic SCI was performed at two different levels in order to determine whether these outcomes demonstrated a level dependence. High-(T3) and low-(T10) thoracic SCI both result in flaccid hindlimb paralysis, but have different effects on the level of supraspinal autonomic control. CV and metabolic function were assessed at several times post-injury to investigate changes over time. Animals with acute high-thoracic SCI displayed resting hypotension that resolved with time post-injury. However, their capacity to control blood pressure (BP) in response to physiological stimuli remained deficient; animals with high-thoracic SCI displayed pronounced orthostatic hypotension (OH) and severe episodes of sensory stimulation-induced hypertension known as autonomic dysreflexia (AD). The resting BP and heart rate of animals with low-thoracic SCI, and their ability to respond to orthostatic stress, was indistinguishable from sham controls. Lipid metabolism was also disordered by SCI in a level-dependent pattern. Animals with high-thoracic SCI carried increased white adipose tissue and had higher circulating triacylglycerol levels compared to animals with low-thoracic SCI and sham controls. However, there was no difference in the distribution of cholesterol-carrying lipoproteins. Carbohydrate metabolism in animals with SCI did not support the diabetic profile suggested by the lipid results. Overall, animals with SCI were more sensitive to glucose and insulin than sham-injured animals. The pronounced ketone response to fasting in animals with high-thoracic SCI suggests that there are diverse effects on substrate metabolism. This work introduces simple tests that can be performed to investigate several important and understudied autonomic outcomes of SCI. The results reveal the importance of the intact autonomic nervous system in regulating CV and metabolic function. The disparity between motor and autonomic function encourages modifying our current conventions so that we stratify subjects by their autonomic injury level and their motor deficits.
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Kuzmanov, Uros. "Metabolic function of cytoplasmic methylenetetrahydrofolate Dehydrogenase-Cyclohydrolase-Synthetase activities." Thesis, McGill University, 2005. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=98741.

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The NADP-dependent trifunctional methylenetetrahydrofolate Dehydrogenase-Cyclohydrolase-Synthetase (DCS) is responsible for the interconversion of one-carbon substituted tetrahydrofolates (THFs) required for methylation reactions and nucleotide synthesis in the cytoplasm of mammalian cells. A spontaneously immortalized DCS null fibroblast cell line was found to be a purine auxotroph due to a lack of 10-formylTHF required for de novo purine synthesis (Christensen et al. 2005). Using a retroviral infection system the DCS null fibroblasts were infected with constructs designed to express wild type DCS or proteins with D and S activities inactivated by point mutations. Western analysis and activity assays confirmed protein expression. All constructs rescued the cell line from purine auxotrophy showing that one-carbon substituted THF derived from cytoplasmic serine and mitochondrial formate can be utilized in purine synthesis. Supported by previous studies, radiolabeling experiments tracing incorporation of exogenous 3-14C serine and 14C formate demonstrated that mitochondrial formate is the preferred source of one-carbon units for purine synthesis in these cells.
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Olagaray, Katie E. "Bioactive nutrients for improved metabolic function of dairy cattle." Thesis, Kansas State University, 2017. http://hdl.handle.net/2097/35448.

