Tesi sul tema "Secretion stress"
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Smart, Darren. "Stressors & LH secretion in the ewe". Thesis, University of Liverpool, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.333607.
Parker, Victoria Joanne. "Hypothalamic mechanisms mediating inhibition of prolactin secretion following stress in early pregnant mice". Thesis, University of Edinburgh, 2012. http://hdl.handle.net/1842/6485.
Kim, Beob Gyun. "INFLUENCES OF CHROMIUM (III) PICOLINATE ON PIGS UNDER THERMAL, IMMUNE OR DIETARY STRESS, AND ON ADRENAL STEROID SECRETION". UKnowledge, 2007. http://uknowledge.uky.edu/gradschool_diss/560.
Kosti, Ourania. "Intra-adrenal mechanisms in the control of steroid secretion and the response to stress". Thesis, Queen Mary, University of London, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.411344.
Weber, Barbara. "Stress response and virulence in Vibrio anguillarum". Doctoral thesis, Umeå : Institutionen för molekylärbiologi (Teknisk-naturvetenskaplig fakultet), Umeå universitet, 2010. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-33269.
Marin, Marie-France. "Immediate and delayed effects of stress on a reactivitated declarative long-term memory trace". Thesis, McGill University, 2009. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=116034.
Pilgrim, Kamala. "Mechanisms underlying cortisol reactivity to stress in low and high socioeconomic status individuals : role of naturally-occurring attentional biases". Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=116040.
Valiquette, Luc François. "Association between self-reported childhood maltreatment and cortisol profiles in psychotic patients". Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=112314.
Alharake, Jawad. "Study of genetic factors involved in enzyme secretion in hyperproductive strains of Trichoderma reesei". Electronic Thesis or Diss., université Paris-Saclay, 2023. http://www.theses.fr/2023UPASB061.
Fossil fuels are a major contributor to global warming, and their non-renewable nature is an impediment for building sustainable societies. In this context, second generation biofuels represent an attractive and more environmentally friendly alternative. The process of second-generation biofuel production consists of several steps including a physicochemical pretreatment of lignocellulosic (non-edible) biomass, the enzymatic hydrolysis of cellulose into glucose and the fermentation of simple sugars into biofuels, such as bioethanol. One of the main bottlenecks for a large implementation of this process is, however, the relatively high cost of hydrolytic enzymes, namely cellulases, used to deconstruct the pretreated lignocellulosic biomass into fermentable sugars.The filamentous fungus Trichoderma reesei is the preferred choice for industrial production of cellulases since it has hyperproduction and hypersecretion capacities. Industrial strains of T. reesei can secrete up to 100 g/L of cellulases in controlled industrial fermenters. In particular, the mutant strain Rut- C30 is a reference hyperproducer strain, but our incomplete understanding of its enhanced secretion system complicates further improvement of its hypersecretion capacity by genetic engineering. Therefore, this work aimed at unravelling the regulatory pathways controlling secretion and the secretion stress response in order to identify bottlenecks and to develop new strains with enhanced secretion capacity in the future.To this end, transcriptomic data were generated from cultivations of T. reesei Rut-C30 in different secretion stress conditions which allowed to identify potential components of secretion regulation that were targeted for deletion. As a complementary approach, mining of transcriptomic data obtained with other filamentous fungi in secretion stress conditions revealed further target genes potentially involved in the regulation of the secretion pathway. Finally, nine genes were deleted in the Rut-C30 strain, and the resulting strains phenotypically characterized. All of them displayed reduced growth and showed altered protein secretion behavior. RNA sequencing was performed on ∆res2, ∆rpn4 and ∆snd1 mutant strains and compared to that of Rut-C30 in the same culture conditions. Neither of the three transcription factors impacts transcription of genes involved in secretion or the secretion stress response in our conditions. However, in all three mutants, genes encoding enzymes of lipid metabolism are differentially expressed which could affect secretion in an indirect way. The results represent first clues to alleviate bottlenecks in secretion in T. reesei Rut-C30 and pave the way to develop strains with still improved secretion capacity
Solà, Tapias Núria. "The involvement of the three main inflammatory bowel disease pathways and the secretion of trypsin proteolytic activity on intestinal epithelial cells". Thesis, Toulouse 3, 2018. http://www.theses.fr/2018TOU30049/document.
Crohn's disease (CD) and Ulcerative colitis (UC) are two forms of Inflammatory Bowel Disease (IBD), a chronic inflammatory pathology affecting the digestive tract. Patients suffer from relapsing flares, diarrhea, abdominal pain and bleeding. Although the molecular mechanisms of IBD are poorly understood, recent data suggest that IBD occurs in genetically predisposed individuals developing an abnormal immune response to intestinal microbes after, being exposed to specific environmental triggers. Genetic studies have reported more than 170 polymorphisms susceptible to be involved in IBD pathogenesis. The strongest associations have highlighted three main pathways altered in IBD including bacterial sensing (NOD2, CD), autophagy (ATG16L1 and IRGM, CD) and endoplasmic reticulum stress (ER-Stress) (XBP1, UC). The role of intestinal barrier function is also strongly implicated in IBD pathogenesis, and is modulated by factors present in the lumen derived from microbiota, food or at a molecular level, by factors such as proteases. In IBD pathophysiology, the inflammatory process is characterized by impaired intestinal biology including disruption of tight junctions and leaky gut, decreased amount of Paneth and Goblet cells, and translocation of luminal antigens triggering inflammation. Previous studies have demonstrated an increased level of active serine proteases in the stools and tissues of IBD patients, supposing that proteases originate from infiltrated immune cells, pancreatic secretion or microbiota. However, our team has reported that intestinal epithelial cells are a major source of serine proteases, in particular trypsin-like enzymes, are released by a stressed epithelium in pathogenic context such as irritable bowel syndrome. In this project, we aimed at better understanding whether the three main pathways involved in IBD (Nod2, autophagy, ER-stress) could be linked to an epithelial release of trypsin and reciprocally, if epithelial trypsin is able to induce or modulate these three IBD pathways. We confirmed that trypsin-like activity was significantly higher in biopsies from UC and CD patients compared to healthy controls. In Caco-2 monolayers cultured in transwells, secreted trypsin-like proteolytic activity remained stable upon NOD2 stimulation but decreased under autophagy induction. Thapsigargin (Tg) stimulation a well-known ER-stress inducer, enhanced the apical release of trypsin-like activity in Caco2 cells. [...]
