Relevant bibliographies by topics / Beta-cell mass

Contents

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

Academic literature on the topic 'Beta-cell mass'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "Beta-cell mass"

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Bach, Jean-François, Christian Boitard, and Claude Carnaud. "Preservation of beta cell mass." Journal of Autoimmunity 3, no. 1 (February 1990): 45. http://dx.doi.org/10.1016/0896-8411(90)90010-p.

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Bouwens, Luc, and Ilse Rooman. "Regulation of Pancreatic Beta-Cell Mass." Physiological Reviews 85, no. 4 (October 2005): 1255–70. http://dx.doi.org/10.1152/physrev.00025.2004.

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Beta-cell mass regulation represents a critical issue for understanding diabetes, a disease characterized by a near-absolute (type 1) or relative (type 2) deficiency in the number of pancreatic beta cells. The number of islet beta cells present at birth is mainly generated by the proliferation and differentiation of pancreatic progenitor cells, a process called neogenesis. Shortly after birth, beta-cell neogenesis stops and a small proportion of cycling beta cells can still expand the cell number to compensate for increased insulin demands, albeit at a slow rate. The low capacity for self-replication in the adult is too limited to result in a significant regeneration following extensive tissue injury. Likewise, chronically increased metabolic demands can lead to beta-cell failure to compensate. Neogenesis from progenitor cells inside or outside islets represents a more potent mechanism leading to robust expansion of the beta-cell mass, but it may require external stimuli. For therapeutic purposes, advantage could be taken from the surprising differentiation plasticity of adult pancreatic cells and possibly also from stem cells. Recent studies have demonstrated that it is feasible to regenerate and expand the beta-cell mass by the application of hormones and growth factors like glucagon-like peptide-1, gastrin, epidermal growth factor, and others. Treatment with these external stimuli can restore a functional beta-cell mass in diabetic animals, but further studies are required before it can be applied to humans.
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Prasadan, Krishna, Chiyo Shiota, Xiao Xiangwei, David Ricks, Joseph Fusco, and George Gittes. "A synopsis of factors regulating beta cell development and beta cell mass." Cellular and Molecular Life Sciences 73, no. 19 (April 22, 2016): 3623–37. http://dx.doi.org/10.1007/s00018-016-2231-0.

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Dybala, Michael P., Scott K. Olehnik, Jonas L. Fowler, Karolina Golab, J. Michael Millis, Justyna Golebiewska, Piotr Bachul, Piotr Witkowski, and Manami Hara. "Pancreatic beta cell/islet mass and body mass index." Islets 11, no. 1 (January 2, 2019): 1–9. http://dx.doi.org/10.1080/19382014.2018.1557486.

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Kalra, Sanjay, and Yashdeep Gupta. "Beta-cell Insufficiency." European Endocrinology 13, no. 02 (2017): 51. http://dx.doi.org/10.17925/ee.2017.13.02.51.

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‘B eta-cell failure’ is a frequently used term to describe the structural and functional inability of the cells to fulfil their metabolic responsibility. This editorial reviews the anatomy and physiology of the beta cell, and describes factors which regulate this. The authors focus on semantics, comparing the phrases ‘beta-cell failure’, ‘functional mass’, and ‘beta-cell insufficiency’. They suggest the use of ‘beta-cell insufficiency’, with descriptors such as ‘partial’ and ‘complete’, or ‘reversible’ and ‘irreversible’, to convey betacell dysfunction in type 2 diabetes. A three-phase taxonomic structure: beta-cell sufficiency, partial/reversible beta-cell insufficiency and complete/irreversible beta-cell insufficiency, is proposed as a tool to understand pathophysiology and facilitate therapeutic decision-making.
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Bock, T., A. Kyhnel, B. Pakkenberg, and K. Buschard. "The postnatal growth of the beta-cell mass in pigs." Journal of Endocrinology 179, no. 2 (November 1, 2003): 245–52. http://dx.doi.org/10.1677/joe.0.1790245.