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Master of Science
Department of Animal Sciences and Industry
Barry J. Bradford
Dairy cows undergo many homeorhetic adaptations during the transition to lactation. Although many of the physiological processes - including increased lipolysis and postpartum inflammation - are adaptive, exaggerated responses can contribute to metabolic disease and reduced milk production. L-carnitine has been shown to increase hepatic oxidation of fatty acids and reduce hepatic lipid accumulation in early lactation cows; however, L-carnitine is degraded in the rumen. An experiment using 4 ruminally-cannulated Holstein heifers in a split plot design demonstrated that the relative bioavailability of L-carnitine was greater when delivered abomasally than ruminally. There was a dose × route interaction and a route effect for increases in plasma carnitine above baseline, with increases above baseline being greater across all dose levels (1, 3, and 6 g L-carnitine/d) when infused abomasally compared to ruminally. A second experiment used 56 lactating Holstein cows in a randomized complete block design to evaluate 2 rumen-protected products (40COAT and 60COAT) compared to crystalline L-carnitine at doses targeting 3 and 6 g/d carnitine. Although crystalline and 40COAT were effective in linearly increasing carnitine concentrations, only subtle responses were seen for the 60COAT, which were less than that for crystalline carnitine in plasma, milk, and urine. Ineffectiveness of rumen-protected products to increase carnitine concentrations beyond crystalline may have been due to over-encapsulation that hindered liberation of the carnitine and its absorption in the small intestine. Although L-carnitine has the potential to reduce postpartum hepatic lipidosis, effective rumen protection of L-carnitine while maintaining intestinal availability needs further investigation. Plant polyphenols have anti-inflammatory properties and when administered during the transition period, have been shown to increase milk production. An experiment used 122 multiparous Holstein cows in a randomized block design to determine the effect of short term (5-d; SBE5) and long term (60-d; SBE60) administration of Scutellaria baicalensis extract (SBE)on whole-lactation milk yield, 120-d milk component yield, and early lactation milk markers of inflammation. Whole-lactation milk yield was increased for SBE60 compared to control, but was not different for SBE5 compared to control. Greater total pellet intake, milk lactose yield, and reduced SCC during wk 1-9 for SBE60 compared to control, all could have contributed to the observed sustained increase in milk yield. Milk production parameters were not different for SBE5 compared to control. No treatment effects were observed for BCS or milk markers of inflammation (haptoglobin) and metabolic function (β-hydroxybutyrate). Overall, long term administration of S. baicalensis effectively increased milk production, however the mechanism by which this was achieved is unknown. Although routes of administration to effectively achieve their physiological responses were different between L-carnitine (abomasal delivery) and SBE (feeding), both bioactive nutrients can improve the metabolic function of early lactation dairy cows.
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Dubé, Nadia Marie-Noël. "Protein tyrosine phosphatase 1B regulates metabolic, oncogenic, and hematopoietic function." Thesis, McGill University, 2004. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=85155.

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Protein tyrosine phosphatase 1B (PTP1B) is a ubiquitously expressed enzyme that is involved in multiple signaling pathways. Biochemical and substrate trapping studies have implicated PTP1B in the dephosphorylation of various tyrosine kinases, including the EGFR, PDGFR, IR, IGF-IR, JAK2, p210Bcr-Abl, and Src. Of particular interest, gene-targeting studies in mice have established PTP1B as a critical physiological regulator of metabolism by attenuating insulin and leptin signaling. Indeed, PTP1B null mice exhibit resistance to diet-induced diabetes and obesity. Although PTP1B is involved in signaling pathways that contribute to oncogenesis, PTP1B null mice do not develop spontaneous tumors. Therefore, my doctoral research focuses on identifying the physiological significance of PTP1B in these pathways. Our laboratory has previously demonstrated that PTP1B modulates leptin signaling via the tyrosine kinase JAK2. Accordingly, I have shown that PTP1B dephosphorylates JAK2 in a growth hormone (GH)-dependent manner, thus negatively regulating GH signaling and downstream effectors such as STAT3 and STAT5. Consequently, mice lacking PTP1B remain sensitive to GH action after starvation. In addition, I showed that the absence of PTP1B could improve glycemia during streptozotocin-induced type 1 diabetes. In the second part of my research, I have elucidated the mechanism for the previously reported decreased ERK activation in PTP1B null fibroblasts. I demonstrated that Ras activity is reduced in these cells, which is due to increased p120RasGAP expression and p62Dok hyperphosphorylation. Both of these molecules negatively regulate Ras activity by promoting the intrinsic GTPase activity of Ras, leading to decreased ERK activation. Finally, I developed a mouse model of cancer to study the role of PTP1B in tumorigenesis. Since the majority of cancers harbor mutations in p53, I generated p53/PTP1B double null mice. In the absence of p53, PTP1B heterozygous
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Sharma, Rakesh. "Cellular immune function and metabolic abnormalities in chronic heart failure." Thesis, Imperial College London, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.406373.

