Journal articles: 'Beta-cell mass'

1

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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9

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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10

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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11

Sabir, Shakila, Ammara Saleem, Muhammad Akhtar, Muhammad Saleem, and Moosa Raza. "Increasing beta cell mass to treat diabetes mellitus." Advances in Clinical and Experimental Medicine 27, no. 9 (July 18, 2018): 1309–15. http://dx.doi.org/10.17219/acem/74452.

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12

Montaña, E., S. Bonner-Weir, and G. C. Weir. "Transplanted beta cell response to increased metabolic demand. Changes in beta cell replication and mass." Journal of Clinical Investigation 93, no. 4 (April 1, 1994): 1577–82. http://dx.doi.org/10.1172/jci117137.

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13

Wang, Chaoxun, Xiaopan Chen, Xiaoying Ding, Yanju He, Chengying Gu, and Ligang Zhou. "Exendin-4 Promotes Beta Cell Proliferation via PI3k/Akt Signalling Pathway." Cellular Physiology and Biochemistry 35, no. 6 (2015): 2223–32. http://dx.doi.org/10.1159/000374027.

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Background/Aims: Prevention of diabetes requires maintenance of a functional beta-cell mass, the postnatal growth of which depends on beta cell proliferation. Past studies have shown evidence of an effect of an incretin analogue, Exendin-4, in promoting beta cell proliferation, whereas the underlying molecular mechanisms are not completely understood. Methods: Here we studied the effects of Exendin-4 on beta cell proliferation in vitro and in vivo through analysing BrdU-incorporated beta cells. We also analysed the effects of Exendin-4 on beta cell mass in vivo, and on beta cell number in vitro. Then, we applied specific inhibitors of different signalling pathways and analysed their effects on Exendin-4-induced beta cell proliferation. Results: Exendin-4 increased beta cell proliferation in vitro and in vivo, resulting in significant increases in beta cell mass and beta cell number, respectively. Inhibition of PI3K/Akt signalling, but not inhibition of either ERK/MAPK pathway, or JNK pathway, significantly abolished the effects of Exendin-4 in promoting beta cell proliferation. Conclusion: Exendin-4 promotes beta cell proliferation via PI3k/Akt signaling pathway.

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Sekiguchi, Yukari, Junya Owada, Hisashi Oishi, Tokio Katsumata, Kaori Ikeda, Takashi Kudo, and Satoru Takahashi. "Noninvasive Monitoring of ^|^beta;-Cell Mass and Fetal ^|^beta;-Cell Genesis in Mice Using Bioluminescence Imaging." Experimental Animals 61, no. 4 (2012): 445–51. http://dx.doi.org/10.1538/expanim.61.445.

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15

Vetere, Amedeo, and Bridget K. Wagner. "Chemical Methods to Induce Beta-Cell Proliferation." International Journal of Endocrinology 2012 (2012): 1–8. http://dx.doi.org/10.1155/2012/925143.

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Pancreatic beta-cell regeneration, for example, by inducing proliferation, remains an important goal in developing effective treatments for diabetes. However, beta cells have mainly been considered quiescent. This “static” view has recently been challenged by observations of relevant physiological conditions in which metabolic stress is compensated by an increase in beta-cell mass. Understanding the molecular mechanisms underlining these process could open the possibility of developing novel small molecules to increase beta-cell mass. Several cellular cell-cycle and signaling proteins provide attractive targets for high throughput screening, and recent advances in cell culture have enabled phenotypic screening for small molecule-induced beta-cell proliferation. We present here an overview of the current trends involving small-molecule approaches to induce beta-cell regeneration by proliferation.

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Hutton, J. C., and H. W. Davidson. "Getting beta all the time: discovery of reliable markers of beta cell mass." Diabetologia 53, no. 7 (April 22, 2010): 1254–57. http://dx.doi.org/10.1007/s00125-010-1762-4.

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17

Inaishi, Jun, and Yoshifumi Saisho. "Beta-Cell Mass in Obesity and Type 2 Diabetes, and Its Relation to Pancreas Fat: A Mini-Review." Nutrients 12, no. 12 (December 16, 2020): 3846. http://dx.doi.org/10.3390/nu12123846.

