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Dissertations / Theses on the topic 'Pancreatic beta-cell'

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Published: 4 June 2021

Last updated: 25 July 2025

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1

Barlow, Jonathan. "Mitochondrial involvement in pancreatic beta cell glucolipotoxicity." Thesis, University of Plymouth, 2015. http://hdl.handle.net/10026.1/3314.

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High circulating glucose and non-esterified free fatty acid (NEFA) levels can cause pancreatic β-cell failure. The molecular mechanisms of this β-cell glucolipotoxicity are yet to be established conclusively. In this thesis by exploring mitochondrial energy metabolism in INS-1E insulinoma cells and isolated pancreatic islets, a role of mitochondria in pancreatic β-cell glucolipotoxicity is uncovered. It is reported that prolonged palmitate exposure at high glucose attenuates glucose-stimulated mitochondrial respiration which is coupled to ADP phosphorylation. These mitochondrial defects coinci

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2

Cui, Ju, and 崔菊. "Kinesin-1 in pancreatic beta cell and renal epithelial cell." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hdl.handle.net/10722/197835.

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3

Hanna, Katie. "Novel mechanisms of glucolipotoxic pancreatic beta cell death." Thesis, Nottingham Trent University, 2018. http://irep.ntu.ac.uk/id/eprint/35356/.

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Glucolipotoxicity (GLT) is the term given to the combined and damaging effect of increased glucose and fatty acid levels on pancreatic beta cells (β-cells) (Poitout et al, 2010). There is mounting evidence that glucolipotoxicity is the cause of the decline in β-cell function found in type 2 diabetes (T2D). T2D is a chronic metabolic disorder characterised by sustained elevated blood glucose and free fatty acids, with a continuously increasing prevalence (Olokoba et al, 2012). It is estimated 415 million people currently are living with diabetes and 193 million are undiagnosed, of those 90% are

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4

Hill, Jennifer. "Bacterial Regulation of Host Pancreatic Beta Cell Development." Thesis, University of Oregon, 2018. http://hdl.handle.net/1794/23140.

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Diabetes is a metabolic disease characterized by the loss of functional pancreatic beta cells. The incidence of diabetes has risen rapidly in recent decades, which has been attributed at least partially to alterations in host-associated microbial communities, or microbiota. It is hypothesized that the loss of important microbial functions from the microbiota of affected host populations plays a role in the mechanism of disease onset. Because the immune system also plays a causative role in diabetes progression, and it is well documented that immune cell development and function are regulated b

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5

Westermark, Pål. "Models of the metabolism of the pancreatic beta-cell." Doctoral thesis, KTH, Numerical Analysis and Computer Science, NADA, 2005. http://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-408.

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<p>The pancreatic β-cell secretes insulin in response to a raised blood glucose level. Deficiencies in this control system are an important part of the etiology of diabetes. The biochemical basis of glucose-stimulated insulin secretion is incompletely understood, and a more complete understanding is an important component in the quest for better therapies against diabetes.</p><p>In this thesis, mathematical modeling has been employed in order to increase our understanding of the biochemical principles that underlie glucosestimulated insulin secretion of the pancreatic β-cell. The modeling effo

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6

Pinnick, Katherine Elizabeth. "Pancreatic fat accumulation and effects on beta cell function." Thesis, University of Oxford, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.492051.

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Type 2 Diabetes Mellitus (T2DM) is characterised by impaired pancreatic 13-cell function resulting in inadequate insulin secretion. The mechanisms involved in 13-cell dysfunction are largely unknown. Elevated fasting plasma non-esterified fatty acid (NEFA) concentrations have been identified as a risk factor for the development of T2DM. The work in this thesis investigates functional effects of NEFA on the 13-cell. Prolonged exposure to elevated NEFA has previously been associated with impaired insulin secretion, reduced insulin content and altered gene expression and lipid metabolism in the 1

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7

Yang, Yu Hsuan Carol. "Identification and characterization of pancreatic beta-cell survival factors." Thesis, University of British Columbia, 2014. http://hdl.handle.net/2429/46424.

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8

Hughes, Jonathan Martyn. "Streptozotocin and sugar transport in pancreatic beta cell lines." Thesis, University of Bath, 1993. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.386772.

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9

Duffy, Joan. "Effects of insulin sensitising agents on pancreatic beta cell function." Thesis, University of Ulster, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.399052.