Hickman, Cristina Fontes Lindemann. "Environmental factors affecting interferon-τ expression and secretion by in vitro produced bovine blastocysts". Thesis, University of Edinburgh, 2010. http://hdl.handle.net/1842/4399.
Zimmermann, Ulrich, Konstanze Spring, Hans-Ulrich Wittchen, Hubertus Himmerich, R. Landgraf, Manfred Uhr e Florian Holsboer. "Arginine vasopressin and adrenocorticotropin secretion in response to psychosocial stress is attenuated by ethanol in sons of alcohol-dependent fathers". Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2013. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-110031.
Gallo, Marco. "misc-1/OGC is a new stress response gene and regulator of apoptosis, germline stem cell proliferation and insulin secretion". Thesis, University of British Columbia, 2010. http://hdl.handle.net/2429/27092.
Zimmermann, Ulrich, Konstanze Spring, Hans-Ulrich Wittchen, Hubertus Himmerich, R. Landgraf, Manfred Uhr e Florian Holsboer. "Arginine vasopressin and adrenocorticotropin secretion in response to psychosocial stress is attenuated by ethanol in sons of alcohol-dependent fathers". Technische Universität Dresden, 2004. https://tud.qucosa.de/id/qucosa%3A26808.
Hammer, Jared Louis. "Changes In Threonyl-Trna Synthetase Expression And Secretion In Response To Endoplasmic Reticulum Stress By Monensin In Ovarian Cancer Cells". ScholarWorks @ UVM, 2017. http://scholarworks.uvm.edu/graddis/764.
Madec, Iltud. "Effets du sémiochimique MHUSA (Mother Hens' Uropygial Secretion Analogue) sur le stress des poulets de chair : approches zootechnique, physiologique et comportementale". Phd thesis, Toulouse, INPT, 2008. http://oatao.univ-toulouse.fr/7819/1/madec.pdf.
Gumpper, Kristyn Nicole. "Maintaining Cardiac and Gastric Physiology: TRIM Proteins as Central Factors in Regulation of Organ Homeostasis at the Cellular Level". The Ohio State University, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=osu1563287863754715.
Sá, Maria Joana Giraldes Pereira Côrte-Real Corrêa de. "Natural IgM secretion in health and disease : genetic control and role in type 1 diabetes". Doctoral thesis, Universidade Técnica de Lisboa. Faculdade de Medicina Veterinária, 2012. http://hdl.handle.net/10400.5/4232.
Germline-encoded autoreactive natural antibodies (NAbs) of the IgM isotype are secreted and circulate as a result of basal immune system stimulation, and constitute an important first line of defense against microorganism invasion, bridging the innate and the adaptive immune responses. NAbs are mostly secreted by positively selected B1a cells, and have been claimed to have a protective role against autoimmunity. Nevertheless, NAbs binding to cell surface self-antigens could have implications in the initiation of autoimmunity. Article I focused on the genetic control of NAbs secretion in healthy mice. Importantly, interferon regulatory factor 4 (Irf4), a transcription factor required for plasma cell differentiation and antibody secretion, was identified as the most probable candidate for the control of homeostatic serum IgM levels in the mouse. Type 1 diabetes (T1D) is a complex autoimmune disease that develops spontaneously in humans and is pathogenically similar in the non-obese-diabetic (NOD) mouse model. B cells are necessary in the NOD diabetogenic process, and the presence of anti-pancreatic beta cell antibodies is the earliest manifestation of T1D. Article II revealed that NOD peritoneal cavity B1a cells are more prone to spontaneously secrete NAbs that recognize pancreatic beta cell autoantigens, which could promote T1D either by enhancing professional antigen presentation of islet antigens, by activating the complement cascade or by directly promoting beta cell damage and self-antigens release. The studies reported in article III have explored these possibilities and have proven that NAbs of NOD B1a cells origin could bind and directly induce oxidative stress on pancreatic beta cells. Moreover, these studies have shown that NOD B1a cells have a lower threshold for innate-like stimulation and have established a link between NOD B1a cells properties, NAbs specificities and impact of IgM binding on beta cells physiology. Finally, article IV provides evidence that early treatment with antibodies that evoke NOD B1a cells proliferation and differentiation into IgM secreting cells correlates with T1D precipitation. In conclusion, this thesis has shown that Irf4 is a critical player in the genetic network that controls IgM secretion in healthy individuals, and that in the NOD mouse model of T1D, a lower threshold for innate like stimulation of peritoneal cavity B1a cells contributes to a naturally increased state of B1a cells activation and autoreactive IgM secretion, determining the initiation and/or contributing to the fueling of beta cells autoimmunity.