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Studies of the postnatal growth of the beta-cell mass in rats have revealed some unexpected and apparently paradoxical results, the most prominent being a beta-cell mass plateau in the early phase of life. We have studied the postnatal growth of the beta-cell mass in the domestic pig to investigate its development in a larger mammal. The pancreases from a total of 86 male pigs from 5 to 100 days of age were studied. The beta-cell mass increased linearly from day 5 to day 40, reached a plateau from day 40 to day 60, and then increased further into adulthood. The relative beta-cell mass (beta-cell mass per body mass) was increased in the early postnatal period but reached a constant level from day 60, after which there was a linear relationship between the beta-cell mass and the body mass. There were high rates of both beta-cell apoptosis and mitosis at 50 and 60 days of age, while the Volume-weighted mean islet Volume increased from birth and reached a plateau at approximately 60 days of age. A beta-cell mass plateau early in life accompanied by a wave of beta-cell apoptosis coinciding with the relative beta-cell mass decreasing to reach a constant level, and a linear relationship between the beta-cell mass and the body mass in later life is exactly what has previously been reported in rats. The coincidence of these events in both rats and pigs, although occurring at different ages in the two species, suggests a causal relationship as previously suggested in a proposed explanatory model for postnatal beta-cell growth.
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Nacher, V., M. Pérez-Maraver, R. Jara, J. Soler, and E. Montanya. "Beta cell mass after transplantation of cryopreserved islets." Transplantation Proceedings 31, no. 6 (September 1999): 2560. http://dx.doi.org/10.1016/s0041-1345(99)00500-x.

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Saudek, Frantisek, Carl-Henrik Brogren, and Srirang Manohar. "Imaging the Beta-Cell Mass: Why and How." Review of Diabetic Studies 5, no. 1 (2008): 6–12. http://dx.doi.org/10.1900/rds.2008.5.6.

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Kim, Hail, Yukiko Toyofuku, Francis C. Lynn, Eric Chak, Toyoyoshi Uchida, Hiroki Mizukami, Yoshio Fujitani, et al. "Serotonin regulates pancreatic beta cell mass during pregnancy." Nature Medicine 16, no. 7 (June 27, 2010): 804–8. http://dx.doi.org/10.1038/nm.2173.

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Prato, S. Del, W. J. Wishner, J. Gromada, and B. J. Schluchter. "beta-Cell mass plasticity in type 2 diabetes." Diabetes, Obesity and Metabolism 6, no. 5 (September 2004): 319–31. http://dx.doi.org/10.1111/j.1462-8902.2004.00360.x.

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Dissertations / Theses on the topic "Beta-cell mass"

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Zhou, Luxian. "Functional study of beta cell mass regulation in vivo." Thesis, University of Warwick, 2010. http://wrap.warwick.ac.uk/34648/.

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Those key factors, supporting re-expansion of beta cell numbers after injury in various model systems, are largely unknown. Insulin-like growth factor II (IGF-II), an important member from the IGF family, plays a critical role in supporting cell division and differentiation during ontogeny, but its role in the adult is not known. In this study we investigated the effect of IGF-II in beta cell regeneration. An in vivo model of „switchable‟ c-Myc-induced beta cell ablation, pIns-c-MycERTAM (Pelengaris, Khan et al. 2002), which exhibits beta cell regeneration once Myc is deactivated, is employed in this study of the IGF-II function. Here we show for the first time that IGF-II is re-expressed in the adult pancreas following beta cell injury. Moreover, whereas a 90% beta cell ablation was induced in both pIns-cMycERTAM/IGF-II WT (MIG) and pIns-cMycERTAM/IGF-II KO (MIGKO) mice, a recovery up to 3 months was performed. By investigating the beta cell mass and numbers our results demonstrate that re-expression of IGF-II is important in supporting the beta cell regeneration in adult mice. Moreover this study supports the utility of using such ablation-recovery models for identifying other potential factors critical for underpinning successful beta cell regeneration in vivo. Both Myc and PML contribute to the regulation of apoptosis. Recent studies suggest that Myc and PML may interact at several levels in control of cell fate. Here we examined whether loss of the PML protein, which has been shown to regulate apoptosis via the p53 pathway, can prevent or affect c-Myc-induced beta cell apoptosis in pIns-c-MycERTAM transgenic mice. Together with the Applied Neuroinformatics Group at the University of Bielefeld in Germany, we have been developing and validating a machine learning based system to analyze beta and alpha cell numbers (Herold, Zhou et al. 2009). Comparative results between traditional techniques and this new method are presented here.
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Austin, Emily. "Homeostatic regulation of induced [beta]-cell mass expansion in mice." Thesis, McGill University, 2006. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=101701.