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Kohlhaas, Christine Frederike. "Metabolic regulation of human vascular endothelial cell function in vitro." Thesis, University of Glasgow, 2008. http://theses.gla.ac.uk/348/.

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The vascular endothelium contributes to the maintenance of vascular health by regulating vascular tone and leukocyte adhesion, amongst others. The vasoregulatory actions of the endothelium are mediated through coordinated release of vasodilators such as nitric oxide (NO) and prostacyclin, and vasoconstrictors such as endothelin-1 and thromboxane A2. Endothelial NO is the principal vasodilator in the vasculature and is produced by endothelial nitric oxide synthase (eNOS). Insulin is a vasoactive hormone that exerts its vasodilatory effects through eNOS-mediated NO production. Endothelial function is impaired in a number of disorders, including insulin resistance, diabetes and atherosclerosis, leading to dysregulated vasodilation as well as increased monocyte adhesion and plaque formation (atherosclerosis). The underlying molecular mechanisms leading to endothelial dysfunction are still in question. The work presented in this thesis addressed this question by investigating how insulin signalling and eNOS-mediated NO and superoxide production in human vascular endothelial cells are affected under experimental hyperinsulinaemia (chapter 3) and experimental hyperglycaemia (chapter 4). Atherogenic processes in human aortic endothelial cells (HAEC) were investigated by assessing monocyte adhesion under experimental hyperinsulinaemia (chapter 3), and by determining the contribution of NO and AMP-dependent kinase (AMPK) activity to the regulation of endothelial chemokine production (chapter 6). The potential of insulin to modify the subcellular distribution of eNOS was investigated in chapter 5. Clinical hyperinsulinaemia correlates with attenuated NO-mediated vasodilation, but it is not clear how hyperinsulinaemia impairs eNOS-mediated NO production. The present study modelled hyperinsulinaemia in HAEC and demonstrated a blunted response of hyperinsulinaemic cells to Ca2+-stimulated, but not insulin-stimulated eNOS-mediated NO synthesis. To address the underlying mechanisms responsible, the protein expression levels of components of the metabolic and mitogenic insulin signalling pathways, and of the metabolic energy sensor, AMPK, were quantified. Experimental hyperinsulinaemia slightly and non-significantly increased basal and insulin-stimulated eNOSS1177 phosphorylation in a time-dependent manner, and the levels of eNOST495 increased following acute insulin stimulation under these conditions. No marked dysregulation of individual insulin signalling pathway components was identified as a potential cause, but increased activating AMPKT172 phosphorylation was found to be a potential cause of increased unstimulated eNOSS1177 phosphorylation under experimental hyperinsulinaemia. Monocyte adhesion to hyperinsulinaemic HAEC did not differ from control HAEC, indicating that experimental hyperinsulinaemia did not act as a proatherogenic factor in the present study. Overt diabetes was simulated by experimental hyperglycaemia in human umbilical vein endothelial cells (HUVEC) and its effect on insulin-stimulated eNOS phosphorylation and endothelial superoxide production assessed. Insulin tended to stimulate phosphorylation of eNOSS615 and eNOSS1177, and decrease phosphorylation of eNOSS114, eNOST495 and eNOSS633 under control conditions. Experimental hyperglycaemia slightly reduced basal phosphorylation of Ser633 and significantly reduced insulin-stimulated phosphorylation of Ser114, but mildly increased basal Ser615 phosphorylation, indicating some dysregulation of eNOS phosphorylation. The upstream components of the metabolic insulin signalling pathway were not impaired in hyperglycaemic conditions. The subcellular localisation of eNOS is thought to have implications for its function. This study showed that eNOS localises to the plasma membrane, the nucleus, the cytoplasm and, primarily, the perinuclear area of HAEC. Insulin stimulation did not affect this distribution. Phospho-eNOS species were found primarily at the plasma membrane, and insulin may modulate the abundance of an intracellular eNOST495 species. Previous work in our laboratory on AMPK-mediated reduction of adhesion molecule expression has lead to the investigation of AMPK- and NO-mediated regulation of chemokine production in the present study. Inhibition of NO synthesis increased the production of monocyte chemoattractant protein (MCP)-1 in HAEC. AMPK activity downregulated TNFα-stimulated MCP-1 expression, and this was NO-dependent in the short-term, but may be NO-independent during prolonged AMPK activation. These data implicate NO and AMPK as antiatherogenic mediators in vascular endothelial cells in vitro. Taken together, the data in this thesis provide further insight into some of the molecular mechanisms involved in endothelial function and their response to hyperinsulinaemia, hyperglycaemia and proatherogenic stimulation.
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Arora, Teresa. "Sleep and its association with metabolic function across the lifespan." Thesis, University of Birmingham, 2012. http://etheses.bham.ac.uk//id/eprint/3343/.