RESUMO Secreção de IgM natural na saúde e na doença: controlo genético e papel na diabetes tipo 1 - Os autoanticorpos naturais (NAbs) da classe IgM existem no organismo na ausência de imunização e constituem uma primeira linha de defesa fundamental contra infecções. Os NAbs são secretados maioritariamente por células B1a e a sua ligação a autoantigénios na superfície celular pode ter implicações para a iniciação de autoimunidade. O trabalho descrito no artigo I focou-se na compreensão do controlo genético da secreção de NAbs em murganhos saudáveis. Este estudo identificou o interferon regulatory factor 4 (Irf4), um factor de transcrição necessário para a diferenciação de plasmócitos e secreção de anticorpos, como o candidato mais provável para o controlo da homeostasia dos níveis de IgM circulante no murganho. A diabetes tipo 1 (T1D) é uma doença autoimune complexa que se desenvolve espontaneamente nos humanos e que tem uma patogenia semelhante no murganho NOD (non-obese-diabetic). Os linfócitos B são necessários para o processo diabético do NOD, em que a presença de anticorpos anti-células beta pancreáticas é uma das manifestações mais precoces. O artigo II revelou que as células B1a da cavidade peritoneal do NOD têm uma elevada predisposição para secretarem NAbs que reconhecem autoantigénios de células beta pancreáticas e que podem promover o desenvolvimento de T1D quer pelo aumento da apresentação de autoantigénios, quer pela activação da cascata do sistema de complemento, quer pela indução directa de danos nas células beta pancreáticas. A investigação descrita no artigo III provou que os NAbs secretados por células B1a do NOD têm a capacidade de se ligarem e induzirem stress oxidativo nas células beta do pâncreas. Estes estudos revelaram ainda que as células B1a do NOD têm um limiar reduzido para activação inata e estabeleceram uma relação entre as propriedades das células B1a do NOD, as especificidades dos NAbs e o impacto da ligação de IgM na fisiologia das células beta. Finalmente, o artigo IV evidenciou que a indução de proliferação e diferenciação das células B1a em células secretoras de IgM contribui para o início da T1D. Esta tese demonstrou que o Irf4 é um factor de transcrição com um papel fundamental no controlo da secreção de IgM em animais saudáveis e que, no murganho NOD, as células B1a da cavidade peritoneal têm um menor limiar para estimulação inata, que contribui para o seu estado de activação e para a secreção de IgM autoreactiva, determinando a iniciação e/ou contribuindo para a progressão da diabetes tipo 1.
Fundação para a Ciência e Tecnologia; Instituto Gulbenkian da Ciência
Patrick-Melin, Amy J. "Effect of 7 Days Aerobic Exercise on Insulin Sensitivity, Oxidative Stress, TLR2/TLR4 Cell Surface Expression and Cytokine Secretion in Sedentary Obese Adults". Kent State University / OhioLINK, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=kent1310918543.
Roma, Leticia Prates. "Mecanismos moleculares do efeito citotoxico da dexametasona em linhagens de celulas beta e ilhotas pancreaticas". [s.n.], 2009. http://repositorio.unicamp.br/jspui/handle/REPOSIP/314413.
Tese (doutorado) - Universidade Estadual de Campinas, Instituto de Biologia
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Resumo:Introdução/Objetivos. A produção de espécies reativas de oxigênio (EROs) faz parte de diversos processos fisiológicos. Nos últimos anos, o aumento de EROs têm sido associado ao desenvolvimento de diversas doenças, dentre elas o Diabetes Mellitus Tipo 2. As células beta pancreáticas são notadamente mais suscetíveis ao estresse oxidativo devido a sua baixa capacidade antioxidativa, resultado da menor expressão e atividade de enzimas antioxidantes como superóxido dismutase e peroxidases. A dexametasona, um glicocorticóide sintético, tem efeitos diabetogênicos e citotóxicos em células produtoras de insulina e ilhotas pancreáticas. Entretanto, os mecanismos pelos quais a dexametasona atua sobre as células-alvo não estão bem esclarecidos. Dessa forma, nosso objetivo foi analisar se a dexametasona induz estresse oxidativo em células produtoras de insulina RINm5F e ilhotas pancreáticas. Utilizamos três modelos: 1) células RINm5F controle, que são extremamente sensíveis ao estresse oxidativo; 2) células RINm5F superexpressando a enzima catalase (RINm5F.Cat), que são resistente ao estresse oxidativo e 3) ilhotas de ratos adultos cultivadas por 72 h com dexametasona (Dexa) e ilhotas tratadas concomitantemente com dexametasona e o antioxidante N-acetilcisteína (Dexa+NAC). Resultados: Aumento na produção de EROs foi observado em células RINm5F tratadas com dexametasona. O tratamento com dexametasona aumentou a atividade/clivagem da caspase-3 e apoptose em células RINm5F após 3 dias de cultura. Expressão protéica e atividade de Cu/ZnSOD estava aumentada após o tratamento com dexametasona, enquanto que a expressão/atividade de MnSOD não foi modulada pelo corticóide. A superexpressão da catalase em linhagens de célula beta previniu todos os efeitos citotóxicos da dexametasona, inclusive a morte celular. Elevados níveis de Cu/ZnSOD podem favorecer o aumento na geração de EROs e conseqüentemente, apoptose. Da mesma forma, ilhotas tratadas com dexametasona apresentaramaumento na produção de EROs, efeito que foi revertido quando as ilhotas foram tratadas concomitantemente com dexametasona e NAC. Redução na secreção de insulina estimulada por glicose foi observada em ilhotas cultivadas com dexametasona. O tratamento com dexametasona e NAC restaurou a secreção de insulina a níveis próximos aos controles. Uma menor produção deNAD(P)H no grupo Dexa foi observado, sendo que o grupo Dexa+NAC mostrou níveis semelhantes ao grupo controle. Não ocorreram diferenças nas concentrações intracelulares de cálcio estimulado por glicose em nenhum dos grupos. A dexametasona reduziu a expressão gênica da sinaptotagmina VII, enquanto no grupo Dexa+NAC houve um aumento da expressão desse gene em ilhotas pancreáticas. Interessantemente, o tratamento com NAC diminuiu a expressão gênica da Cu/ZnSOD. Conclusões: Nossos resultados indicam que as ações da dexametasona em células produtoras de insulina e ilhotas pancreáticas são mediadas através do aumento do estresse oxidativo, sendo a Cu/ZnSOD importante nesse processo. A superexpressão da catalase e o uso do antioxidante n-acetilcisteína previnem contra os efeitos citotóxicos do glicocorticóide.