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Current therapies do not prevent the devastating complications associated with type 1 and 2 diabetes. Novel therapies seek to restore a functional beta-cell mass through stimulating endogenous beta-cell mass expansion. Whilst there is considerable evidence that the beta-cell mass is under homeostatic regulation in the normal pancreas, it is unclear if such regulation exists in the context of induced beta-cell mass expansion. The aim of this study was to demonstrate that beta-cell mass expansion resulting from the induction of islet cell neogenesis is subject to long-term homeostatic control in the normoglycemic mouse adult pancreas.
A pentadecapeptide fragment of Islet Neogenesis Associated Protein (INGAP 104-118) was administered daily to adult C57BL/6J mice for 12 weeks. Four animals from the INGAP104-118 treatment group and control group were sacrificed each week. The pancreas was removed from each mouse and stained for insulin. beta-cell mass was calculated as the organ weight multiplied by the percent of insulin+ area of total tissue area. Contrary to our expectations, there was no change in the total beta-cell mass in INGAP104-118-treated animals compared to control. Reanalysis of the stained tissue sections was preformed, and insulin+ structures were classified as being: (1) a duct islet, (2) a cluster of insulin+ cells, or (3) a mature islet. The density (#/mm2) of duct islets, clusters, and total structures in INGAP 104-118-treated animals was significantly increased; conversely, the density of mature islets was significantly decreased. The increase in cluster density suggests that INGAP104-118 induced neogenesis in the pancreas of treated animals. Poisson regression revealed 9th order polynomial time trends in the structure densities. Though these time trends differed between the classes of structures, they were identical in INGAP104-118 and control animals for each class of structure, suggesting an external stimulus was acting equally on both groups.
While this study did not determine if there is homeostatic regulation of induced beta-cell mass expansion, it did reveal important aspects for the design of a future study to address this issue. The definitions for structure classification must be well-established and rates of beta-cell replication should be determined.
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Lipsett, Mark Andrew. "Pharmacological induction of Islet Neogenesis and subsequent beta-cell mass expansion." Thesis, McGill University, 2006. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=103170.