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Type 2 diabetes (T2DM) is characterized by insulin resistance and beta-cell dysfunction. Although insulin resistance is assumed to be a main pathophysiological feature of the development of T2DM, recent studies have revealed that a deficit of functional beta-cell mass is an essential factor for the pathophysiology of T2DM. Pancreatic fat contents increase with obesity and are suggested to cause beta-cell dysfunction. Since the beta-cell dysfunction induced by obesity or progressive decline with disease duration results in a worsening glycemic control, and treatment failure, preserving beta-cell mass is an important treatment strategy for T2DM. In this mini-review, we summarize the current knowledge on beta-cell mass, beta-cell function, and pancreas fat in obesity and T2DM, and we discuss treatment strategies for T2DM in relation to beta-cell preservation.

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18

Chintinne, Marie, Geert Stangé, Bart Denys, Zhidong Ling, Peter In ‘t Veld, and Daniel Pipeleers. "Beta Cell Count Instead of Beta Cell Mass to Assess and Localize Growth in Beta Cell Population following Pancreatic Duct Ligation in Mice." PLoS ONE 7, no. 8 (August 30, 2012): e43959. http://dx.doi.org/10.1371/journal.pone.0043959.

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19

Golson, Maria, Courtney Warfield, and Maureen Gannon. "Activated FoxM1 in beta cell mass expansion and recovery." Developmental Biology 356, no. 1 (August 2011): 229. http://dx.doi.org/10.1016/j.ydbio.2011.05.383.

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20

Meier, J. J. "Beta cell mass in diabetes: a realistic therapeutic target?" Diabetologia 51, no. 5 (March 4, 2008): 703–13. http://dx.doi.org/10.1007/s00125-008-0936-9.

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21

Plaisance, Valérie, Gérard Waeber, Romano Regazzi, and Amar Abderrahmani. "Role of MicroRNAs in Islet Beta-Cell Compensation and Failure during Diabetes." Journal of Diabetes Research 2014 (2014): 1–12. http://dx.doi.org/10.1155/2014/618652.

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Pancreatic beta-cell function and mass are markedly adaptive to compensate for the changes in insulin requirement observed during several situations such as pregnancy, obesity, glucocorticoids excess, or administration. This requires a beta-cell compensation which is achieved through a gain of beta-cell mass and function. Elucidating the physiological mechanisms that promote functional beta-cell mass expansion and that protect cells against death, is a key therapeutic target for diabetes. In this respect, several recent studies have emphasized the instrumental role of microRNAs in the control of beta-cell function. MicroRNAs are negative regulators of gene expression, and are pivotal for the control of beta-cell proliferation, function, and survival. On the one hand, changes in specific microRNA levels have been associated with beta-cell compensation and are triggered by hormones or bioactive peptides that promote beta-cell survival and function. Conversely, modifications in the expression of other specific microRNAs contribute to beta-cell dysfunction and death elicited by diabetogenic factors including, cytokines, chronic hyperlipidemia, hyperglycemia, and oxidized LDL. This review underlines the importance of targeting the microRNA network for future innovative therapies aiming at preventing the beta-cell decline in diabetes.

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Tarabra, Elena, Stella Pelengaris, and Michael Khan. "A Simple Matter of Life and Death—The Trials of Postnatal Beta-Cell Mass Regulation." International Journal of Endocrinology 2012 (2012): 1–20. http://dx.doi.org/10.1155/2012/516718.

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Pancreatic beta-cells, which secrete the hormone insulin, are the key arbiters of glucose homeostasis. Defective beta-cell numbers and/or function underlie essentially all major forms of diabetes and must be restored if diabetes is to be cured. Thus, the identification of the molecular regulators of beta-cell mass and a better understanding of the processes of beta-cell differentiation and proliferation may provide further insight for the development of new therapeutic targets for diabetes. This review will focus on the principal hormones and nutrients, as well as downstream signalling pathways regulating beta-cell mass in the adult. Furthermore, we will also address more recently appreciated regulators of beta-cell mass, such as microRNAs.

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Couri, Carlos Eduardo Barra, and Júlio César Voltarelli. "Potencial role of stem cell therapy in type 1 diabetes mellitus." Arquivos Brasileiros de Endocrinologia & Metabologia 52, no. 2 (March 2008): 407–15. http://dx.doi.org/10.1590/s0004-27302008000200029.

