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Journal articles on the topic 'Pancreatic beta-cell'

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Published: 4 June 2021

Last updated: 11 March 2023

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1

Rastogi, D. P., A. C. Saxena, and Sunil Kumar. "Pancreatic beta-cell regeneration." British Homeopathic Journal 77, no. 03 (July 1988): 147–51. http://dx.doi.org/10.1016/s0007-0785(88)80071-1.

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Abstract Cephalendra, indica ∅ (41% v/v alcoholic extract of the wild variety of Cephalendra indica Naud.), on regular administration in doses ranging from 25 μml to 75 μml/100 g of body weight (gbw) by the oral or intraperitoneal (ip) route produced a significant fall in blood sugar level in alloxan-induced diabetic rats. Biochemical studies showed stabilization of blood sugar level in 70% of cases of fourteen to twenty days after withdrawal of the drug. Histopathological studies revealed regeneration of pancreatic β cells. The hypothesis is that the drug acts through the hypothalamo-hypophysial-pancreatic axis, producing selective regeneration of β cells. The drug may indirectly release inhibitory factors from hypothalamic neurons, inhibiting the secretion of growth hormone and triggering insulin secretion from β cells. The therapeutic action of the drug on pancreatic β cells and lack of acute and subacute toxicity may open up new prospects in the treatment of diabetes mellitus.

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2

Thermos, K., M. D. Meglasson, J. Nelson, K. M. Lounsbury, and T. Reisine. "Pancreatic beta-cell somatostatin receptors." American Journal of Physiology-Endocrinology and Metabolism 259, no. 2 (August 1, 1990): E216—E224. http://dx.doi.org/10.1152/ajpendo.1990.259.2.e216.

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The characteristics of somatostatin (SRIF) receptors in rat pancreatic beta-cells were investigated using rat islets and the beta-cell line HIT-T15 (HIT). The biochemical properties of the SRIF receptors were examined with 125I-labeled des-Ala-1,Gly-2-desamino-Cys-3-[Tyr-11]- dicarba3,14-somatostatin (CGP 23996). 125I-CGP 23996 bound to SRIF receptors in HIT cells with high affinity and in a saturable manner. The binding of 125I-CGP 23996 to SRIF receptors was blocked by SRIF analogues with a rank order of potency of somatostatin 28 (SRIF-28) greater than D-Trp-8-somatostatin greater than somatostatin 14 (SRIF-14). To investigate the physical properties of the HIT cell SRIF receptor, the receptor was covalently labeled with 125I-CGP 23996 using photo-cross-linking techniques. 125I-CGP 23996 specifically labeled a protein of 55 kDa in HIT cell membranes. The size of the SRIF receptor in HIT cells is similar to the size of the SRIF receptor labeled with 125I-CGP 23996 in membranes of freshly isolated islets, suggesting that the physical properties of SRIF receptors in HIT cells and rat islet cells are similar. The binding studies suggest that beta-cells predominantly express a SRIF-28-preferring receptor. In freshly isolated islets, glucose- and arginine-stimulated insulin release was effectively blocked by SRIF-28 but not by SRIF-14. SRIF-14 did inhibit arginine-stimulated glucagon secretion from freshly isolated islets. The dissociation of the inhibitory effects of SRIF-28 and SRIF-14 on insulin and glucagon release from freshly isolated islets suggests that the two peptides act through different receptors in islets to regulate hormone secretion.

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3

Grossman, E., J. Tao, D. Lee, and A. Chong. "QUANTIFYING PANCREATIC BETA-CELL REGENERATION." Transplantation 86, Supplement (July 2008): 143. http://dx.doi.org/10.1097/01.tp.0000332375.84668.26.

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4

Grossman, Eric J., Jing Tao, David D. Lee, and Anita S. Chong. "Quantifying pancreatic beta-cell regeneration." Journal of the American College of Surgeons 207, no. 3 (September 2008): S106—S107. http://dx.doi.org/10.1016/j.jamcollsurg.2008.06.272.

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5

Bigam, David L., and A. M. James Shapiro. "Pancreatic transplantation: Beta cell replacement." Current Treatment Options in Gastroenterology 7, no. 5 (October 2004): 329–41. http://dx.doi.org/10.1007/s11938-004-0046-9.

