Relevant bibliographies by topics / Β-cell of pancreas

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

Academic literature on the topic 'Β-cell of pancreas'

Author: Grafiati
Published: 3 June 2025
Last updated: 31 July 2025

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Journal articles on the topic "Β-cell of pancreas"

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Ma, Haiting, Katherine J. Wert, Dmitry Shvartsman, Douglas A. Melton та Rudolf Jaenisch. "Establishment of human pluripotent stem cell-derived pancreatic β-like cells in the mouse pancreas". Proceedings of the National Academy of Sciences 115, № 15 (2018): 3924–29. http://dx.doi.org/10.1073/pnas.1702059115.

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Type 1 diabetes is characterized by autoimmune destruction of β cells located in pancreatic islets. However, tractable in vivo models of human pancreatic β cells have been limited. Here, we generated xenogeneic human pancreatic β-like cells in the mouse pancreas by orthotopic transplantation of stem cell-derived β (SC-β) cells into the pancreas of neonatal mice. The engrafted β-like cells expressed β cell transcription factors and markers associated with functional maturity. Engrafted human cells recruited mouse endothelial cells, suggesting functional integration. Human insulin was detected i
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Beamish, Christine A., Sofia Mehta, Brenda J. Strutt, Subrata Chakrabarti, Manami Hara та David J. Hill. "Decrease in Ins+Glut2LO β-cells with advancing age in mouse and human pancreas". Journal of Endocrinology 233, № 3 (2017): 229–41. http://dx.doi.org/10.1530/joe-16-0475.

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The presence and location of resident pancreatic β-cell progenitors is controversial. A subpopulation of insulin-expressing but glucose transporter-2-low (Ins+Glut2LO) cells may represent multipotent pancreatic progenitors in adult mouse and in human islets, and they are enriched in small, extra-islet β-cell clusters (<5 β cells) in mice. Here, we sought to identify and compare the ontogeny of these cells in mouse and human pancreata throughout life. Mouse pancreata were collected at postnatal days 7, 14, 21, 28, and at 3, 6, 12, and 18 months of age, and in the first 28 days after β-cell m
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Butler, Alexandra E., Sangeeta Dhawan, Jonathan Hoang та ін. "β-Cell Deficit in Obese Type 2 Diabetes, a Minor Role of β-Cell Dedifferentiation and Degranulation". Journal of Clinical Endocrinology & Metabolism 101, № 2 (2016): 523–32. http://dx.doi.org/10.1210/jc.2015-3566.

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Abstract Context: Type 2 diabetes is characterized by a β-cell deficit and a progressive defect in β-cell function. It has been proposed that the deficit in β-cells may be due to β-cell degranulation and transdifferentiation to other endocrine cell types. Objective: The objective of the study was to establish the potential impact of β-cell dedifferentiation and transdifferentiation on β-cell deficit in type 2 diabetes and to consider the alternative that cells with an incomplete identity may be newly forming rather than dedifferentiated. Design, Setting, and Participants: Pancreata obtained at
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Bohuslavova, Romana, Ondrej Smolik, Jessica Malfatti та ін. "NEUROD1 Is Required for the Early α and β Endocrine Differentiation in the Pancreas". International Journal of Molecular Sciences 22, № 13 (2021): 6713. http://dx.doi.org/10.3390/ijms22136713.

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Diabetes is a metabolic disease that involves the death or dysfunction of the insulin-secreting β cells in the pancreas. Consequently, most diabetes research is aimed at understanding the molecular and cellular bases of pancreatic development, islet formation, β-cell survival, and insulin secretion. Complex interactions of signaling pathways and transcription factor networks regulate the specification, growth, and differentiation of cell types in the developing pancreas. Many of the same regulators continue to modulate gene expression and cell fate of the adult pancreas. The transcription fact
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Mwangi, Simon M., Yousef Usta, Shreya M. Raja та ін. "Glial cell line-derived neurotrophic factor enhances neurogenin3 gene expression and β-cell proliferation in the developing mouse pancreas". American Journal of Physiology-Gastrointestinal and Liver Physiology 299, № 1 (2010): G283—G292. http://dx.doi.org/10.1152/ajpgi.00096.2010.