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Current therapies for diabetes mellitus are insufficient to prevent the devastating complications associated with this disease. A novel approach for the treatment of diabetes is the restoration of an insulin-producing beta-cell mass through the stimulation of endogenous progenitor cells. Thus, the aim of this thesis was to determine if pharmacological initiation of islet neogenesis and subsequent beta-cell mass expansion will lead to the reversal of hyperglycaemia in a response that is under homeostatic regulation and has efficacy in humans.
A pentadecapeptide fragment of Islet Neogenesis Associated Protein (INGAP 104-108), was administered to normoglycaemic hamsters and was found to result in an expanded beta-cell mass as measured by immunohistochemical morphometric analysis. This expansion was shown to occur through the transformation of duct- and acinar-associated progenitors. In order to determine if this therapeutic approach would be effective in mammals other than hamsters, INGAP 104-108 was administered to normoglycaemic mice, dogs and monkeys, hyperglycaemic mice, and to human pancreatic tissue cultures.
INGAP104-108 administration led to a dose-dependent increase of beta-cell mass in mice, with similar trends observed in dogs. Similarly, administration of INGAP104-108 to normoglycaemic monkeys for 90 days resulted in profound areas of islet neogenesis. Administration of INGAP104-108 to diabetic mice resulted in restoration of euglycaemia and a dramatic increase in beta-cell mass. Furthermore, INGAP104-108 administration to cultured human acinar tissue, led to the formation of insulin-producing islet-like structures. These results suggest that INGAP 104-108 therapy has the ability to reverse a diabetic state and could be effective in humans. However, it was necessary to determine whether the continual stimulation of islet neogenesis through INGAP 104-108 administration is a safe therapeutic approach.
The beta-cell mass dynamics of euglycaemic mice administered INGAP 104-108 at various doses for 31 or 90 days were determined. beta-cell mass was greatly increased at 31 days of therapy, though by 90 days of therapy there was no difference in total beta cell mass between all treatment groups. However, there were marked instances of islet neogenesis in mice treated with INGAP104-108 for 90 days. This elevation in islet neogenesis was tempered by decreased beta-cell replication and increased beta-cell apoptosis, resulting in no overall difference in total beta-cell mass. These results suggest that inherent homeostatic regulation persisted to maintain a net beta-cell mass that matched the physiological need, even in the setting of continual induction of islet neogenesis.
INGAP104-108 therapy has been shown to expand the insulin-producing beta-cell mass in a safe homeostatic manner and reverse diabetic hyperglycaemia. These findings suggest that a novel pharmacological agent for the successful stimulation of beta-cell mass expansion is within reach, enabling new therapeutic modalities for the treatment of diabetes.
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Fieldus, Warren Edward. "Beta-cell mass dynamics in the BioBreeding rat model of autoimmune diabetes." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape9/PQDD_0024/MQ51340.pdf.

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Mészáros, Gergő. "CaMK1D controls β-cell mass and glucose homeostasis." Thesis, Strasbourg, 2015. http://www.theses.fr/2015STRAJ035.

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Le diabètes mellites de type 2 (T2DM) est caractérisé par une hyperglycémie provenant d’une dérégulation de la sécrétion d’insuline combinée avec une altération de l’action de l’insuline. CaMK1D est un nouveau gène identifié, dont le rôle reste à explorer. Dans l’étude exposée ici, j’ai montré que CaMK1D a un effet majeur sur la régulation du glucose. J’ai observé une réduction exceptionnelle des taux de glucose sanguins à jeun, ce qui entraine une amélioration globale de la tolérance au glucose. Les souris mutantes montrent une augmentation conséquente dans les niveaux sanguins d’insuline. Les souris invalidées pour CaMK1D présentent des ilots pancréatiques de taille plus importante due à une hypertrophie des cellules béta. De plus, les souris mutantes sont protégées contre la stéatose hépatique. Dans l’ensemble, mon travail met en évidence le nouveau rôle clé de CaMK1D chez les cellules béta et apporte plus de compréhension quant à son rôle lors du développement du T2DM
Type 2 diabetes mellitus (T2DM) is characterized by hyperglycemia resulting from defects in insulin secretion in combination with impaired insulin action. CaMK1D represents one potential candidate gene, the in vivo function remained elusive. In this work, I have found that CaMK1D plays a central role in blood glucose regulation. Pancreas-specific CaMK1D knockout mice display dramatically reduced fasting blood glucose levels leading to an overall improved glucose tolerance. CaMK1D knockout mice show markedly higher ad libitum and fasting insulin levels. Interestingly, pancreas-specific CaMK1D knockout mice display islet hyperplasia caused by beta-cell hypertrophy. Furthermore, conditional knockout mice are protected against high-fat feeding-induced hepatic steatosis. Overall, my work establishes an essential role of CaMK1D in pancreatic beta-cells and provides further understanding about its role in the development of T2DM
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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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Eriksson, Olof. "Imaging Islets of Langerhans by Positron Emission Tomography : Quantification of Beta-Cell Mass in the Native Pancreas and the Islet Graft." Doctoral thesis, Uppsala universitet, Enheten för radiologi, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-136372.