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Type 1 diabetes mellitus is the result of the autoimmune response against pancreatic beta-cell(s). At the time of clinical diagnosis near 70% of beta-cell mass is been destroyed as a consequence of the auto-destruction that begins months or even years before the clinical diagnosis. Although marked reduction of chronic complications was seen after development and progression of insulin therapy over the years for type 1 diabetic population, associated risks of chronic end-organ damage and hypoglycemia still remain. Besides tight glucose control, beta-cell mass preservation and/or increase are known to be other important targets in management of type 1 diabetes as long as it reduces chronic microvascular complications in the eyes, kidneys and nerves. Moreover, the larger the beta-cell mass, the lower the incidence of hypoglycemic events. In this article, we discuss some insights about beta-cell regeneration, the importance of regulation of the autoimmune process and what is being employed in human type 1 diabetes in regard to stem cell repertoire to promote regeneration and/or preservation of beta-cell mass.

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Cantley, James, Aimee Davenport, Laurène Vetterli, Nandor J. Nemes, P. Tess Whitworth, Ebru Boslem, Le May Thai, et al. "Disruption of beta cell acetyl-CoA carboxylase-1 in mice impairs insulin secretion and beta cell mass." Diabetologia 62, no. 1 (October 17, 2018): 99–111. http://dx.doi.org/10.1007/s00125-018-4743-7.

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25

Liu, Z., K. Tanabe, E. Bernal-Mizrachi, and M. A. Permutt. "Mice with beta cell overexpression of glycogen synthase kinase-3β have reduced beta cell mass and proliferation." Diabetologia 51, no. 4 (January 25, 2008): 623–31. http://dx.doi.org/10.1007/s00125-007-0914-7.

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26

Fontés, G., B. Zarrouki, D. K. Hagman, M. G. Latour, M. Semache, V. Roskens, P. C. Moore, et al. "Glucolipotoxicity age-dependently impairs beta cell function in rats despite a marked increase in beta cell mass." Diabetologia 53, no. 11 (July 14, 2010): 2369–79. http://dx.doi.org/10.1007/s00125-010-1850-5.

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27

Chintinne, M., G. Stangé, B. Denys, P. In ‘t Veld, K. Hellemans, M. Pipeleers-Marichal, Z. Ling, and D. Pipeleers. "Contribution of postnatally formed small beta cell aggregates to functional beta cell mass in adult rat pancreas." Diabetologia 53, no. 11 (July 20, 2010): 2380–88. http://dx.doi.org/10.1007/s00125-010-1851-4.

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28

Salas, Elisabet, Nabil Rabhi, Philippe Froguel, and Jean-Sébastien Annicotte. "Role of Ink4a/Arf Locus in Beta Cell Mass Expansion under Physiological and Pathological Conditions." Journal of Diabetes Research 2014 (2014): 1–7. http://dx.doi.org/10.1155/2014/873679.

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The ARF/INK4A (Cdkn2a) locus includes the linked tumour suppressor genes p16INK4a and p14ARF (p19ARF in mice) that trigger the antiproliferative activities of both RB and p53. With beta cell self-replication being the primary source for new beta cell generation in adult animals, the network by which beta cell replication could be increased to enhance beta cell mass and function is one of the approaches in diabetes research. In this review, we show a general view of the regulation points at transcriptional and posttranslational levels of Cdkn2a locus. We describe the molecular pathways and functions of Cdkn2a in beta cell cycle regulation. Given that aging reveals increased p16Ink4a levels in the pancreas that inhibit the proliferation of beta cells and decrease their ability to respond to injury, we show the state of the art about the role of this locus in beta cell senescence and diabetes development. Additionally, we focus on two approaches in beta cell regeneration strategies that rely on Cdkn2a locus negative regulation: long noncoding RNAs and betatrophin.

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Wang, Jingjing, and Hongjun Wang. "Oxidative Stress in Pancreatic Beta Cell Regeneration." Oxidative Medicine and Cellular Longevity 2017 (2017): 1–9. http://dx.doi.org/10.1155/2017/1930261.

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Pancreatic β cell neogenesis and proliferation during the neonatal period are critical for the generation of sufficient pancreatic β cell mass/reserve and have a profound impact on long-term protection against type 2 diabetes (T2D). Oxidative stress plays an important role in β cell neogenesis, proliferation, and survival under both physiological and pathophysiological conditions. Pancreatic β cells are extremely susceptible to oxidative stress due to a high endogenous production of reactive oxygen species (ROS) and a low expression of antioxidative enzymes. In this review, we summarize studies describing the critical roles and the mechanisms of how oxidative stress impacts β cell neogenesis and proliferation. In addition, the effects of antioxidant supplements on reduction of oxidative stress and increase of β cell proliferation are discussed. Exploring the roles and the potential therapeutic effects of antioxidants in the process of β cell regeneration would provide novel perspectives to preserve and/or expand pancreatic β cell mass for the treatment of T2D.