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Glial cell line-derived neurotrophic factor (GDNF) is a factor produced by glial cells that is required for the development of the enteric nervous system. In transgenic mice that overexpress GDNF in the pancreas, GDNF has been shown to enhance β-cell mass and improve glucose control, but the transcriptional and cellular processes involved are not known. In this study we examined the influence of GDNF on the expression of neurogenin3 (Ngn3) and other transcription factors implicated in early β-cell development, as well as on β-cell proliferation during embryonic and early postnatal mouse pancre
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Garcia, Cathy, Aarthi Venkat, Daniel McQuaid, et al. "Abstract PR-05: Endocrine beta-cell stress promotes pancreatic ductal adenocarcinoma through endocrine-exocrine cell crosstalk." Cancer Research 84, no. 17_Supplement_2 (2024): PR—05—PR—05. http://dx.doi.org/10.1158/1538-7445.pancreatic24-pr-05.

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Abstract For a long time, the pancreas was thought to have separate cellular compartments that functioned distinctly from one another. The endocrine pancreas (islets of Langerhans) regulates glucose homeostasis, while the exocrine pancreas (acini and ducts) produces and secretes digestive enzymes. However, it has recently become clear that the endocrine and exocrine compartments communicate with one another, and dysfunction in one leads to dysfunction in the other, resulting in diabetes or pancreatitis. However, whether and how the endocrine pancreas drives the development of pancreatic ductal
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Kobayashi, Masaki, Osamu Kikuchi, Tsutomu Sasaki та ін. "FoxO1 as a double-edged sword in the pancreas: analysis of pancreas- and β-cell-specific FoxO1 knockout mice". American Journal of Physiology-Endocrinology and Metabolism 302, № 5 (2012): E603—E613. http://dx.doi.org/10.1152/ajpendo.00469.2011.

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Diabetes is characterized by an absolute or relative deficiency of pancreatic β-cells. New strategies to accelerate β-cell neogenesis or maintain existing β-cells are desired for future therapies against diabetes. We previously reported that forkhead box O1 (FoxO1) inhibits β-cell growth through a Pdx1-mediated mechanism. However, we also reported that FoxO1 protects against β-cell failure via the induction of NeuroD and MafA. Here, we investigate the physiological roles of FoxO1 in the pancreas by generating the mice with deletion of FoxO1 in the domains of the Pdx1 promoter (P-FoxO1-KO) or t
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Riz, Michela, Morten Gram Pedersen, Gianna Maria Toffolo, et al. "Minimal modeling of insulin secretion in the perfused rat pancreas: a drug effect case study." American Journal of Physiology-Endocrinology and Metabolism 306, no. 6 (2014): E627—E634. http://dx.doi.org/10.1152/ajpendo.00603.2013.

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The experimental protocol of the perfused rat pancreas is commonly used to evaluate β-cell function. In this context, mathematical models become useful tools through the determination of indexes that allow the assessment of β-cell function in different experimental groups and the quantification of the effects of antidiabetic drugs, secretagogues, or treatments. However, a minimal model applicable to the isolated perfused rat pancreas has so far been unavailable. In this work, we adapt the C-peptide minimal model applied previously to the intravenous glucose tolerance test to obtain a specific
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Perfetti, Riccardo, Jie Zhou, Máire E. Doyle, and Josephine M. Egan. "Glucagon-Like Peptide-1 Induces Cell Proliferation and Pancreatic-Duodenum Homeobox-1 Expression and Increases Endocrine Cell Mass in the Pancreas of Old, Glucose-Intolerant Rats." Endocrinology 141, no. 12 (2000): 4600–4605. http://dx.doi.org/10.1210/endo.141.12.7806.

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Abstract Glucose homeostasis in mammals is maintained by insulin secretion from the β-cells of the islets of Langerhans. Type 2 diabetes results either from primary β-cell failure alone and/or a failure to secrete enough insulin to overcome insulin resistance. Here, we show that continuous infusion of glucagon-like peptide-1 (7–36) (GLP-1; an insulinotropic agent), to young and old animals, had effects on the β-cell of the pancreas other than simply on the insulin secretory apparatus. Our previous studies on a rodent model of glucose intolerance, the aging Wistar rat, show that a plateau in is
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Wiebe, Peter O., Jay D. Kormish, Venus T. Roper, et al. "Ptf1a Binds to and Activates Area III, a Highly Conserved Region of the Pdx1 Promoter That Mediates Early Pancreas-Wide Pdx1 Expression." Molecular and Cellular Biology 27, no. 11 (2007): 4093–104. http://dx.doi.org/10.1128/mcb.01978-06.