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Obesity and accompanied metabolic dysfunction are global public health problems. A better understanding of factors contributing to obesity and metabolic disease development is needed, particularly lifestyle behaviours including sleep. Sleep duration has been suggested to be a contributor to obesity and metabolic dysfunction development. This thesis examines the relationships between sleep, obesity, and metabolic function in different age groups and ethnicities. The thesis also presents a model for experimental sleep manipulation that can be used to understand the underlying mechanisms for the associations among sleep duration, obesity, and metabolic dysfunction. The studies and findings were as follows: 1. Cross-sectional data from young South Asian children in Birmingham showed that ‘inadequate' sleep duration, unlike findings from different population studies, was not associated with overweight/obesity. 2. Cross-sectional data from a population of adolescents in the Midlands showed that short sleep duration was associated with increased odds of overweight/obesity. 3. Cross-sectional data from older Chinese from Guangzhou, China, showed that total long sleep duration was associated with increased odds of the metabolic syndrome. 4. Data from the experimental sleep model revealed that reducing sleep over a prolonged period is more achievable than sleep extension.
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Ferreira, Matias Maria. "Targeting the metabolic environment to modulate T cell effector function." Thesis, Montpellier, 2019. http://www.theses.fr/2019MONTT020.

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L’activation des cellules T est initiée suite à la rencontre avec un antigène spécifique. Les études réalisées pour mieux comprendre ce processus d’activation se sont principalement focalisées sur le rôle des cellules présentatrices d'antigènes et des cytokines. Toutefois, des données récentes soulignent également l'importance du microenvironnement métabolique pour soutenir l’augmentation des besoins énergétiques et biosynthétiques liés à la stimulation antigénique. Cette reprogrammation métabolique est conditionnée par la disponibilité en nutriments et la teneur en oxygène qui peuvent être altérés en conditions pathologiques, comme dans des tumeurs. En effet, plusieurs groupes dont le nôtre ont montré qu’en cas de faible disponibilité en nutriments, une compétition peut se créer entre les cellules tumorales et les cellules T, impactant de ce fait négativement leurs fonctions anti-tumorales. Cet effet est dû, du moins en partie, aux profils métaboliques distincts des sous-populations de cellules T; alors que les cellules T effectrices (dont les cellules Th1) sont fortement glycolytiques, les cellules T régulatrices suppressives (Treg) présentent un métabolisme plus mixte avec des niveaux accrus d'oxydation lipidique. Il est donc important de déterminer comment les changements métaboliques des cellules T anti-tumorales affectent leur persistance et leur fonctionnalité. Ainsi, j'ai entrepris des travaux afin d’évaluer si le niveau d’expression du transporteur de glucose Glut1 permettait d’identifier et de sélectionner des cellules T ayant des fonctions effectrices distinctes. Nous avons confirmé cette hypothèse et notamment montré que les cellules T exprimant un niveau élevé de Glut1 possèdent un potentiel de sécrétion d’IFNg accru.De plus, nos travaux montrent que la disponibilité en nutriments extracellulaires est un élément clé pour la différenciation terminale des cellules Th1. En effet, l'activation des cellules T CD4 naïves en conditions limitantes en glutamine induit leur différenciation en cellules Treg Foxp3+. Plus surprenant encore, cette carence induit un blocage de la différenciation Th1 même lors d’une polarisation vers ce lignage. De plus, en conditions de carence en