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6

Russ, Holger A., Limor Landsman, Christopher L. Moss, Roger Higdon, Renee L. Greer, Kelly Kaihara, Randy Salamon, Eugene Kolker, and Matthias Hebrok. "Dynamic Proteomic Analysis of Pancreatic Mesenchyme Reveals Novel Factors That Enhance Human Embryonic Stem Cell to Pancreatic Cell Differentiation." Stem Cells International 2016 (2016): 1–9. http://dx.doi.org/10.1155/2016/6183562.

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Current approaches in human embryonic stem cell (hESC) to pancreatic beta cell differentiation have largely been based on knowledge gained from developmental studies of the epithelial pancreas, while the potential roles of other supporting tissue compartments have not been fully explored. One such tissue is the pancreatic mesenchyme that supports epithelial organogenesis throughout embryogenesis. We hypothesized that detailed characterization of the pancreatic mesenchyme might result in the identification of novel factors not used in current differentiation protocols. Supplementing existing hESC differentiation conditions with such factors might create a more comprehensive simulation of normal development in cell culture. To validate our hypothesis, we took advantage of a novel transgenic mouse model to isolate the pancreatic mesenchyme at distinct embryonic and postnatal stages for subsequent proteomic analysis. Refined sample preparation and analysis conditions across four embryonic and prenatal time points resulted in the identification of 21,498 peptides with high-confidence mapping to 1,502 proteins. Expression analysis of pancreata confirmed the presence of three potentially important factors in cell differentiation: Galectin-1 (LGALS1), Neuroplastin (NPTN), and the Lamininα-2 subunit (LAMA2). Two of the three factors (LGALS1 and LAMA2) increased expression of pancreatic progenitor transcript levels in a published hESC to beta cell differentiation protocol. In addition, LAMA2 partially blocks cell culture induced beta cell dedifferentiation. Summarily, we provide evidence that proteomic analysis of supporting tissues such as the pancreatic mesenchyme allows for the identification of potentially important factors guiding hESC to pancreas differentiation.

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7

Laughlin, Maren. "Why Image the Pancreatic Beta Cell?" Current Medicinal Chemistry-Immunology, Endocrine & Metabolic Agents 4, no. 4 (December 1, 2004): 251–52. http://dx.doi.org/10.2174/1568013043357482.

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8

Smith, W. G. J., I. Hanning, D. G. Johnston, and C. B. Brown. "Pancreatic Beta-cell Function in CAPD." Nephrology Dialysis Transplantation 3, no. 4 (1988): 448–52. http://dx.doi.org/10.1093/oxfordjournals.ndt.a091696.

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9

Diedisheim, Marc, Masaya Oshima, Olivier Albagli, Charlotte Wennberg Huldt, Ingela Ahlstedt, Maryam Clausen, Suraj Menon, et al. "Modeling human pancreatic beta cell dedifferentiation." Molecular Metabolism 10 (April 2018): 74–86. http://dx.doi.org/10.1016/j.molmet.2018.02.002.

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10

Poitout, Vincent, Julie Amyot, Meriem Semache, Bader Zarrouki, Derek Hagman, and Ghislaine Fontés. "Glucolipotoxicity of the pancreatic beta cell." Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids 1801, no. 3 (March 2010): 289–98. http://dx.doi.org/10.1016/j.bbalip.2009.08.006.

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11

Shen, Mary, Eric S. Orwoll, John E. Conte, and Melvin J. Prince. "Pentamidine-induced pancreatic beta-cell dysfunction." American Journal of Medicine 86, no. 6 (June 1989): 726–28. http://dx.doi.org/10.1016/0002-9343(89)90457-9.

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12

Pipeleers, D. G. "Heterogeneity in pancreatic beta-cell population." Diabetes 41, no. 7 (July 1, 1992): 777–81. http://dx.doi.org/10.2337/diabetes.41.7.777.

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13

Smit, Jan WA, and Michaela Diamant. "Genetically defined pancreatic beta cell failure." Pharmacogenomics 3, no. 5 (September 2002): 669–78. http://dx.doi.org/10.1517/14622416.3.5.669.

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14

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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15

Stützer, I., D. Esterházy, and M. Stoffel. "The pancreatic beta cell surface proteome." Diabetologia 55, no. 7 (March 31, 2012): 1877–89. http://dx.doi.org/10.1007/s00125-012-2531-3.