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ABSTRACT The critical pancreatic transcription factor Pdx1 is expressed throughout the pancreas early but enriched in insulin-producing β cells postnatally. Previous studies showed that the 5′ conserved promoter regions areas I and II (Pdx1 PB) direct endocrine cell expression, while an adjacent region (Pdx1 XB) containing conserved area III directs transient β-cell expression. In this study, we used Cre-mediated lineage tracing to track cells that activated these regions. Pdx1 PBCre mediated only endocrine cell recombination, while Pdx1 XBCre directed broad and early recombination in the deve
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Dissertations / Theses on the topic "Β-cell of pancreas"

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Papadopoulou, Stella. "FGFs and Wnts in pancreatic growth and β-cell function". Doctoral thesis, Umeå universitet, Umeå centrum för molekylär medicin (UCMM), 2005. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-528.

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Mesenchymal-epithelial interactions are pivotal for proper pancreatic growth and development. The pancreatic progenitor cells present in the early pancreatic anlagen proliferate and eventually give rise to all pancreatic cell types. The Fibroblast Growth Factor 2b (FGFR2b) high-affinity ligand Fibroblast Growth Factor 10 (FGF10) has been linked to pancreatic epithelial cell proliferation and we have previously shown that Notch signalling controls pancreatic cell differentiation via lateral inhibition. By overexpressing FGF10 under the control of the Ipf1/Pdx1 promoter in mice, we have shown th
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Kassem, Mohamad. "Etude in vivo et in vitro du vieillissement des îlots pancréatiques : impact de la sénescence endothéliale et des microparticules sur la fonction des îlots." Thesis, Strasbourg, 2017. http://www.theses.fr/2017STRAJ007/document.

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Ce travail scientifique a abordé la problématique du vieillissement des îlots pancréatiques et l’effet de la senescence endothéliale et des microparticules (MPs) sur la fonction des îlots. Nous avons exploré l’impact du vieillissement du pancréas sur la morphologie, le devenir et la fonction de l’îlot pancréatique par analyse comparative entre pancréas de rats jeunes et d’âge moyen et le rôle des MPs endothéliales pro-sénescentes sur la fonction des îlots et leur sénescence prématurée. Nos résultats in vivo montrent que le pancréas est un organe précocement sensible au stress oxydant s’accumul
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Cohrs, Christian M., Julia K. Panzer, Denise M. Drotar та ін. "Dysfunction of Persisting β Cells Is a Key Feature of Early Type 2 Diabetes Pathogenesis". Elsevier, 2020. https://tud.qucosa.de/id/qucosa%3A73294.

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Type 2 diabetes is characterized by peripheral insulin resistance and insufficient insulin release from pancreatic islet β cells. However, the role and sequence of β cell dysfunction and mass loss for reduced insulin levels in type 2 diabetes pathogenesis are unclear. Here, we exploit freshly explanted pancreas specimens from metabolically phenotyped surgical patients using an in situ tissue slice technology. This approach allows assessment of β cell volume and function within pancreas samples of metabolically stratified individuals. We show that, in tissue of pre-diabetic, impaired glucose-to
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Hoarau, Emmanuelle. "Etude du rôle des espèces réactives de l'oxygène dans le développement du pancréas." Thesis, Sorbonne Paris Cité, 2015. http://www.theses.fr/2015PA05T007.

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Le pancréas est un organe hétérogène composé d’une partie exocrine, responsable de la synthèse d’enzymes pour la digestion, et d’une partie endocrine, essentielle pour l’homéostasie glucidique. Notamment la sécrétion d’insuline par les cellules β contrôle la glycémie. Les dysfonctionnements des cellules β sont une des causes du diabète, première épidémie non infectieuse au monde. Il est actuellement possible d’en traiter les symptômes mais pas de le guérir. De nombreux laboratoires recherchent un protocole idéal de production de cellules β afin de pouvoir greffer ces cellules aux patients. L’i
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Müller, Laura Mara. "Study of novel molecular defects in human pancreas dysfunction." Doctoral thesis, Humboldt-Universität zu Berlin, 2021. http://dx.doi.org/10.18452/22597.

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Diabetes ist ein weltweites Problem, das durch den Verlust oder die Dysfunktion der Insulin-produzierenden β-Zellen des Pankreas verursacht wird. In seltenen Fällen entsteht Diabetes durch eine Mutation in einem einzigen Gen. Diese monogenetischen Formen des Diabetes können zur Identifizierung neuer Regulatoren der β-Zellen-Entwicklung und -Funktion beitragen. In der vorliegenden Arbeit habe ich neue putative Diabetes-assoziierte Gene untersucht, die zuvor durch „Next-Generation“ Sequenzierung in einer Gruppe von Kindern und Jugendlichen mit idiopathischem Diabetes festgestellt wurden. Insbe
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Sumners, Lindsay Hart. "Chickens from lines artificially selected for juvenile low and high body weight differ in glucose homeostasis and pancreas physiology." Diss., Virginia Tech, 2015. http://hdl.handle.net/10919/51238.