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10

Halvorsen, Tanya L. "Growth regulation and differentiation in the human pancreatic beta cell /." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2001. http://wwwlib.umi.com/cr/ucsd/fullcit?p3000408.

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11

Cosentino, C. "ROLE OF TRNA MODIFYING ENZYMES IN PANCREATIC BETA CELL DEMISE." Doctoral thesis, Università degli Studi di Milano, 2015. http://hdl.handle.net/2434/335205.

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Transfer RNAs (tRNAs) are small molecules of 70-80 nucleotides with a crucial role in protein synthesis. tRNAs once transcribed are highly modified and the methylation is the most common modification. Several enzymes are responsible of tRNA modification and their function is necessary to regulate the stability, the aminoacylation and the rigidity of the structure of tRNAs. De-aminoacylated or degraded tRNAs can act as important signal molecules in the cells, activating different pathways of stress response. For this reason is not surprising that mutations in genes codifying for tRNA modifying

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12

Tsang, Siu-wai. "Involvement of Pdzd2 in the regulation of pancreatic beta-cell functions." View the Table of Contents & Abstract, 2007. http://sunzi.lib.hku.hk/hkuto/record/B39716430.

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13

Tsang, Siu-wai, and 曾少慧. "Involvement of Pdzd2 in the regulation of pancreatic beta-cell functions." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B39793746.

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14

Nishi, Kiyoto. "Nardilysin Is Required for Maintaining Pancreatic β-Cell Function". 京都大学 (Kyoto University), 2017. http://hdl.handle.net/2433/225463.

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15

Cromwell, Diane. "Pancreatic beta-cell actions of nutrients and metabolizable nutrient ester derivatives." Thesis, University of Ulster, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.494335.

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16

Tym, Amy. "Effect of protein glycation by methylglyoxal on pancreatic beta cell function." Thesis, University of Warwick, 2014. http://wrap.warwick.ac.uk/61717/.

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Methylglyoxal is a physiological dicarbonyl metabolite and potent argininedirected glycating agent. It often modifies proteins at functional sites producing loss of positive charge, structural distortion and inactivation. Plasma methylglyoxal is increased in hyperglycaemia associated with diabetes and is linked to the development of vascular complications of diabetes – particularly nephropathy, retinopathy and neuropathy. The effects of dicarbonyl glycation on beta cells and involvement in early stage dysfunction and development of type 2 diabetes mellitus are not known. The aim of this projec

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17

Zhang, Wen. "Mechanism of genistein in the regulation of pancreatic beta-cell proliferation." Thesis, Virginia Tech, 2007. http://hdl.handle.net/10919/35772.

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This study was designed to examine the effect of genistein, a botanical derived primarily from legumes, on pancreatic Î²-cell proliferation and the related molecular mechanisms. Diabetes mellitus is a major and growing public health problem worldwide. Both in type 1 (T1D) and type 2 diabetes (T2D), the deterioration of glycemic control over time is primarily caused by an inadequate mass and progressive dysfunction of Î²-cells. Therefore, the search for novel, safe and cost-effective agents that can enhance islet Î²-cell proliferation, thereby preserving Î²-cell mass, could be one of the essen

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18

Yan, Zhongyu. "Charaterization of Chlorpyrifos Toxicity on the Pancreatic Beta Cell Line RINm5f." Wright State University / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=wright1290111576.

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19

Mercier, Reuben. "Identification and function of new regulators of pancreatic beta cell differentiation." Electronic Thesis or Diss., Strasbourg, 2024. http://www.theses.fr/2024STRAJ007.

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La différenciation in vitro des cellules souches pluripotentes induites humaines (hiPSC) en cellules bêta productrices d'insuline (SC-Beta) offre de grandes promesses pour le développement d'une thérapie de remplacement cellulaire contre le diabète de type 1, une pathologie résultant d'une attaque auto-immune contre les cellules bêta, entraînant une déficience en insuline et donc une incapacité à réguler la glycémie. Ces protocoles ont été optimisés au fil des ans mais produisent encore des cellules SC-Beta immatures, à la production suboptimale d'insuline en réponse au glucose. Ce frein est p

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20

Weng, Chen. "SINGLE-CELL TRANSCRIPTOMICS OF HUMAN PANCREATIC ISLETS IN DIABETES AND ΒETA CELL DIFFERENTIATION". Case Western Reserve University School of Graduate Studies / OhioLINK, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=case1612882103714773.