Abstract: Introduction/Aims: Reactive oxygen species (ROS) play a dual role on living organisms, being involved in many physiological processes and also being linked to the development of several pathologies, including the type 2 diabetes mellitus. Pancreatic beta cells are very sensitive to oxidative stress because of their low antioxidant capacity, wich results from their low expression and activity of antioxidant enzymes, especially peroxidases. Dexamethasone is a synthetic diabetogenic glucocorticoid that induces cytotoxic effects on pancreatic beta cells. However, the precise mechanisms of dexamethasone toxicity on target cells are not fully understood. The aim of the present study was to analyzed whether dexamethasone induces oxidative stress in insulinproducing cells and pancreatic islets. Experimental design: The experiments were performed using 3 models: 1) RINm5F control cells, extremely sensitive to oxidative stress; 2) RINm5F cells overexpressing the enzyme catalase (RINm5F.Cat), very resistant to oxidative stress and 3) rat pancreatic islets cultured for 72 h with dexamethasone (Dexa) or cultured concomitantly with dexamethasone and the antioxidant N-acetylcysteine (Dexa+NAC). Results: An increased generation of reative oxygen species (ROS) was observed in dexamethasone-treated insulinproducing cells together with an increase in caspase-3 activity and apoptosis rate. Interestingly, exposure to dexamethasone increased the cytosolic superoxide dismutase Cu/ZnSOD protein expression and activity, while the mitochondrial MnSOD isoform was not affected by the glucocorticoid. Overexpression of catalase in insulin-producing cells prevented all the cytotoxic effects of dexamethasone. Pancreatic islets cultured in the presence of dexamethasone (Dexa) for 72 h showed increased ROS production. Glucose-stimulated insulin secretion was decreased after Dexa treatment. Intracellular ROS levels were decreased and the insulin secretion capacitywas recovered by concomitant treatment with Dexa+NAC. The total insulin content and intracellular Ca+2 levels were not modulated in either Dexa or Dexa+NAC groups. There was a decrease in the NAD(P)H production rate, used as an indicator of viability, after dexamethasone treatment. Concomitant incubation with NAC returned viability to control levels. Dexamethasone also decreased SYT VII gene expression; in contrast, the Dexa+NAC group showed increased expression of SYT VII compared to controls. Surprisingly, treatment with NAC decreased the gene expression of the antioxidant enzyme, Cu/ZnSOD. Conclusions: The cytotoxic effects of dexamethasone in RINm5F insulin-producing cells and pancreatic islets are primarily ROS-mediated. High levels of expression and activity of the Cu/ZnSOD might favour the generation of ROS. The overexpression of catalase and the use of the antioxidant Nacetylcysteine counteract the cytotoxic effects of dexamethasone.
Doutorado
Fisiologia
Doutor em Biologia Funcional e Molecular
Alvarenga, Santos Buiate Ester. "ESTABLISHMENT OF BIOTROPHY BY THE MAIZE ANTHRACNOSE PATHOGEN COLLETOTRICHUM GRAMINICOLA: USE OF BIOINFORMATICS AND TRANSCRIPTOMICS TO ADDRESS THE POTENTIAL ROLES OF SECRETION, STRESS RESPONSE, AND SECRETED PROTEINS". UKnowledge, 2015. http://uknowledge.uky.edu/plantpath_etds/17.
Stewart, Benjamin J. "Characterization of the effects of the lipid peroxidation products 4-hydroxynonenal and 4-oxononenal on hepatic lipid accumulation, VLDL assembly, secretion, and microtubules : relevance to alcoholic liver disease /". Connect to full text via ProQuest. Limited to UCD Anschutz Medical Campus, 2008.
Typescript. Includes bibliographical references (leaves 111-122). Free to UCD affiliates. Online version available via ProQuest Digital Dissertations;
Botermans, Jos A. M. "Feeding environment for growing-finishing pigs : effects of competition for feed and feeding frequency on performance, behaviour, injuries, plasma cortisol and exocrine pancreatic secretion /". Alnarp : Swedish Univ. of Agricultural Sciences (Sveriges lantbruksuniv.), 1999. http://epsilon.slu.se/avh/1999/91-576-5744-0.pdf.
Khalili-Mahani, Najmeh 1971. "Observing the stressed brain : magnetic resonance imaging of the neural correlates of hypothalamic pituitary adrenal axis function". Thesis, McGill University, 2009. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=115857.
Schulz, Simone [Verfasser], e Reinhold [Akademischer Betreuer] Läßle. "Validity and Maintenance of Binge Eating Disorder. Laboratory and naturalistic studies on the role of negative affect, stress-induced eating and cortisol secretion in obese women with BED / Simone Schulz ; Betreuer: Reinhold Läßle". Trier : Universität Trier, 2014. http://d-nb.info/119780692X/34.