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Type 1 and 2 Diabetes Mellitus are a growing health problem throughout the world. There is an increasing  need for methodologies, which are both reliable and non-invasive to measure the amount of insulin-producing tissue (Beta-cell mass, or BCM), as well as rapidly quantify changes in the BCM due to the onset of disease, beta-cell replacement therapy, or other treatments. Positron Emission Tomography (PET) is a non-invasive, quantitative functional imaging technique which can be used to study dynamical or static processes inside the body. In this thesis, we present a study protocol for in vivo imaging of the most common form of beta- cell replacement therapy; islet transplantation. Islets were labeled with the PET tracer, 2-deoxy-2[18F]fluoro-D-glucose ([18F]FDG), and administered intra-portally, while the recipient was monitored by PET/CT. The hepatic distribution of the islets was highly heterogeneous, and around 25% (human) or 50% (porcine) of the administered islets could not be found in the liver after completed transplantation, confirming previous reports of considerable cell injury during the procedure leading to low hepatic engraftment. Native BCM in the pancreas can potentially be quantified using a PET tracer with sufficiently high specificity, but the major obstacle is the relative low amounts of insulin producing tissue (only 1-2% of the pancreatic volume). Two tetrabenazine analogues, [18F]FE-(+)-DTBZ and [18F]FE-(+)-DTBZ-d4, are ligands to VMAT2, which is expressed in islet tissue. Both analogues were investigated and characterized as potential BCM imaging agents both in vitro and in vivo.  Both tracers exhibited high preferential binding to islet tissue compared to exocrine pancreatic tissue. However, the specificity was not high enough to overcome the obscuring exocrine signal in vivo (7-10% of the signal originating from specific islet tracer uptake). This thesis demonstrates that it is possible to quantitatively assess islet transplantation by PET imaging. In vivo determination of native pancreatic BCM is, in theory, possible with both [18F]FE-(+)-DTBZ and [18F]FE-(+)-DTBZ-d4, but tracer analogues with higher islet specificity is needed for quantification of smaller BCM changes with physiological impact.
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Bowden, Gregory David [Verfasser]. "The Design, Synthesis, and Radiosynthesis Optimization of Novel Approaches towards the In Vivo PET Imaging of Beta Cell Mass / Gregory David Bowden." Tübingen : Universitätsbibliothek Tübingen, 2021. http://d-nb.info/1239644361/34.

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Espes, Daniel. "Engraftment of Pancreatic Islets in Alternative Transplantation Sites and the Feasibility of in vivo Monitoring of Native and Transplanted Beta-Cell Mass." Doctoral thesis, Uppsala universitet, Institutionen för medicinsk cellbiologi, 2016. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-282953.