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21

Watson, Maria. "The role of palmitate in skeletal muscle cell insulin resistance and pancreatic beta cell dysfunction." Thesis, University of Dundee, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.505620.

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22

Jeffrey, Kristin Danielle. "Novel pathways in fatty-acid induced apoptosis in the pancreatic beta-cell." Thesis, University of British Columbia, 2007. http://hdl.handle.net/2429/31378.

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Pancreatic β-cell death is a critical event in the pathogenesis of all forms of diabetes. Type 2 diabetes is caused by the combination of acquired factors such as elevated circulating fatty acids as well as genetic factors. In this study, we show that the free fatty acid palmitate increases markers of endoplasmic stress and apoptosis in pancreatic β-cells. Carboxypeptidase E (CPE), an enzyme involved in the processing of insulin, was identified as the major down-regulated protein spot during palmitate-induced apoptosis using Cy-dye 2D gel proteomics in both the MIN6 β-cell line and human

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23

Stokesberry, Susan Anne. "Functional effects of temperature on pancreatic beta-cell insulin secretion and integrity." Thesis, University of Ulster, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.422895.

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24

Rodrigues, Costa Ana, Celia M. Antunes, and Júlio Cruz-Morais. "Abnormal regulation of pancreatic beta cell Na,K-ATPase on glucose intolerant rats." Bachelor's thesis, Springer Berlin, 2010. http://hdl.handle.net/10174/3307.

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Background and aims: Glucose (G) is the most important physiological insulin secretagogue. It is widely accepted that, in pancreatic -cell, G evoked early ionic events such as membrane depolarization and Ca2+ influx through voltage dependent Ca2+ channels triggers insulin exocytosis. However, the role of other electrogenic systems, namely ionic pumps, to these events remains essentially uninvestigated. It is known that the activity of Na,K-ATPase is modified in type 2 diabetes (T2D). The pump is responsible for maintaining Na+ and K+ gradients across the plasma membrane and generates a net ou

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25

Manesso, Erica. "DYNAMICS OF PANCREATIC BETA CELLS: Evidence for Beta Cell Turnover and Attempted Regeneration in Diabetes from Sources of Beta Cells other than Beta Cell Replication in Rats, Monkeys, and Humans." Doctoral thesis, Università degli studi di Padova, 2010. http://hdl.handle.net/11577/3426591.

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Since the fundamental defect in both type 1 (T1DM) and type 2 diabetes (T2DM) is beta cell failure, there is increasing interest in the capacity, if any, for beta cell regeneration. In this context quantitative analysis of beta cell turnover becomes essential to permit investigation of the mechanisms that regulate it. For example, how does beta cell mass adapt to obesity? How is beta cell mass preserved during aging? How does beta cell mass expand during childhood? In collaboration with the Larry Hillblom Islet Research at David Geffen School of Medicine, University of California Los Angeles

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26

Ullsten, Sara. "The Impact of Pancreatic Islet Vascular Heterogeneity on Beta Cell Function and Disease." Doctoral thesis, Uppsala universitet, Institutionen för medicinsk cellbiologi, 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-330805.

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Diabetes Mellitus is a group of complex and heterogeneous metabolic disorders characterized by hyperglycemia. Even though the condition has been extensively studied, its causes and complex pathologies are still not fully understood. The occurring damage to the pancreatic islets is strikingly heterogeneous. In type 1 diabetes, the insulin producing beta cells are all destroyed within some islets, and similarly in type 2 diabetes, some islets may be severely affected by amyloid. At the same time other islets, in the near vicinity of the ones that are affected by disease, may appear fully normal

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27

Yuan, Yuan. "Small-Molecule Modulators of Pancreatic Ductal Cells: Histone Methyltransferases and \(\beta\)-Cell Transdifferentiation." Thesis, Harvard University, 2012. http://dissertations.umi.com/gsas.harvard:10637.

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Small molecules are important not only for treating human diseases but also for studying disease-related biological processes. This dissertation focuses on the effects of small molecules on pancreatic ductal adenocarcinoma cells. Here, I describe the discovery of two small-molecule tool compounds and their applications for interrogating the biological processes related to two distinct diseases in the human pancreas. First, BRD4770 was identified as a histone methyltransferase inhibitor through a target-based biochemical approach, and was used as a probe to study the function of methyltransfera

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28

Owen, R. A. "The role of transglutaminase in stimulus-secretion coupling in the pancreatic #beta#-cell." Thesis, Nottingham Trent University, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.384731.