glutamine, nous avons découvert que l'alpha-cétoglutarate (aKG), un métabolite dérivé de la glutamine, rétablit cette différenciation terminale Th1. J'ai ensuite évalué l'impact de l’aKG dans les processus de différenciation Th1/Treg en condition non limitante en glutamine. Mes données montrent que, dans des conditions de polarisation Th1, l’ajout d’aKG améliore la différenciation des cellules T CD4 naïfs en cellules Th1 et augmente la production d’IFNg. A l’inverse, l’ajout d’aKG s’accompagne d’une diminution des cellules Foxp3+ et d’une augmentation de la sécrétion de cytokines inflammatoires dans des conditions de polarisation Treg. L'altération de la différenciation des cellules T médiée par l'aKG est notamment associée à une phosphorylation oxydative (OXPHOS) accrue ; ainsi, l'ajout d’un inhibiteur du cycle de Krebs et du complexe mitochondrial II /succinate déshydrogénase, atténue le blocage de la différenciation Treg induit par l'aKG. De façon remarquable, ces modifications de l'équilibre Th1/Treg médiées par l'aKG sont maintenues in vivo et impactent le devenir de cellules T exprimant un récepteur chimérique anti-tumoral (CAR) injectées chez des souris porteuses de tumeurs. En résumé, nos données montrent qu'une faible teneur en aKG intracellulaire liée à une disponibilité limitée en glutamine, favorise un phénotype Treg, alors que des niveaux élevés d’aKG modifient l'équilibre vers un phénotype Th1.En conclusion, les données générées au cours de ma thèse devraient permettre le développement de stratégies permettant de sélectionner des cellules T ayant des propriétés effectrices anti-tumorales améliorées
T 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
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Foglesong, Grant. "Lifestyle Improvements Enhance Metabolic Function and Mitigate Breast Cancer Progression." The Ohio State University, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=osu1490266217799202.

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Pathare, Neeti C. "Metabolic adaptations following disuse and their impact on skeletal muscle function." [Gainesville, Fla.] : University of Florida, 2005. http://purl.fcla.edu/fcla/etd/UFE0010024.

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Thesis (Ph.D.)--University of Florida, 2005.
Typescript. Title from title page of source document. Document formatted into pages; contains 171 pages. Includes Vita. Includes bibliographical references.
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Books on the topic "Metabolic function"

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name, No. Metabolic profiling: Its role in biomarker discovery and gene function analysis. Boston, MA: Kluwer Academic, 2003.

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Harrigan, George G., and Royston Goodacre, eds. Metabolic Profiling: Its Role in Biomarker Discovery and Gene Function Analysis. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4615-0333-0.

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Brown, A. M. Metabolic substrates other than glucose support axon function in central white mater. New York, N.Y: Wiley-Liss, Inc., 2001.

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Canada. Dept. of Fisheries and Oceans. Physical and Chemical Sciences Branch. Protocols for measuring mixed function oxygenases of fish liver. Mont-Joli, Qué: Physical and Chemical Sciences Branch, Dept. of Fisheries and Oceans, 1991.

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Bronner, Felix, Mary C. Farach-Carson, and Helmtrud I. Roach, eds. Bone-Metabolic Functions and Modulators. London: Springer London, 2012. http://dx.doi.org/10.1007/978-1-4471-2745-1.

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Dhalla, Naranjan S., Grant N. Pierce, and Robert E. Beamish, eds. Heart Function and Metabolism. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4613-2053-1.