Kuehn, Carina Brigitte. "Développement et études comparatives de méthodes pour améliorer la survie et les fonctions de cellules productrices d'insuline et d'îlots pancréatiques endocriniens porcins en conditions de culture in vitro et de stress apoptotiques". Thèse, Université de Sherbrooke, 2014. http://hdl.handle.net/11143/5411.
Cerrato, Giulia. "Oleate : An Atypical Cellular Stress Inducer That Stalls Protein Secretion Oleate-Induced Aggregation of LC3 at the Trans-Golgi Network Is Linked to a Protein Trafficking Blockade A Genome-Wide RNA Interference Screen Disentangles the Golgi Tropism of LC3 Live Cell Imaging of LC3 Dynamics". Thesis, université Paris-Saclay, 2021. http://www.theses.fr/2021UPASL023.
Distinct classes of fatty acids (FAs) (saturated or cis-/trans-unsaturated carbon chains) impact on cellular and organismal physiology in a different manner. Interestingly, these diverse categories have a profound (but different) effect on autophagy, the conserved intracellular degradation mechanism that maintains energy homeostasis and protects cells against stress. Oleate, the most abundant endogenous and dietary cis-unsaturated FA, has the atypical property to induce the redistribution of the LC3 protein (peculiar sign of autophagy) in a non-canonical fashion and preferentially to the Golgi apparatus. Intrigued by these observations, which might be related to the health-improving effects of cis-unsaturated FAs (and the notorious toxicity of trans-unsaturated and saturated FAs), we decided to explore the mechanisms causing the oleate-induced relocation of LC3 to the Golgi apparatus. To achieve this goal, a robotized RNA interference genome-wide screen led to the identification of multiple genes involved in the Golgi-related protein transport, as well as in the integrated stress response. Follow-up experiments revealed that oleate affected the subcellular morphology of the Golgi apparatus, correlating with a blockade of conventional (Golgi-dependent) protein secretion that caused secretory cargo to be stalled at the level of the trans-Golgi network. The inhibition of protein secretion was observed using several experimental systems, both in vitro and in vivo. Moreover, a systematic screen searching for other chemical entities that mimic the oleate-induced cellular effects led to the identification of several compounds belonging to rather different pharmacological classes. These “oleate mimetics” also shared with oleate the capacity to block conventional protein secretion, supporting the notion that this pathway of Golgi perturbation is indeed of pharmacological relevance. In conclusion, this research work shows that oleate represents a class of molecules that act on the Golgi apparatus to cause the recruitment of LC3 and to stall protein secretion
Nyblom, Hanna K. "Glucotoxicity in Insulin-Producing β-Cells". Doctoral thesis, Uppsala University, Department of Medical Cell Biology, 2007. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-8309.
Background and aims: Type 2 diabetes mellitus is connected with elevated glucose levels, which cause impaired glucose-stimulated insulin secretion (GSIS) and degeneration of β-cells. Mechanisms for such glucotoxic effects were explored in the present study.
Materials and methods: INS-1E cells were cultured for 5 days in 5.5, 11, 20 or 27 mM glucose in the presence or absence of AMPK-agonist AICAR. GSIS was determined from INS-1E cells and islets obtained from type 2 diabetes and control donors. Human islets and INS-1E cells were functionally characterized (GSIS) and protein profiled (SELDI-TOF MS). Glucose-induced de novo synthesis of fatty acyls (HR-MAS NMR spectroscopy), fatty acid composition (GC-MS), triglyceride content and specific proteins (Western blotting) were determined in INS-1E cells.
Results: Impaired GSIS was observed from INS-1E cells exposed to chronic hyperglycaemia and islets isolated from type 2 diabetics compared to INS-1E cells cultured at normal glucose levels and control islets, respectively. Several glucose-regulated proteins were found when type 2 diabetes and control islets or mitochondria from INS-1E cells cultured at different glucose concentrations were protein profiled. Glucose induced lipid de novo synthesis of both saturated and unsaturated fatty acids in specific proportions. Glucose-induced impairment of function and mass was reverted by inclusion of AICAR, which lowered levels of pro-apoptotic protein CHOP but left triglyceride content unaffected.
Conclusions: Impaired GSIS and increased apoptosis observed in β-cells after prolonged exposure to elevated glucose concentrations involved accumulation of lipid species in specific proportions, AMPK-inactivation, ER-stress activation and complex, coordinated changes in expression patterns of mitochondrial and human islet proteins.
Mühlhan, Markus, Ulrike Lüken, Jens Siegert, Hans-Ulrich Wittchen, Michael N. Smolka e Clemens Kirschbaum. "Enhanced Sympathetic Arousal in Response to fMRI Scanning Correlates with Task Induced Activations and Deactivations". Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2014. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-127271.
Mühlhan, Markus, Ulrike Lüken, Jens Siegert, Hans-Ulrich Wittchen, Michael N. Smolka e Clemens Kirschbaum. "Enhanced Sympathetic Arousal in Response to fMRI Scanning Correlates with Task Induced Activations and Deactivations". Public Library of Science, 2013. https://tud.qucosa.de/id/qucosa%3A27292.
Herson, Paco S. "Oxidative stress activates a novel non-selective cation channel in insulin-secreting cells". Thesis, University of Aberdeen, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.265376.
DeAngelis, Cara Marie. "Characterization of the Vibrio cholerae Phage Shock Protein Response". University of Toledo Health Science Campus / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=mco1556723496251854.