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29

Zehri, Aqib Hyder. "Differential Effects of Pulsatile vs. Chronic Hyperglycemia on Fetal Pancreatic Beta Cell Population." Thesis, The University of Arizona, 2011. http://hdl.handle.net/10150/145129.

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30

Germanos, Mark. "A Cab for Insulin: Characterising Cab45 in Pancreatic β-Cells". Thesis, The University of Sydney, 2022. https://hdl.handle.net/2123/29871.

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The pancreatic β-cell is purpose-built for the production and secretion of insulin, the only hormone that can remove glucose from the blood. Insulin is kept inside miniature membrane-bound storage compartments known as secretory granules, and these specialised organelles can readily fuse with the plasma membrane upon cellular stimulation to release insulin into the circulation. At this point in time, the mechanisms that govern the generation of insulin secretory granules are poorly defined. This is pertinent to understanding the molecular pathogenesis of type 2 diabetes, where a reduced popula

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31

Yeo, Wendy Wai Yeng. "Differentiation of skeletal muscle-derived stem cells into beta pancreatic lineage." Thesis, Montpellier, 2015. http://www.theses.fr/2015MONTS091.

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Le diabète de type 1 (DT1) est caractérisé par des niveaux élevés de glucose en raison de la destruction des cellules ß pancréatiques sécrétrices d'insuline. Cependant, les thérapies actuelles de remplacement des cellules bêta du pancréas impliquant la transplantation d'îlots pancréatiques sont techniquement difficiles et limitées par la disponibilité de don d'organes. Bien que les cellules souches embryonnaires et les cellules souches pluripotentes induites soient intensément étudiées, aucune de ces deux sources de cellules souches ne peut être utilisée directement sans le risque de développe

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32

Hartman, Matthew G. "The roles of ATF3 in stress-regulated signal transduction and cell death in pancreatic beta-cells." Connect to resource, 2005. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1116425282.

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Thesis (Ph. D.)--Ohio State University, 2005.<br>Title from first page of PDF file. Document formatted into pages; contains xxiv, 185 p.; also includes graphics. Includes bibliographical references (p. 164-185). Available online via OhioLINK's ETD Center

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33

Preston, Amanda Miriam Clinical School St Vincent's Hospital Faculty of Medicine UNSW. "The role of endoplasmic reticulum stress in beta-cell lipoapoptosis." Publisher:University of New South Wales. Clinical School - St Vincent's Hospital, 2008. http://handle.unsw.edu.au/1959.4/41231.

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Beta-cell failure is a key step in the progression from metabolic disorder to overt type 2 diabetes (T2D). This failure is characterised by both secretory defects and loss of beta-cell mass, the latter most likely through increases in the rate of apoptosis. Although the mechanisms underlying these beta-cell defects are unclear, evidence suggests that chronic exposure of beta-cells to elevated fatty acid (FA) plays a role in disease development in genetically susceptible individuals. Furthermore, it has been postulated that endoplasmic reticulum (ER) stress signalling pathways (the unfolded pro

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34

Mitchell, Ryan. "The effects of type 2 diabetes associated risk loci on pancreatic beta cell function." Thesis, Imperial College London, 2016. http://hdl.handle.net/10044/1/39040.

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The pancreatic islets of Langerhans play a fundamental role in the stabilisation of blood glucose levels. Pancreatic islets are spherical structures composed of multiple cell types, with each individual cell type secreting a peptide hormone, such as insulin and glucagon, which regulates whole body glucose homoeostasis. Defective hormone secretion from islet cells is a hallmark of certain metabolic diseases, including type 2 diabetes mellitus (T2D). The most abundant islet cell type is the pancreatic β-cell, a specialised cell type that secretes the hypoglycaemic hormone insulin in response to

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35

Heister, Paula Maria. "The role of two pore channels (TPCs) in pancreatic beta cell stimulus-secretion coupling." Thesis, University of Oxford, 2012. http://ora.ox.ac.uk/objects/uuid:4bed27d2-e7e4-49ff-8168-aa02b6f9b613.