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Zhao, Xin. "Increase of beta cell mass by beta cell replication, but not neogenesis, in the maternal pancreas in mice." Endocrine Journal 61, no. 6 (2014): 623–28. http://dx.doi.org/10.1507/endocrj.ej14-0040.

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31

Mattsson, Goran, Stella Pelengaris, and Michael Khan. "The Role of c-Myc in Beta Cell Mass Homeostasis." Immunology‚ Endocrine & Metabolic Agents in Medicinal Chemistry 6, no. 2 (April 1, 2006): 179–89. http://dx.doi.org/10.2174/187152206776359966.

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32

Sweet, Ian R., Daniel L. Cook, Åke lernmark, Carla J. Greenbaum, and Kenneth A. Krohn. "Non-Invasive Imaging of Beta Cell Mass: A Quantitative Analysis." Diabetes Technology & Therapeutics 6, no. 5 (October 2004): 652–59. http://dx.doi.org/10.1089/dia.2004.6.652.

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33

Nielsen, J. H., E. D. Galsgaard, A. M ldrup, B. Nissen Friedrichsen, N. Billestrup, J. A. Hansen, Y. C. Lee, and C. Carlsson. "Regulation of beta-cell mass by hormones and growth factors." Diabetes 50, Supplement 1 (February 1, 2001): S25—S29. http://dx.doi.org/10.2337/diabetes.50.2007.s25.

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34

Portha, Bernard, Cécile Tourrel-Cuzin, and Jamileh Movassat. "Activation of the GLP-1 Receptor Signalling Pathway: A Relevant Strategy to Repair a Deficient Beta-Cell Mass." Experimental Diabetes Research 2011 (2011): 1–11. http://dx.doi.org/10.1155/2011/376509.

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Recent preclinical studies in rodent models of diabetes suggest that exogenous GLP-1R agonists and DPP-4 inhibitors have the ability to increase islet mass and preserve beta-cell function, by immediate reactivation of beta-cell glucose competence, as well as enhanced beta-cell proliferation and neogenesis and promotion of beta-cell survival. These effects have tremendous implication in the treatment of T2D because they directly address one of the basic defects in T2D, that is, beta-cell failure. In human diabetes, however, evidence that the GLP-1-based drugs alter the course of beta-cell function remains to be found. Several questions surrounding the risks and benefits of GLP-1-based therapy for the diabetic beta-cell mass are discussed in this review and require further investigation.

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35

Holloway, A. C., J. J. Petrik, J. E. Bruin, and H. C. Gerstein. "Rosiglitazone prevents diabetes by increasing beta-cell mass in an animal model of type 2 diabetes characterized by reduced beta-cell mass at birth." Diabetes, Obesity and Metabolism 10, no. 9 (September 2008): 763–71. http://dx.doi.org/10.1111/j.1463-1326.2007.00808.x.

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Costes, Safia, Gyslaine Bertrand, and Magalie A. Ravier. "Mechanisms of Beta-Cell Apoptosis in Type 2 Diabetes-Prone Situations and Potential Protection by GLP-1-Based Therapies." International Journal of Molecular Sciences 22, no. 10 (May 18, 2021): 5303. http://dx.doi.org/10.3390/ijms22105303.

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Type 2 diabetes (T2D) is characterized by chronic hyperglycemia secondary to the decline of functional beta-cells and is usually accompanied by a reduced sensitivity to insulin. Whereas altered beta-cell function plays a key role in T2D onset, a decreased beta-cell mass was also reported to contribute to the pathophysiology of this metabolic disease. The decreased beta-cell mass in T2D is, at least in part, attributed to beta-cell apoptosis that is triggered by diabetogenic situations such as amyloid deposits, lipotoxicity and glucotoxicity. In this review, we discussed the molecular mechanisms involved in pancreatic beta-cell apoptosis under such diabetes-prone situations. Finally, we considered the molecular signaling pathways recruited by glucagon-like peptide-1-based therapies to potentially protect beta-cells from death under diabetogenic situations.