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Islet transplantation is a possible curative treatment for type 1 diabetes (T1D). Currently the liver dominates as implantation site, despite the many challenges encountered at this site. Acute hypoxia in islets transplanted to muscle and omentum, two possible alternative sites, was prevailing. However, it was rapidly reversed at both implantation sites, in contrast to when islets were transplanted intraportally. At the intramuscular site hypoxia was further relieved by co-transplantation of an oxygen carrier, polymerized hemoglobin, which also improved the functional outcome. The complement system was activated after islet transplantation to muscle, but did not hamper graft function. Both mouse and human islets transplanted to omentum become well re-vascularized and have a functional blood flow and oxygenation comparable with that of endogenous islets. Animals transplanted with islets to the omentum had a superior graft function compared with animals receiving intraportal islet grafts. Alloxan-diabetic animals were cured with a low number of islets both when the islets were implanted in the omentum and muscle. The islet grafts responded adequately to both glucose and insulin and displayed a favorable mRNA gene expression profile. A challenge in diabetes research and in islet transplantation is that there are no established techniques for quantifying beta-cell mass in vivo. By using radiolabeled Exendin-4, a GLP-1 receptor agonist, beta-cell mass after transplantation to muscle of mice was quantified. The results may well be translated to the clinical setting. By comparing the pancreatic accumulation of [11C]5-hydroxy tryptophan ([11C]5-HTP) as detected by positron emission tomography (PET) in T1D patients with that of healthy controls, a 66% decrease was observed. This may in fact represent the loss of beta-cells, taking into account that other cells within the islets of Langerhans are largely unaffected in T1D.  In conclusion, the data presented support the use of alternative implantation sites for islet transplantation. In addition to improving the functional outcome this may enable more transplantations since the number of transplanted islets may be reduced. The techniques investigated for quantifying transplanted and endogenous beta-cell mass may greatly improve our knowledge of the pathophysiology of T1D and become a valuable tool for evaluation of beta-cell mass.
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Cohrs, Christian M., Julia K. Panzer, Denise M. Drotar, Stephen J. Enos, Nicole Kipke, Chunguang Chen, Robert Bozsak, et al. "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-tolerant subjects, β cell volume is unchanged, but function significantly deteriorates, exhibiting increased basal release and loss of first-phase insulin secretion. In individuals with type 2 diabetes, function within the sustained β cell volume further declines. These results indicate that dysfunction of persisting β cells is a key factor in the early development and progression of type 2 diabetes, representing a major target for diabetes prevention and therapy.
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Book chapters on the topic "Beta-cell mass"

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Faintuch, Bluma Linkowski, and Salomao Faintuch. "Progress in Noninvasive Beta-Cell Mass Imaging." In Obesity and Diabetes, 631–39. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-53370-0_46.

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Téllez, Noèlia, and Eduard Montanya. "Determining Beta Cell Mass, Apoptosis, Proliferation, and Individual Beta Cell Size in Pancreatic Sections." In Methods in Molecular Biology, 313–37. New York, NY: Springer US, 2020. http://dx.doi.org/10.1007/978-1-0716-0385-7_21.

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Montaña, Eduard, Susan Bonner-Weir, and Gordon C. Weir. "Beta Cell Replication and Mass in Islet Transplantation." In Advances in Experimental Medicine and Biology, 421–27. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4899-1819-2_55.

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Montanya, Eduard, and Noèlia Téllez. "Pancreatic Remodeling: Beta-Cell Apoptosis, Proliferation and Neogenesis, and the Measurement of Beta-Cell Mass and of Individual Beta-Cell Size." In Methods in Molecular Biology, 137–58. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-59745-448-3_11.

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Bartolome, Alberto, and Carlos Guillén. "Role of the Mammalian Target of Rapamycin (mTOR) Complexes in Pancreatic β-Cell Mass Regulation." In The Pancreatic Beta Cell, 425–69. Elsevier, 2014. http://dx.doi.org/10.1016/b978-0-12-800174-5.00017-x.

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Robertson, R. "Metabolic Measures of Islet Function and Mass After Islet Transplantation." In Islet Transplantation and Beta Cell Replacement Therapy, 193–201. CRC Press, 2007. http://dx.doi.org/10.3109/9781420016512-11.

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Mozar, Anais, Hugo Lin, Katoura Williams, Nagesh Guthalu, Anthony Otero, Connie Chin, Andrew F. Stewart, Adolfo Garcia Ocana, and Rupangi C. Vasavada. "Parathyroid Hormone-Related Protein (PTHrP) 1-36 Markedly Enhances β-Cell Regeneration and Completely Restores β-Cell Mass in a Mouse Model of Partial Pancreatectomy." In BASIC/TRANSLATIONAL - Beta Cell Biology, OR01–2—OR01–2. The Endocrine Society, 2011. http://dx.doi.org/10.1210/endo-meetings.2011.part1.or2.or01-2.