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This thesis presents an investigation into the role of the recently identified two pore channels (TPCs) in Î²-cell stimulus-secretion coupling. TPCs are the receptors for calcium mobilising messenger nicotinic acid adenine dinucleotide phosphate (NAADP) located in the membrane of acidic intracellular calcium stores. It is proposed that they are responsible for the ATP-sensitive potassium channel (Katp channel) independent pathway of stimulus-secretion coupling; and that this pathway is not subordinate to the KAT? channel dependent pathway; but an alternative explanation of stimulus-secretion c

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36

Naghiloo, Sheyda. "Proteomic Pathways to Type 2 Diabetes in the Pancreatic Islet." Thesis, The University of Sydney, 2022. https://hdl.handle.net/2123/29172.

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Unveiling proteomic changes that occur through stages of pathogenesis can provide unparalleled insights into the mechanisms underpinning disease. Using fluorescence-activated cell sorting (FACS) and liquid chromatography mass spectrometry/mass spectrometry (LC-MS/MS), I aimed to characterise the deep proteome of both whole islets and individual islet cell types (alpha, beta, gamma, delta and epsilon) from mice and humans in variable states of health and disease. Acquisition of individual islet cell type proteomes will serve as a window of enquiry into islet cell regulation and intra-cellular c

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37

Kahve, A. "Biophysical and biochemical effects and distribution of fatty acids in pancreatic beta cells and microvascular endothelial cells." Thesis, University of Exeter, 2019. http://hdl.handle.net/10871/36684.

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The incidences of obesity and type 2 diabetes and their complications are increasing globally. The presence of elevated circulating free fatty acids has been associated with the initial dysfunction of pancreatic beta cells and microvascular endothelial cells followed later by their demise. The aim of this thesis was to investigate the mechanisms by which demise occurs, and how it may be prevented. Palmitate, a saturated fatty acid, caused cell death in both INS-1 beta cells and HCMec/D3 microvascular cells, whereas the unsaturated fatty acid oleic acid did not cause cell death, and also protec

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38

Hartman, Matthew George. "The roles of ATF3 in stress-regulated signal transduction and cell death in pancreatic beta-cells." The Ohio State University, 2005. http://rave.ohiolink.edu/etdc/view?acc_num=osu1116425282.

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39

Onyango, David J. "The effects of the adipocyte-secreted proteins resistin and visfatin on the pancreatic beta-cell." Thesis, University of Wolverhampton, 2009. http://hdl.handle.net/2436/89148.

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Adipose tissue secreted proteins (adipokines) have been proposed to form a link between obesity and type 2 diabetes (T2D). Resistin and visfatin are two adipokines which have been previously suggested as having roles in the pancreatic islet. The aim of this study was therefore to investigate the regulatory role of the adipokines resistin and visfatin in the pancreatic beta-cell. In order to do this, pancreatic β-cell lines from rat (BRIN-BD11) and mouse (βTC-6) were used to study the effect of exogenous incubation with physiological and pathological concentrations of resistin and visfatin on d

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40

Turbitt, Julie Michelle. "The role of taurine in the regulation of insulin secretion and pancreatic beta-cell function." Thesis, University of Ulster, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.422896.

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41

Karlsson, Ella. "Studies of neuropeptides in pancreatic beta cell function with special emphasis on islet amyloid polypeptide (IAPP)." Doctoral thesis, Uppsala University, Department of Medical Cell Biology, 2000. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-560.

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<p>The presence of protein amyloid in pancreas and its association to diabetes was first described 100 years ago in 1901, but was not identified as Islet Amyloid Polypeptide (IAPP) until 1986. The aim of the present work was to determine the role of the beta cell hormone, IAPP, in normal pancreatic islet physiology and during early disturbances of islet function.</p><p>Intra-islet peptides, i.e. chromogranin peptides and an extra-islet peptide, i.e. leptin, were studied to identify possible endogenous regulators of IAPP and insulin secretion. Chromogranin-B, but not chromogranin-A or pancreast

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42

Hamamatsu, Keita. "Establishment of non-invasive quantification of pancreatic beta cell mass in mice using SPECT/CT imaging with ¹¹¹In-labeled exendin-4 and its application to evaluation of diabetes treatment effects on pancreatic beta cell mass." Kyoto University, 2020. http://hdl.handle.net/2433/253199.

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43

Tatsuoka, Hisato. "Single-cell Transcriptome Analysis Dissects the Replicating Process of Pancreatic Beta Cells in Partial Pancreatectomy Model." Doctoral thesis, Kyoto University, 2021. http://hdl.handle.net/2433/263543.