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Early pancreatectomy experiments performed in ducks and pigeons at the end of the 19th century revealed that avians, unlike mammals, do not display signs of diabetes. Relative to mammals, birds are considered hyperglycemic, displaying fasting blood glucose concentrations twice that of a normal human. While circulating levels of insulin are similar in avians and mammals, and structure and function of the insulin receptor are also conserved among vertebrate species, birds do not experience deleterious effects of chronic hyperglycemia as observed in mammals. Understanding avian glucose homeost
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Obeid, Joëlle. "Caractérisation de la fonction des β-arrestines dans les cellules β pancréatiques : recherche de nouvelles stratégies thérapeutiques pour le diabète de type 2". Thesis, Montpellier, 2018. http://www.theses.fr/2018MONTT066.

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Les pertes de la fonction et de la masse des cellules beta pancréatiques jouent un rôle central dans le diabète de type 2 (DT2). Les beta-arrestines 1 et 2 (ARRB1 et ARRB2), sont impliquées dans la sécrétion et/ou la survie des cellules beta pancréatiques.Dans une première étude, afin de caractériser précisément la fonction d’ARRB1 dans les cellules beta pancréatiques, nous avons eu pour objectif de générer des souris invalidées spécifiquement dans ces cellules en utilisant le système Cre/lox sous le contrôle du promoteur Ins1. Des études avaient été publiées à partir des deux lignées Ins1Cre-
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Guez, Fanny. "Etude des mécanismes moléculaires impliqués dans le cycle cellulaire des cellules β pancréatiques humaines". Thesis, Paris 5, 2013. http://www.theses.fr/2013PA05T094.

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Le diabète est une maladie qui touche 347 millions de personnes dans le monde (90% ayant un diabète de type 2) (OMS, septembre 2012). Elle se définit par une perturbation de la régulation de l’homéostasie glucidique avec un déficit dans la fonction des cellules ß du pancréas. Dans le diabète de type 1, ce déficit est provoqué par une destruction autoimmune. Dans le diabète de type 2, il est dû à une insulino-résistance périphérique conduisant à un épuisement des cellules ß qui ne peuvent plus maintenir leur fonction. Une stratégie pour restaurer une masse fonctionnelle de cellules ß est, soit
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Auffret, Julien. "Impact des hormones lactogènes sur la cellule β pancréatique et l’adipocyte". Thesis, Paris 11, 2012. http://www.theses.fr/2012PA11T087/document.

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Pour étudier l’impact de la signalisation de la prolactine (PRL), une hormone impliquée dans la proliférationcellulaire sur l’adipocyte et la cellule β pancréatique, deux types cellulaires impliqués dans la balanceénergétique, nous avons caractérisé le phénotype de souris déficientes en récepteur de la PRL (R PRL-/-) sousdifférentes conditions physiopathologiques. Dans un premier temps, nous avons étudié l’impact du R PRL sur ledéveloppement d’une obésité induite par un régime obésogène. Dans un deuxième temps, nous nous sommesintéressés à l’impact du R PRL sur l’ontogenèse des cellules β dura
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Blanc, Marina. "La protéine Bax Inhibitor 1 protège des désordres métaboliques et de la mort cellulaire programmée au sein des cellules β pancréatiques". Electronic Thesis or Diss., Université Côte d'Azur, 2022. http://theses.univ-cotedazur.fr/2022COAZ6031.

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L'obésité est un problème de santé publique majeur au niveau mondial. En France, plus de 50% de la population est en surpoids ou obèse. L'obésité s'accompagne de pathologies incluant le diabète de type 2 (DT2) dont la prévalence ne cesse d'augmenter corrélant à celle de l'obésité. La résistance à l'insuline au sein des tissus périphériques (foie, muscles, tissu adipeux) ainsi qu'une perte progressive des cellules β du pancréas, participent au développement du diabète de type 2. Les cellules β pancréatiques possèdent un Réticulum Endoplasmique (RE) très développé permettant de répondre efficace
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Book chapters on the topic "Β-cell of pancreas"

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Rickels, Michael R. "Defining Outcomes for β-Cell Replacement Therapy." In Transplantation of the Pancreas. Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-031-20999-4_65.