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Hong, JY, M. Brissova, Q. Cai, A. Shostak, and AC Powers. "Proliferating Intra-Islet Endothelial Cells Affect Beta Cell Mass and Regeneration." In The Endocrine Society's 92nd Annual Meeting, June 19–22, 2010 - San Diego, OR32–2—OR32–2. Endocrine Society, 2010. http://dx.doi.org/10.1210/endo-meetings.2010.part3.or2.or32-2.

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Huang, Yao, and Yongchang Chang. "Regulation of Pancreatic Islet Beta-Cell Mass by Growth Factor and Hormone Signaling." In Progress in Molecular Biology and Translational Science, 321–49. Elsevier, 2014. http://dx.doi.org/10.1016/b978-0-12-800101-1.00010-7.

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Chavey, Audrey, Jamileh Movassat, and Bernard Porth. "Impact and Mechanisms of Pancreatic Beta-Cell Mass Programming by Maternal Diabetes - Insight from Animal Model Studies." In Gestational Diabetes. InTech, 2011. http://dx.doi.org/10.5772/23027.

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Conference papers on the topic "Beta-cell mass"

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Gu, Chenjuan, Min Li, Qingyun Li, and Ning Li. "Changes Of Islet Beta Cell Mass And MTOR/HIF1/VEGF-A Pathway In Mice Exposed To Intermittent Hypoxia." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a5371.

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Deden, L., M. Boss, E. Aarts, F. Berends, H. de Boer, E. Hazebroek, and M. Gotthardt. "Pancreatic uptake of radiolabeled exendin as a measure of beta cell mass in T2DM before and after bariatric surgery." In NuklearMedizin 2021 – digital. Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0041-1727078.

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Nguyen, Thienly, Parash Parajuli, Asrar Ahmad, Purba Singh, Sailaja Eragameddy, Gopalakrishnan Ramakrishnan, Laurence Levy, et al. "Abstract B32: Restoration of beta cell mass as a synthetic lethal strategy to overcome oncogenic Kras-driven pancreatic ductal adenocarcinoma." In Abstracts: AACR Precision Medicine Series: Opportunities and Challenges of Exploiting Synthetic Lethality in Cancer; January 4-7, 2017; San Diego, CA. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-8514.synthleth-b32.

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Hollenbach, M., N. Klöting, I. Sommerer, J. Lorenz, M. Heindl, J. Mössner, M. Blüher, and A. Hoffmeister. "p8 deficiency lead to elevated pancreatic beta cell mass but does not contribute to insulin resistance in mice fed with high fat diet." In Viszeralmedizin 2017. Georg Thieme Verlag KG, 2017. http://dx.doi.org/10.1055/s-0037-1604898.

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Al-Meer, S. H., M. A. Amr, A. I. Helal, and A. T. Al-Kinani. "Ultratrace Determination of Strontium-90 in Environmental Soil Samples From Qatar by Collision/Reaction Cell-Inductively Coupled Plasma Mass Spectrometry (CRC-ICP-MS/MS)." In ASME 2013 15th International Conference on Environmental Remediation and Radioactive Waste Management. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/icem2013-96160.

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Abstract:
Because of the very low level of 90Sr in the environmental soil samples and its determination by beta counting may take several weeks, we developed a procedure for ultratrace determination of 90Sr using collision reaction cell-inductively coupled plasma tandem mass spectrometry (CRC-ICP-MS/MS, Agilent 8800). Soil samples were dried at 105 °C and then heated in a furnace at 550 °C to remove any organics present. 500 g of each soil samples were aliquoted into 2000 ml glass beakers. Each Soils samples were soaked in 2 ppm Sr solution carrier to allow determination of chemical yield. The solid to liquid ratio was 1:1. Finally the soil samples were dried at 105 °C. Five hundred milliliters concentrated nitric acid and 250 ml hydrochloric acid volumes were added on 500 g soil samples. The samples were digested on hot plate at 80 °C to prevent spraying with continuous manual mixing. The leachate solution was separated. The solids were rinsed with 500 ml deionized water, warmed on a hot plate and the leachate plus previous leachate were filtered and the total volume was reduced to 500 ml by evaporation. Final leachate volume was transferred to a centrifuge tubes. The centrifuge tubes were centrifuged at 3,500 rpm for 10 min. The leachate was transferred to a 1 L beaker and heated on a hot plate to evaporate the leachate to dryness. The reside was re-dissolved in 100 ml of 2% HNO3 and reduced by evaporation to 10 mL. The solution was measured directly by CRC-ICP-MS/MS by setting the first quadruple analyzer to m/z 90 and introducing oxygen gas into the reaction cell for elimination isobar interference from zirconium-90. The method was validated by measurements of standard reference materials and applied on environmental soil samples. The overall time requirement for the measurement of strontium-90 by CRC-ICP-MS/MS is 2 days, significantly shorter than any radioanalytical protocol currently available.
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Haugh, Matthew G., and Laoise M. McNamara. "The Role of Integrins in Osteocyte Response to Mechanical Stimulus." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80126.