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44

Åkerblom, Björn. "Frk/Shb Signalling in Pancreatic Beta-cells : Roles in Islet Function, Beta-cell Development and Survival as Implicated in Mouse Knockout Models." Doctoral thesis, Uppsala universitet, Institutionen för medicinsk cellbiologi, 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-89348.

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The adaptor protein Shb and the non-receptor tyrosine kinase Frk have been implicated in intracellular signalling in insulin-producing beta cells. In this thesis, knockout mice are used to further elucidate the role of Shb and Frk for beta cell number, cytokine-induced cell death, and glucose homeostasis. In addition, the effect of Shb deficiency upon tumour growth is studied in a mouse model of endogenous tumourigenesis. Previously, overexpression of Frk has been associated with increased beta cell replication, and increased susceptibility to cytokine induced beta cell destruction. To test wh

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45

Herrero, Rodríguez Laura. "Implication of Long-Chain Fatty Acids in Glucose-Induced Insulin Secretion in the Pancreatic Beta-Cell." Doctoral thesis, Universitat de Barcelona, 2004. http://hdl.handle.net/10803/2999.

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INTRODUCTION Carnitine palmitoyltransferase I, which is expressed in the pancreas as the liver isoform (LCPTI), catalyzes the rate-limiting step in the transport of fatty acids into the mitochondria for their oxidation. To directly examine whether the availability of long-chain fatty acyl-CoA affects the regulation of insulin secretion in the Beta-cell, we infected INS(832/13) cells and rat islets with an adenovirus encoding a mutant form of LCPTI (Ad-LCPTI M593S) that is insensitive to its inhibitor malonyl-CoA. C75 is described as a potential drug for treatment of obesity and type 2 diabetes

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46

Miani, MICHELA. "The cross-talk between endoplasmatic reticulum stress and cytokines in pancreatic beta cell inflammation and apoptosis." Doctoral thesis, Universite Libre de Bruxelles, 2013. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/209418.

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La prévalence de l’obésité et du diabète de type 1 (DT1) s’accroit dans le monde à une vitesse alarmante. L’augmentation du poids corporel, de la quantité d’acides gras libres (AGL) circulant et de la résistance à l’insuline peut induire un stress du réticulum endoplasmique (RE) dans les cellules beta du pancréas, ce qui pourrait favoriser l’inflammation. Afin de tester cette hypothèse, nous avons exposé des cellules beta à un léger stress chronique du RE induit par de l’acide ciclopiazonique (ACP) ou l’AGL palmitate et les avons ensuite traitées avec une faible dose d’interleukine 1β (IL-1β)

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47

Du, Xiaoyu. "PLAGL1/ZAC, a transient neonatal diabetes mellitus locus gene, in pancreatic beta-cell development and function." Thesis, McGill University, 2011. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=96741.

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Studies on congenital disorders of the pancreas have contributed to the identification of genes that are critical in beta-cell development and function. Transient neonatal diabetes mellitus (TNDM) is a rare congenital disorder of the pancreas. It involves severe insulin deficiency at birth that reverses over weeks or months but may relapse with diabetes in later life. PLAGL1 (pleiomorphic adenoma gene-like 1, also known as ZAC, zinc finger protein that regulates apoptosis and cell cycle arrest, and LOT1, Lost On Transformation 1) is one of the two possible genes at the TNDM locus and the multi

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48

Patterson, Steven. "Homocysteine and the effects of other amino thiols on pancreatic beta cell function and insulin secretion." Thesis, University of Ulster, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.398994.

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49

Watson, David. "Mechanisms of pancreatic beta cell death induced by cytokines and by reactive oxygen and nitrogen species." Thesis, Keele University, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.502942.

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50

O'Sullivan-Murphy, Bryan M. "Contribution of WFS1 to Pancreatic Beta Cell Survival and Adaptive Alterations in WFS1 Deficiency: A Dissertation." eScholarship@UMMS, 2012. https://escholarship.umassmed.edu/gsbs_diss/590.

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Diabetes mellitus comprises a cohort of genetic and metabolic diseases which are characterized by the hallmark symptom of hyperglycemia. Diabetic subtypes are based on their pathogenetic origins: the most prevalent subtypes are the autoimmune-mediated type 1 diabetes mellitus (T1DM) and the metabolic disease of type 2 diabetes mellitus (T2DM). Genetic factors are major contributory aspects to diabetes development, particularly in T2DM where there is close to 80% concordance rates between monozygotic twins. However, the functional state of the pancreatic β cell is of paramount importance to the

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