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Pourghadamyari, Hossein, Mohammad Rezaei, Mohsen Basiri, Yaser Tahamtani, Behrouz Asgari, Seyedeh-Nafiseh Hassani, Reza Meshkani, Taghi Golmohammadi, and Hossein Baharvand. "Generation of a Transgenic Zebrafish Model for Pancreatic Beta Cell Regeneration." Galen Medical Journal 8 (November 6, 2019): 1056. http://dx.doi.org/10.31661/gmj.v8i0.1056.

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Background: Diabetes is a major worldwide health problem. It is widely accepted that the beta cell mass decreases in type I diabetes (T1D). Accordingly, beta cell regeneration is a promising approach to increase the beta cell mass in T1D patients. However, the underlying mechanisms of beta cell regeneration have yet to be elucidated. One promising avenue is to create a relevant animal model to explore the underlying molecular and cellular mechanisms of beta cell regeneration. The zebrafish can be considered a model in beta cell regeneration studies because the pancreas structure and gene expression pattern are highly conserved between human and zebrafish. Materials and Methods: In this study, the Tol2 transposase was exploited to generate a Tg(Ins:egfp-nfsB) zebrafish model that expressed a fusion protein composed of enhanced green fluorescent protein (EGFP) and nitroreductase (NTR) under control of the Ins promoter. Results: Metronidazole (MTZ) treatment of Tg(ins:egfp-nfsB) zebrafish larvae led to selective ablation of beta cells. Proof-of-concept evidence for beta cell regeneration in the transgenic larvae was observed two days after withdrawal of MTZ. Conclusion: This study suggests that the Tg(ins:egfp-nfsB) zebrafish can be used as a disease model to study beta cell regeneration and elucidate underlying mechanisms during the regeneration process. [GMJ.2019;8:e1056]

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Del Zotto, H., CL Gomez Dumm, S. Drago, A. Fortino, GC Luna, and JJ Gagliardino. "Mechanisms involved in the beta-cell mass increase induced by chronic sucrose feeding to normal rats." Journal of Endocrinology 174, no. 2 (August 1, 2002): 225–31. http://dx.doi.org/10.1677/joe.0.1740225.

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The aim of the present study was to clarify the mechanisms by which a sucrose-rich diet (SRD) produces an increase in the pancreatic beta-cell mass in the rat. Normal Wistar rats were fed for 30 weeks either an SRD (SRD rats; 63% wt/wt), or the same diet but with starch instead of sucrose in the same proportion (CD rats). We studied body weight, serum glucose and triacylglycerol levels, endocrine tissue and beta-cell mass, beta-cell replication rate (proliferating cell nuclear antigen; PCNA), islet neogenesis (cytokeratin immunostaining) and beta-cell apoptosis (propidium iodide). Body weight (g) recorded in the SRD rats was significantly (P<0.05) larger than that of the CD group (556.0+/-8.3 vs 470.0+/-13.1). Both serum glucose and triacylglycerol levels (mmol/l) were also significantly higher (P<0.05) in SRD than in CD rats (serum glucose, 8.11+/-0.14 vs 6.62+/-0.17; triacylglycerol, 1.57+/-0.18 vs 0.47+/-0.04). The number of pancreatic islets per unit area increased significantly (P<0.05) in SRD rats (3.29+/-0.1 vs 2.01+/-0.2). A significant increment (2.6 times) in the mass of endocrine tissue was detected in SRD animals, mainly due to an increase in the beta-cell mass (P=0.0025). The islet cell replication rate, measured as the percentage of PCNA-labelled beta cells increased 6.8 times in SRD rats (P<0.03). The number of apoptotic cells in the endocrine pancreas decreased significantly (three times) in the SRD animals (P=0.03). The cytokeratin-positive area did not show significant differences between CD and SRD rats. The increase of beta-cell mass induced by SRD was accomplished by an enhanced replication of beta cells together with a decrease in the rate of beta-cell apoptosis, without any evident participation of islet neogenesis. This pancreatic reaction was unable to maintain serum glucose levels of these rats at the level measured in CD animals.

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Song, Imane, Sarah Roels, Geert A. Martens, and Luc Bouwens. "Circulating microRNA-375 as biomarker of pancreatic beta cell death and protection of beta cell mass by cytoprotective compounds." PLOS ONE 12, no. 10 (October 17, 2017): e0186480. http://dx.doi.org/10.1371/journal.pone.0186480.