Lipson, Kathryn L. "The Role of Endoplasmic Reticulum Stress Signaling in Pancreatic Beta Cells: a Dissertation". eScholarship@UMMS, 2008. https://escholarship.umassmed.edu/gsbs_diss/363.
Fonseca, Sonya G. "Role of WFS1 in Regulating Endoplasmic Reticulum Stress Signaling: A Dissertation". eScholarship@UMMS, 2009. https://escholarship.umassmed.edu/gsbs_diss/414.
Oslowski, Christine M. "TXNIP is a Mediator of ER Stress-Induced β-Cell Inflammation and Apoptosis: A Dissertation". eScholarship@UMMS, 2012. https://escholarship.umassmed.edu/gsbs_diss/611.
Dugani, Aisha Mohammed. "Effects of dopamine agonists and antagonists on gastric acid secretion and stress ulcer formation". 1987. http://hdl.handle.net/1993/15446.
Chou, Sheng-Hsia, e 周聖夏. "Effects of docosahexaenoic acid deficiency on stress-induced glucocorticoid secretion in adult male rats". Thesis, 2013. http://ndltd.ncl.edu.tw/handle/44595451536292047639.
國立臺灣大學
生理學研究所
101
Most previous studies have focused on rat docosahexaenoic acid (22:6n-3, DHA) deficiency created during brain development via maternal n-3 fatty acid-deficient diet from pregnancy and lactation on adult anxiety and depression behaviors. It has been suggested the anxiety and depression is associated with hypothalamic-pituitary-adrenal axis (HPA axis) responses. The aim of this study was to evaluate whether brain DHA deficiency during post-weaning period would enhance restrain-induced HPA axis responses and anxiety or depression-like behavior in adult male rats. After weaning at postnatal day 21, male rats fed an n-3 fatty acid-deficient or an n-3 fatty acid-adequate diet till sacrificed at postnatal day 70. The DHA levels were significant decreased in hypothalamus and hippocampus and other brain regions in rats fed with n-3 fatty acid-deficient diet compared to the rats fed with n-3 fatty acid-adequate diet during post-weaning period for 7 weeks. The anxiety-like behavior in the elevated plus-maze test and depressive-like behavior in the forced swim test were no difference between groups. The restraint-induced rectal temperature was increased during the restraint, but no difference between groups. The serum corticosterone was significant increased right after restraint in rats fed an n-3 fatty acid-deficient diet. The GR expression in hippocampus and hypothalamus were no difference between groups. The BDNF was significant decreased in hippocampus after restraint in rats fed n-3 fatty acid-deficient diet compared to the rats fed n-3 fatty acid-adequate diet. This study suggest that brain DHA level can be decreased in male rats fed n-3 fatty acid-deficient diet during post-weaning period, and the decreased brain DHA is associated with higher stress-induced serum corticosterone levels.
Huang, Lih-Rong, e 黃麗榕. "Effect of L-Glutamic Acid on Gastric Secretion and Stress-induced Gastric Lesions -- an in Vivo Study". Thesis, 1995. http://ndltd.ncl.edu.tw/handle/29291475582945156334.
台北醫學大學
醫學研究所
83
The effects of L-glutamic acid (L-Glu) on gastric acid secretion were incestigated in vivo. All SD rats were anesthetized with sodium pentobarbital (45 mg/kg, i.p.) after 24 hrs of fasting. The trachea、esophagus、femoral vein and duodenum were catheterized. The stomach was flushed throuth the esophagus cannula via a peristaltic pump with normal saline at room temperature. Acid output was determined by titration (autotitrator VIT90, Radiometer Corp., Corpenhagen, Denmark) of the perfusate with 0.01N NaOH to pH 7.0. after basal secretions were collected for 30 min, and various acid stimulator (histamine, oxotremorine or pentagastrin) were infused for 60 min. In addition, L-glutamic acid (L-Glu) and 6, 7-dinitroquinoxaline-2, 3-dione (DNQX) was infused for 30 min after the infusion of histamine for 30 min. The result was found that infusion with synthetic L-Glu alone had no effect on spontaneous acid secretion. The histamine-(2 mg/kg/hr) and oxotremorine-(1 ug/kg/hr) stimulated acid secretion and were markedly reduced by L-Glu (750 ug/kg/hr), whereas L-Glu had no effect on acid secretion stimulated by pentagestrin (5 ug/kg/hr). Furthermore, this inhibitory effect of L-Glu on hisstamine-stimulated acid secretion was blocked by DNQX (750 ug/kg/hr), a non-DMDA receptor antagonist. On the other hand, L-Glu and it's subtypes including N-meghy1-D-aspartate (NMDA), kainic acid (KA) and quisqualic acid (QA), which functions to protect mucosal damage and reduce cyclic AMP concentration were also investigated in stres-induced gastric lesions. L-Glu and it's eubtypes were administered before cold-restraint stress (4 + 1℃, 2 hrs). The cAMP concentration of cold restraint-induced mucosal lesion was significantly different from the normal stomach. The present study was conducted to evaluate the effect of these drugs on the development of cold and restraint-induced gastric ulcers. Two hours of restraint at 4 + 1℃ resulted in the production of gastric lesions in all mice. The cAMP concentration of cold restraint-induced was inhibited by L-Glu and it's subtypes. L-Glu at 2, 4 and 8 mg/kg i.p. injection 30 min before strss significantly and dose dependently prevented gastric lesions. NMDA at 0.2, 1 and 2 mg/kg , QA at 2 and 5 mg/kg or KA at 1, 2 and 5 mg/kg administered 30 min before stress prevented gastric ulcer in dose dependently. All these results suggest that L-Glu is involved in the inhibition of oxotremorine-and histamine-induced gastric acid secretion via ionotropic non-NMDA receptors. L-Glu and it's subtypes also may participate in a physiological modulation of the gastric mucosal barrier, by increasing resistance to cold restraint-induced gastric lesions in mice.