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Bone is an exceptional material that is efficiently lightweight, possesses excellent mechanical strength and can also adapt itself in response to changes in physical activity by means of coordinated physiological processes known as modelling and remodelling. The response of bone to mechanical loading is thought to be regulated by mechanosensitive osteocyte cells that can direct the alteration of bone mass, by osteoblasts and osteoclasts, and thereby play an important role in optimizing bone strength. The mechanisms by which osteocytes sense their mechanical environment are not well understood. It has been proposed that integrin-based (αVβ3) attachments to ECM on osteocyte cell processes may facilitate mechanosensation in osteocytes [1,2]. While previous studies have shown that integrin beta;1 plays an important role in response to mechanical stimulus, the role of integrin αVβ3 in osteocyte mechanotransduction has yet to be investigated [3,4].
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"Immature teratoma." In 16th Annual International Conference RGCON. Thieme Medical and Scientific Publishers Private Ltd., 2016. http://dx.doi.org/10.1055/s-0039-1685328.

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Introduction: Immature teratoma represents 3% of all teratomas, 1 % of all ovarian cancers and 20% of malignant ovarian germ cell tumors. It is found either in pure form or as a component of a mixed germ cell tumor. It occurs essentially during the first two decades of life. According to WHO, immature teratoma is defined as a teratoma containing a variable amount of immature embryonal type neuroectodermal tissue Case: We present here a report of 23 years old unmarried female who presented with complaint of abdominal pain since 1 month and her CT scan done outside, showed fibroid uterus. She had history of typhoid fever 1 month back for which USG was done which suggested large uterine fibroid. On examination she was hemodynamically stable. On abdominal examination a non-tender supra-pubic mass of 24 weeks size with firm consistency, irregular margin was felt. On investigation CA 125 was 64.90 IU/L, LD- 223, beta HCG- 1.14. On MRI a large abdomino-pelvic lesion, likely left adnexal lesion with multiple cystic areas, with hemorrhage, with ascites and enlarged retroperitoneal lymph nodes with omental infiltration suggestive of a possibility of malignant germ cell tumor. In view of large ovarian tumor, possibly malignant decision for staging laparotomy was taken. Intra-operatively a large irregular vascular solid mass of 20 x 20 cms with bosselated appearance with few cystic lesions over it was seen, arising from left ovary and was sent for frozen section which reported malignant mature teratoma with components of immature teratoma. She underwent laparotomy with left salpingo-oophorectomy with right ovarian biopsy, omentectomy, appendectomy with B/L pelvic lymphadenectomy. Histopathology was suggestive of grade III immature teratoma. In view of grade III immature teratoma, she received chemotherapy (BEP regimen) post-operatively and is currently under follow up. Conclusion: This case reflects the importance of early diagnosis in cases of pelvic masses in young females. Fertility preservation should be considered in young women with germ cell tumors. Patients with grade II or III tumors or a mere advanced stage disease should be treated with adjuvant chemotherapy (BEP) in addition to surgery.
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