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Yazaki, Yoshio, and Seibu Mochizuki, eds. Cellular Function and Metabolism. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-3078-7.

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Storey, Kenneth B., ed. Functional Metabolism. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2004. http://dx.doi.org/10.1002/047167558x.

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Moss, Joel, and Peter Zahradka, eds. ADP-Ribosylation: Metabolic Effects and Regulatory Functions. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2614-8.

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Workshop Conference Hoechst-Werk Albert (1987 Frankfurt, Germany). Muscle ischaemia: Functional and metabolic aspects. Edited by Hudlicka O and Okyayuz-Baklouti I. München: C. Wolf, 1988.

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Book chapters on the topic "Metabolic function"

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Zschocke, Johannes. "Function Tests." In Inherited Metabolic Diseases, 339–55. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-74723-9_34.

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Zschocke, Johannes, and Stefan Kölker. "Function Tests." In Inherited Metabolic Diseases, 505–20. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-662-49410-3_41.

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Jungermann, Kurt. "Metabolic Zonation of Carbohydrate Metabolism in the Liver." In Integration of Mitochondrial Function, 561–79. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4899-2551-0_55.

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Mather, Kieren J., Alain Baron, and Michael J. Quon. "Insulin Action and Endothelial Function." In The Metabolic Syndrome, 107–35. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-60327-116-5_7.

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Touati, Guy, Jan Huber, and Jean-Marie Saudubray. "Diagnostic Procedures: Function Tests and Postmortem Protocol." In Inborn Metabolic Diseases, 59–69. Berlin, Heidelberg: Springer Berlin Heidelberg, 2006. http://dx.doi.org/10.1007/978-3-540-28785-8_3.

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Fernandes, J., and J. M. Saudubray. "Diagnostic Procedures: Function Tests and Postmortem Protocol." In Inborn Metabolic Diseases, 41–46. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-662-03147-6_2.

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Fernandes, J., J. M. Saudubray, and J. Huber. "Diagnostic Procedures: Function Tests and Postmortem Protocol." In Inborn Metabolic Diseases, 43–51. Berlin, Heidelberg: Springer Berlin Heidelberg, 2000. http://dx.doi.org/10.1007/978-3-662-04285-4_2.

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Harvey, Jenni. "Leptin and Cognitive Function." In Metabolic Syndrome and Neurological Disorders, 485–500. Chichester, UK: John Wiley & Sons Ltd, 2013. http://dx.doi.org/10.1002/9781118395318.ch30.

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Fischer, R., J. Drossard, S. Schillberg, O. Artsaenko, N. Emans, and J. M. Naehring. "Modulation of Plant Function and Plant Pathogens by Antibody Expression." In Metabolic Engineering of Plant Secondary Metabolism, 87–109. Dordrecht: Springer Netherlands, 2000. http://dx.doi.org/10.1007/978-94-015-9423-3_5.

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Chen, Xinpu, and Sridevi Devaraj. "Endothelial function and metabolic syndrome." In International Textbook of Diabetes Mellitus, 1046–50. Chichester, UK: John Wiley & Sons, Ltd, 2015. http://dx.doi.org/10.1002/9781118387658.ch71.

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Conference papers on the topic "Metabolic function"

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Long, Haixia, Shulei Wu, and Haiyan Fu. "Improving Metabolic Flux Estimation of Metabolic Networks by QPSO with Penalty Function." In 2014 Tenth International Conference on Computational Intelligence and Security (CIS). IEEE, 2014. http://dx.doi.org/10.1109/cis.2014.49.

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Robert, Martin, Douglas Murray, Masayuki Honma, Kenji Nakahigashi, Tomoyoshi Soga, and Masaru Tomita. "Extracellular metabolite dynamics and temporal organization of metabolic function in E. coli." In 2012 ICME International Conference on Complex Medical Engineering (CME). IEEE, 2012. http://dx.doi.org/10.1109/iccme.2012.6275650.