Diamond, Scott Lee. "Effect of laminar shear stress on gene regulation, protein synthesis, and protein secretion by cultured human endothelial cells". Thesis, 1990. http://hdl.handle.net/1911/16336.
Subramaney, Ugasvaree. "Personality style, cortisol secretion and the inflammatory response to trauma exposure in a cohort of South African metro police cadets: a prospective, longitudinal study". Thesis, 2012. http://hdl.handle.net/10539/11051.
Chen, Yu-Ting, e 陳育廷. "Role of oxidative stress in the development of mild portal endotoxemia-induced chronic hepatic inflammation and impairment of pancreatic insulin secretion". Thesis, 2008. http://ndltd.ncl.edu.tw/handle/11640773136953732044.
國防醫學院
生理學研究所
96
Portal endotoxemia has been considered as a key pathogenic factor in chronic hepatic inflammation, which have shown to highly associate with metabolic syndrome and type 2 diabetes. Our previous study demonstrated that low-dose intraportal endotoxin infusion could induce chronic hepatic inflammation and impair endocrine pancreatic function. This study was to further test the role of oxidative stress in the pathogenesis of the portal endotoxemia-induced damages in liver and pancreas. from normal rats and fructose-induced insulin resistant rats with fatty liver. Chronic portal infusion was performed under the status of normal and fatty liver condition with portal catheterization connected to lipopolysaccharide (LPS, 0.42 ng/kg/min) or saline-filled osmotic mini-pump for 4 weeks. The rats with intraportal LPS infusion were further divided into two subgroups combined with or without α-Lipoic acid treatment (60 mg/kg/day, P.O.). Our results showed that mild portal endotoxemia created by low-dose intraportal LPS infusion induced subacute hepatic and pancreatic inflammation indicated by the increases in tissue contents of TNF-alpha, IL-6 and superoxide both in normal and fructose-fed rats. Portal LPS infusion significantly attenuated glucose-stimulated insulin secretion shown in hyperglycermic clamp study, but increased plasma amylase, CRP, superoxide levels and WBC count in normal rats. α-Lipoic acid administration significantly alleviated the portal endotoxemia -induced pathological changes in liver and pancreas by histological examination. α-Lipoic acid also reduced plasma amylase, CRP and superoxide production in normal rats with portal LPS infusion. Fructose-induced attenuation in insulin-stimulated glucose uptake was further deteriorated in those with portal LPS infusion and was partially reversed in those LPS-treated rats with α-Lipoic acid administration. Fructose-induced increases in plasma amylase, CRP, superoxide, and WBC counts were further deteriorated in those with LPS treatment. α- Lipoic acid significantly attenuated the detrimental effects of portal endotoxemia on the above-mentioned parameters in fructose-fed rats. These results showed that α-Lipoic acid effectively attenuated portal endotoxemia-induced hepatic inflammation and pancreatic insulin secretion, implicating that augmentation of oxidative stress is crucial for the detrimental effects of chronic portal endotoxemia on liver and pancreas in normal rats and fructose-fed rats, an animal model of metabolic syndrome with fatty liver.
"Phycocyanin protects INS-1E pancreatic beta cells against human islet amyloid polypeptide-induced apoptosis through attenuating oxidative stress and mitochondrial dysfunction". Thesis, 2010. http://library.cuhk.edu.hk/record=b6075047.
It is widely accepted that human islet amyloid polypeptide (hIAPP) aggregation plays an important role in the loss of insulin-producing pancreatic beta cells. Insulin secretion impairment and cell apoptosis can be due to mitochondrial dysfunction in pancreatic beta cells. hIAPP-induced cytotoxicity is mediated by the generation of reactive oxygen species (ROS). Phycocyanin (PC) is a natural compound from blue-green algae that is widely used as food supplement. Currently, little information is available about the effect of hIAPP on mitochondrial function of beta cells and protection of PC against hIAPP-induced cytotoxicity. In this thesis, I hypothesize that hIAPP may impair beta cell function with the involvement of mitochrondrial dysfunction, and this effects could be attenuated by PC. Therefore, the aim of this study was to investigate the role of mitochondria in hIAPP-induced apoptosis, the in vitro protective effects of PC and explore the underlying mechanisms.
It was found that hIAPP induced apoptosis in INS-1E cells with the disruption of mitochondrial function, as evidenced by ATP depletion, mitochondrial mass reduction, mitochondrial fragmentation and loss of mitochondrial membrane potential (DeltaPsim). Further molecular analysis showed that hIAPP induced changes in the expression of Bcl-2 family members, release of cytochrome c and apoptosis-inducing factor (AIF) from mitochondria into cytosol, activation of caspases and cleavage of poly (ADP-ribose) polymerase. Interestingly, the hIAPP-induced mitochondrial dysfunction in INS1-E cells was effectively restored by co-treatment with PC.
Our results showed that hIAPP inhibited the INS-1E cell growth in a dose-dependent manner. However, cytotoxicity of hIAPP was significantly attenuated by co-incubation of the cells with PC. hIAPP induced DNA fragmentation and chromatin condensation, which were key characteristics of cell apoptosis. These changes were inhibited by PC as examined by TUNEL assay and DAPI staining. Moreover, PC significantly prevented the hIAPP-induced overproduction of intracellular ROS and malonaldehyde (MDA), as well as changes of activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) enzymes. Furthermore, hIAPP triggered the activation of mitogen-activated protein kinases (MAPKs) such as c-Jun N-terminal kinase (JNK) and p38 kinase, and these effects were effectively suppressed by PC.