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40

Sayers, Sophie R., Rebecca L. Beavil, Nicholas H. F. Fine, Guo C. Huang, Pratik Choudhary, Kamila J. Pacholarz, Perdita E. Barran, et al. "Structure-functional changes in eNAMPT at high concentrations mediate mouse and human beta cell dysfunction in type 2 diabetes." Diabetologia 63, no. 2 (November 15, 2019): 313–23. http://dx.doi.org/10.1007/s00125-019-05029-y.

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Abstract Aims/hypothesis Progressive decline in functional beta cell mass is central to the development of type 2 diabetes. Elevated serum levels of extracellular nicotinamide phosphoribosyltransferase (eNAMPT) are associated with beta cell failure in type 2 diabetes and eNAMPT immuno-neutralisation improves glucose tolerance in mouse models of diabetes. Despite this, the effects of eNAMPT on functional beta cell mass are poorly elucidated, with some studies having separately reported beta cell-protective effects of eNAMPT. eNAMPT exists in structurally and functionally distinct monomeric and dimeric forms. Dimerisation is essential for the NAD-biosynthetic capacity of NAMPT. Monomeric eNAMPT does not possess NAD-biosynthetic capacity and may exert distinct NAD-independent effects. This study aimed to fully characterise the structure-functional effects of eNAMPT on pancreatic beta cell functional mass and to relate these to beta cell failure in type 2 diabetes. Methods CD-1 mice and serum from obese humans who were without diabetes, with impaired fasting glucose (IFG) or with type 2 diabetes (from the Body Fat, Surgery and Hormone [BodyFatS&H] study) or with or at risk of developing type 2 diabetes (from the VaSera trial) were used in this study. We generated recombinant wild-type and monomeric eNAMPT to explore the effects of eNAMPT on functional beta cell mass in isolated mouse and human islets. Beta cell function was determined by static and dynamic insulin secretion and intracellular calcium microfluorimetry. NAD-biosynthetic capacity of eNAMPT was assessed by colorimetric and fluorescent assays and by native mass spectrometry. Islet cell number was determined by immunohistochemical staining for insulin, glucagon and somatostatin, with islet apoptosis determined by caspase 3/7 activity. Markers of inflammation and beta cell identity were determined by quantitative reverse transcription PCR. Total, monomeric and dimeric eNAMPT and nicotinamide mononucleotide (NMN) were evaluated by ELISA, western blot and fluorometric assay using serum from non-diabetic, glucose intolerant and type 2 diabetic individuals. Results eNAMPT exerts bimodal and concentration- and structure-functional-dependent effects on beta cell functional mass. At low physiological concentrations (~1 ng/ml), as seen in serum from humans without diabetes, eNAMPT enhances beta cell function through NAD-dependent mechanisms, consistent with eNAMPT being present as a dimer. However, as eNAMPT concentrations rise to ~5 ng/ml, as in type 2 diabetes, eNAMPT begins to adopt a monomeric form and mediates beta cell dysfunction, reduced beta cell identity and number, increased alpha cell number and increased apoptosis, through NAD-independent proinflammatory mechanisms. Conclusions/interpretation We have characterised a novel mechanism of beta cell dysfunction in type 2 diabetes. At low physiological levels, eNAMPT exists in dimer form and maintains beta cell function and identity through NAD-dependent mechanisms. However, as eNAMPT levels rise, as in type 2 diabetes, structure-functional changes occur resulting in marked elevation of monomeric eNAMPT, which induces a diabetic phenotype in pancreatic islets. Strategies to selectively target monomeric eNAMPT could represent promising therapeutic strategies for the treatment of type 2 diabetes.

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Yang, Weixia, Yinan Jiang, Yan Wang, Ting Zhang, Qun Liu, Chaoban Wang, Grant Swisher, et al. "Placental growth factor in beta cells plays an essential role in gestational beta-cell growth." BMJ Open Diabetes Research & Care 8, no. 1 (March 2020): e000921. http://dx.doi.org/10.1136/bmjdrc-2019-000921.