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Mycek, M. A., W. Zhong, and P. Urayama. "Investigating cellular metabolic function using fluorescence lifetime imaging microscopy." In Biomedical Topical Meeting. Washington, D.C.: OSA, 2004. http://dx.doi.org/10.1364/bio.2004.fh8.

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Liotino, Vito, Maria Rosaria Vulpi, Anna Castrovilli, Cosimo Tortorella, Giuseppina Piazzolla, Mafalda Candigliota, and Onofrio Resta. "Metabolic Syndrome negatively affects pulmonary function in COPD patients." In ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.pa3620.

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Wielscher, Matthias, Cosetta Minelli, Andre Amaral, Juha Auwinen, Sylvain Sebert, Debbie Jarvis, and Marjo-Riitta Jarvelin. "Cardio metabolic traits and lung function: A Mendelian Randomization study." In ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.pa1277.

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Georgakoudi, Irene, Dimitra Pouli, Zhiyi Liu, Yang Zhang, and Christopher Polleys. "Multiparametric, label-free two-photon imaging of metabolic function (Conference Presentation)." In Unconventional Optical Imaging II, edited by Corinne Fournier, Marc P. Georges, and Gabriel Popescu. SPIE, 2020. http://dx.doi.org/10.1117/12.2566323.

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Kohno, Susumu, Shunsuke Kitajima, Nobunari Sasaki, Hayato Muranaka, and Chiaki Takahashi. "Abstract LB-130: The metabolic function of RB tumor suppressor gene." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-lb-130.

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Meslem, Nacim, and Vincent Fromion. "Lyapunov function for irreversible linear metabolic pathways with allosteric and genetic regulation." In 2011 50th IEEE Conference on Decision and Control and European Control Conference (CDC-ECC 2011). IEEE, 2011. http://dx.doi.org/10.1109/cdc.2011.6160805.

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Qinghua Zhou, Dan Wang, and Momiao Xiong. "Dynamic flux balance analysis of metabolic networks using the penalty function methods." In 2007 IEEE International Conference on Systems, Man and Cybernetics. IEEE, 2007. http://dx.doi.org/10.1109/icsmc.2007.4413786.

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Zhang, Ji, Natalya Pavlova, Richard White, and Craig Thompson. "Abstract 2670: Non-metabolic function of asparagine in regulating global protein translation." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-2670.

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Reports on the topic "Metabolic function"

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House, Geoffrey Lehman. Identifying bacterial signals and metabolic functions in fungal genomes. Office of Scientific and Technical Information (OSTI), November 2018. http://dx.doi.org/10.2172/1483486.

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Arp, Daniel, and Luis Sayavedra-Soto. Metabolomic Functional Analysis of Bacterial Genomes: Final Report. Office of Scientific and Technical Information (OSTI), January 2008. http://dx.doi.org/10.2172/951563.

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Edwards, Jeremy, S. Metabolic engineering of deinococcus radiodurans based on computational analysis and functional genomics. Office of Scientific and Technical Information (OSTI), February 2005. http://dx.doi.org/10.2172/836597.

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Harwood, Caroline S. Integrating large-scale functional genomics data to dissect metabolic networks for hydrogen production. Office of Scientific and Technical Information (OSTI), December 2012. http://dx.doi.org/10.2172/1057459.

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Hofmockel, Kirsten. Microbial drivers of global change at the aggregate scale: linking genomic function to carbon metabolism and warming. Office of Scientific and Technical Information (OSTI), June 2019. http://dx.doi.org/10.2172/1524429.

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Yang, Jia-ming, Yun Luo, Jia-hong Zhang, Qin-qin Liu, Qiang Zhu, Hua Ye, Yan-long Niu, et al. Effects of WB-EMS and Protein Supplementation on Body Composition, Physical Function, Metabolism and Inflammatory Biomarkers in Middle-Aged and Elderly Patients with Sarcopenic Obesity: A Meta-Analysis of Randomized Controlled Trials. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, September 2021. http://dx.doi.org/10.37766/inplasy2021.9.0096.

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