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Maulis, Matthew, and Roberto Gianani. "β-Cell Regeneration in Human Pancreas." In Advances in Experimental Medicine and Biology. Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-5441-0_23.

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Leahy, Jack L. "β-Cell Dysfunction and Chronic Hyperglycaemia." In Molecular Basis of Pancreas Development and Function. Springer US, 2001. http://dx.doi.org/10.1007/978-1-4615-1669-9_3.

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Bonner-Weir, Susan, and Gordon C. Weir. "Mechanisms of Postnatal β-Cell Mass Regulation." In Molecular Basis of Pancreas Development and Function. Springer US, 2001. http://dx.doi.org/10.1007/978-1-4615-1669-9_17.

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Hayek, Alberto, Gillian M. Beattie, and Fred Levine. "Gene Therapeutic Approaches for β-Cell Replacement." In Molecular Basis of Pancreas Development and Function. Springer US, 2001. http://dx.doi.org/10.1007/978-1-4615-1669-9_23.

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McDaniel, Michael L., Jerry R. Colca, Nirmala Kotagal, and Paul E. Lacy. "Regulation and Role of Intracellular Ca2+ in Insulin Secretion by the β Cell." In The Diabetic Pancreas. Springer US, 1985. http://dx.doi.org/10.1007/978-1-4757-0348-1_9.

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Evans, Julie C., Timothy M. Frayling, and Andrew T. Hattersley. "Clinical Consequences of Defects in β-Cell Genes." In Molecular Basis of Pancreas Development and Function. Springer US, 2001. http://dx.doi.org/10.1007/978-1-4615-1669-9_19.

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Kulkarni, Rohit N., and C. Ronald Kahn. "Genetic models of Insulin Resistance:Alterations in β-cell biology." In Molecular Basis of Pancreas Development and Function. Springer US, 2001. http://dx.doi.org/10.1007/978-1-4615-1669-9_18.

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Efrat, Shimon. "Development of β-cell Lines for Transplantation in Type 1 Diabetes Mellitus." In Molecular Basis of Pancreas Development and Function. Springer US, 2001. http://dx.doi.org/10.1007/978-1-4615-1669-9_22.

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Brass, Barry J. "Endocrine pancreas: mechanisms of insulin secretion by the β-cells; interactions among insulin, glucagon and somatostatin." In Principles of Diabetes Mellitus. Springer US, 2004. http://dx.doi.org/10.1007/978-1-4757-6260-0_3.

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Conference papers on the topic "Β-cell of pancreas"

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Mendoza-Elias, Joshua E., José Oberholzer, and Yong Wang. "Microfluidics for Live-Cell Imaging Pancreatic Islets of Langerhans for Human Transplant." In ASME 2014 4th Joint US-European Fluids Engineering Division Summer Meeting collocated with the ASME 2014 12th International Conference on Nanochannels, Microchannels, and Minichannels. American Society of Mechanical Engineers, 2014. http://dx.doi.org/10.1115/fedsm2014-21159.

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Since the introduction of the Edmonton Protocol in 2000, islet transplantation has been emerging as promising therapy for Type I diabetes mellitus (T1DM) and currently is the only therapy that can achieve glycemic control without the need for exogenous insulin. Transplanting islet cells has several advantages over transplanting a whole pancreas in that it involves only a minor surgical procedure with low morbidity and mortality, and at a significantly lower cost. However, an obstacle to realizing this goal is a lack of an islet potency index as required by the U.S. Food and Drug Administration
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Reports on the topic "Β-cell of pancreas"

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Yibchok-anun, Sirinthorn, Wijit Banlunara, and Sirichai Adisakwattana. Antidiabetic effects, mechanisms of of p-methoxy-trans-cinnamic acid. Faculty of Veterinary Science, Chulalongkorn University, 2008. https://doi.org/10.58837/chula.res.2008.81.

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p-Methoxycinnamic acid (p-MCA) is a cinnamic acid derivative that shows various pharmacologic actions such as neuroprotective and hepatoprotective activities. To examine the insulinotropic activity of p-MCA, the perfused rat pancreas and a pancreatic β-cell line, INS-1 were used in the studies. P-MCA increased insulin secretion from the perfused rat pancreas and INS-1 cells in a concentration-dependent manner. In addition, p-MCA increased intracellular Ca²⁺ concentration ([Ca²⁺]i) in INS-1 cells. The p-MCA-induced insulin secretion and rise in [Ca²⁺]i were markedly inhibited in the absence of
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