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ObjectivePancreatic beta cells proliferate in response to metabolic requirements during pregnancy, while failure of this response may cause gestational diabetes. A member of the vascular endothelial growth factor family, placental growth factor (PlGF), typically plays a role in metabolic disorder and pathological circumstance. The expression and function of PlGF in the endocrine pancreas have not been reported and are addressed in the current study.Research design and methodsPlGF levels in beta cells were determined by immunostaining or ELISA in purified beta cells in non-pregnant and pregnant adult mice. An adeno-associated virus (AAV) serotype 8 carrying a shRNA for PlGF under the control of a rat insulin promoter (AAV–rat insulin promoter (RIP)–short hairpin small interfering RNA for PlGF (shPlGF)) was prepared and infused into mouse pancreas through the pancreatic duct to specifically knock down PlGF in beta cells, and its effects on beta-cell growth were determined by beta-cell proliferation, beta-cell mass and insulin release. A macrophage-depleting reagent, clodronate, was coapplied into AAV-treated mice to study crosstalk between beta cells and macrophages.ResultsPlGF is exclusively produced by beta cells in the adult mouse pancreas. Moreover, PlGF expression in beta cells was significantly increased during pregnancy. Intraductal infusion of AAV–RIP–shPlGF specifically knocked down PlGF in beta cells, resulting in compromised beta-cell proliferation, reduced growth in beta-cell mass and impaired glucose tolerance during pregnancy. Mechanistically, PlGF depletion in beta cells reduced islet infiltration of trophic macrophages, which appeared to be essential for gestational beta-cell growth.ConclusionsOur study suggests that increased expression of PlGF in beta cells may trigger gestational beta-cell growth through recruited macrophages.

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42

Ritzel, Robert, A. "Therapeutic approaches based on beta-cell mass preservation and/or regeneration." Frontiers in Bioscience Volume, no. 14 (2009): 1835. http://dx.doi.org/10.2741/3345.

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Dhanvantari, Savita. "Imaging Functional Beta Cell Mass: Can we See Islets Clearly Now?" Current Molecular Imaginge 1, no. 1 (September 1, 2012): 44–54. http://dx.doi.org/10.2174/2211555211201010044.

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Ackermann, Amanda M., and Maureen Gannon. "Pancreatic beta cell mass regeneration and expansion — a role for FoxM1?" Developmental Biology 306, no. 1 (June 2007): 395. http://dx.doi.org/10.1016/j.ydbio.2007.03.585.

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Inaishi, Jun, Yoshifumi Saisho, and Hiroshi Itoh. "Effects of Obesity and Diabetes on Beta-Cell Mass in Japanese." Pancreas - Open Journal 1, no. 2 (August 2, 2016): e11-e13. http://dx.doi.org/10.17140/poj-1-e004.

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Klee, Philippe, Smaragda Lamprianou, Anne Charollais, Dorothée Caille, Rossella Sarro, Manon Cederroth, Jacques-Antoine Haefliger, and Paolo Meda. "Connexin Implication in the Control of the Murine Beta-Cell Mass." Pediatric Research 70, no. 2 (August 2011): 142–47. http://dx.doi.org/10.1203/pdr.0b013e318220f106.

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Levitsky, Lynne L., Goli Ardestani, and David B. Rhoads. "Role of growth factors in control of pancreatic beta cell mass." Current Opinion in Pediatrics 26, no. 4 (August 2014): 475–79. http://dx.doi.org/10.1097/mop.0000000000000110.

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Bronsart, Laura L., Christian Stokes, and Christopher H. Contag. "Chemiluminescence Imaging of Superoxide Anion Detects Beta-Cell Function and Mass." PLOS ONE 11, no. 1 (January 11, 2016): e0146601. http://dx.doi.org/10.1371/journal.pone.0146601.

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Domínguez-Bendala, Juan, Luca Inverardi, and Camillo Ricordi. "Regeneration of pancreatic beta-cell mass for the treatment of diabetes." Expert Opinion on Biological Therapy 12, no. 6 (April 16, 2012): 731–41. http://dx.doi.org/10.1517/14712598.2012.679654.

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Barbosa-Sampaio, Helena C., Bo Liu, Robert Drynda, Ana M. Rodriguez de Ledesma, Aileen J. King, James E. Bowe, Cédric Malicet, et al. "Nupr1 deletion protects against glucose intolerance by increasing beta cell mass." Diabetologia 56, no. 11 (July 31, 2013): 2477–86. http://dx.doi.org/10.1007/s00125-013-3006-x.

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Journal articles on the topic 'Beta-cell mass'

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