Taken together, I have demonstrated for the first time the involvement of mitochondrial dysfunction in hIAPP-induced INS-1E cell apoptosis, which was attenuated by PC through attenuating oxidative stress, modulating JNK and p38 pathways and reducing mitochondrial dysfunction.
Li, Xiaoling.
Adviser: Juliana Chung Ngor Chan.
Source: Dissertation Abstracts International, Volume: 73-01, Section: B, page: .
Thesis (Ph.D.)--Chinese University of Hong Kong, 2010.
Includes bibliographical references (leaves 150-159).
Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web.
Electronic reproduction. [Ann Arbor, MI] : ProQuest Information and Learning, [201-] System requirements: Adobe Acrobat Reader. Available via World Wide Web.
Abstract also in Chinese.
Barbeau, Annie. "Rôle de l'estérification des acides gras dans la régulation de la sécrétion d'insuline et le stress métabolique induits par le glucose". Thèse, 2012. http://hdl.handle.net/1866/7063.
Diabetes is a chronic disease of glucose homeostasis characterized by hyperglycemia and the result of a failure of insulin secretion in combination or not with impaired insulin action. Overnutrition and lack of physical activity in individuals who have acquired or inherited genetic predispositions lead to insulin resistance. During the period of compensation where the concentration of plasma fatty acids is high, hyperinsulinemia fully compensates for the insulin resistance of target tissues and blood sugar is normal. Glucose promotes insulin secretion through its metabolism by the pancreatic β cell. According to the classical model of glucose-induced insulin secretion, the increase in the ATP/ADP ratio resulting from glycolysis and glucose oxidation induces the closure of KATP channels thus changing membrane potential followed by an influx of Ca2+. This influx of Ca2+ allows the exocytosis of secretory granules containing insulin. Several nutrients like fatty acids are capable of potentiating insulin secretion. However, the classical model does not explain the potentiation of insulin secretion by fatty acids. To explain the potentiating effect of fatty acids, our laboratory has proposed a complementary model in which malonyl-CoA derived from glucose anaplerotic metabolism inhibits carnitine palmitoyltransferase 1, the enzyme catalyzing the limiting step of fatty acid oxidation, thereby promoting their esterification and thus the formation signaling derivatives. The anaplerotic model of insulin secretion predicts that malonyl-CoA derived from glucose metabolism inhibits β-oxidation of fatty acids and increases the availability of acyl-CoA or non esterified fatty acids. Thus, lipid molecules can act as coupling factors for insulin exocytosis. Fatty acid-derived signalling molecules that are active remain to be identified. Work performed by our laboratory has shown that increasing the partition of fatty acids toward β-oxidation reduced glucose-induced insulin secretion, suggesting that derivatives of fatty acid esterification are important for the potentiation of insulin secretion. Indeed, at high concentrations of glucose, fatty acids are esterified into lysophosphatidic acid (LPA), phosphatidic acid (PA) and diacylglycerol (DAG) and subsequently in triglycerides (TG). The present study established the relative importance fatty acid esterification in the production of factors potentiating insulin secretion. We hypothesized that molecules derived from the process of esterification of fatty acid (eg lysophosphatidic acid (LPA) and diacylglycerol (DAG)) act as metabolic signals and are responsible for the modulation of the secretion of insulin in the presence of fatty acids. Thus, the level of expression of key enzymes controlling the process of esterification has been altered by molecular biology approaches to increase distribution of fatty acids toward esterification in the β cell. The expression of various isoforms of glycerol-3-phosphate acyltransferase (GPAT), which catalyzes the first step of esterification of fatty acids was increased and inhibited. The effects of GPAT isoenzyme modulation on the esterification process, on β-oxidation and on glucose-induced insulin secretion were investigated. The various approaches we used have changed the levels of DAG and TG without altering insulin secretion induced by glucose in the presence or absence of fatty acids. Thus, the results of this study do not suggest a role for de novo synthesis of glycerolipid intermidiates via esterification of fatty acids in the potentiation of insulin secretion. However, the esterification of fatty acids is an integral part of a TG/fatty acid cycle with its counterpart lipolysis. Moreover, parallel studies conducted by colleagues of the laboratory have demonstrated a role for lipolysis and a cycle TG/fatty acid in the potentiation of insulin secretion by fatty acids. In parallel with our studies of the mechanisms of insulin secretion involving fatty acids, our laboratory is also interested in the negative effects of fatty acids on the β cell. The glucolipotoxicity resulting from chronic exposure to saturated fatty acids in the presence of high glucose concentrations is of particular interest in the context of obesity rates. The microsomal isoform of GPAT was also used as a molecular tool under glucolipotoxicity conditions to study the role of de novo synthesis of complex lipids in the context of decompensation when β-cell function decreases. Increased esterification of fatty acids by the overexpression of microsomal isoform of GPAT has increased the toxic effects of fatty acids in the context of glucolipotoxicity. Thus, our results allow us to conclude that the distribution of lipids toward esterification and a decrease in β-oxidation is instrumental in glucolipotoxicity.
Narayanan, Niju. "Molecular and Genetic Strategies to Enhance Functional Expression of Recombinant Protein in Escherichia coli". Thesis, 2009. http://hdl.handle.net/10012/4721.
Décary, Simon. "Amélioration de la fonction pancréatique par l'activité physique chez le rat diabétique de type 2". Thèse, 2008. http://hdl.handle.net/1866/7740.