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16

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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17

Rane, Sushil, G. "Cell cycle control of pancreatic beta cell proliferation." Frontiers in Bioscience 5, no. 1 (2000): d1. http://dx.doi.org/10.2741/rane.

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18

Rane, Sushil G. "Cell cycle control of pancreatic beta cell proliferation." Frontiers in Bioscience 5, no. 3 (2000): d1–19. http://dx.doi.org/10.2741/a492.

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19

Logsdon, C. D., L. Keyes, and R. D. Beauchamp. "Transforming growth factor-beta (TGF-beta 1) inhibits pancreatic acinar cell growth." American Journal of Physiology-Gastrointestinal and Liver Physiology 262, no. 2 (February 1, 1992): G364—G368. http://dx.doi.org/10.1152/ajpgi.1992.262.2.g364.

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Effects of transforming growth factor (TGF)-beta 1 on mouse pancreatic acinar cell growth and rapid intracellular responses to cholecystokinin (CCK) were examined in vitro. TGF-beta 1 inhibited [3H]thymidine incorporation stimulated by either the CCK analogue caerulein, epidermal growth factor, or insulin. TGF-beta 1 inhibition of growth stimulated by a maximal dose of caerulein (1 nM) was dose dependent with one-half maximal effects occurring at approximately 5 pM and maximal inhibition seen with 30 pM. In contrast to its effects on CCK-stimulated [3H]thymidine incorporation, TGF-beta 1 had no effect on CCK-stimulated increases in amylase release or intracellular Ca2+ concentration. To determine whether TGF-beta 1 might be an autocrine growth regulator, pancreatic mRNA was probed for the presence of TGF-beta 1 transcripts. TGF-beta 1 mRNA was not detected in whole pancreas but was detectable with increasing abundance over time in primary cultures of pancreatic acinar cells. The appearance of the TGF-beta 1 mRNA corresponded to the period of rapid cellular proliferation in vitro. These results suggest that TGF-beta 1 may be an autocrine growth inhibitor in the pancreas and that the inhibitory effects of TGF-beta 1 on pancreatic acinar cell growth occur at sites distal to those involved in stimulus-secretion coupling.

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20

Hosseini, Azar, Reza Shafiee-Nick, and Ahmad Ghorbani. "Pancreatic beta cell protection/regeneration with phytotherapy." Brazilian Journal of Pharmaceutical Sciences 51, no. 1 (March 2015): 1–16. http://dx.doi.org/10.1590/s1984-82502015000100001.

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Although currently available drugs are useful in controlling early onset complications of diabetes, serious late onset complications appear in a large number of patients. Considering the physiopathology of diabetes, preventing beta cell degeneration and stimulating the endogenous regeneration of islets will be essential approaches for the treatment of insulin-dependent diabetes mellitus. The current review focused on phytochemicals, the antidiabetic effect of which has been proved by pancreatic beta cell protection/regeneration. Among the hundreds of plants that have been investigated for diabetes, a small fraction has shown the regenerative property and was described in this paper. Processes of pancreatic beta cell degeneration and regeneration were described. Also, the proposed mechanisms for the protective/regenerative effects of such phytochemicals and their potential side effects were discussed.

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21

Zhao, Huan, Kathy O. Lui, and Bin Zhou. "Pancreatic beta cell neogenesis: Debates and updates." Cell Metabolism 33, no. 11 (November 2021): 2105–7. http://dx.doi.org/10.1016/j.cmet.2021.10.007.

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22

Barlow, Jonathan P., and Thomas P. Solomon. "Skeletal-muscle To Pancreatic Beta-cell Crosstalk." Medicine & Science in Sports & Exercise 49, no. 5S (May 2017): 347. http://dx.doi.org/10.1249/01.mss.0000517827.55828.b1.

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23

Kohler, Martin, Daniel Nyqvist, Tilo Moede, Helene Wahlstedt, Over Cabrera, Ingo Leibiger, and Per-Olof Berggren. "Imaging of Pancreatic Beta-Cell Signal-Transduction." Current Medicinal Chemistry-Immunology, Endocrine & Metabolic Agents 4, no. 4 (December 1, 2004): 281–99. http://dx.doi.org/10.2174/1568013043357275.

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24

Rulifson, I. C., S. K. Karnik, P. W. Heiser, D. ten Berge, H. Chen, X. Gu, M. M. Taketo, R. Nusse, M. Hebrok, and S. K. Kim. "Wnt signaling regulates pancreatic beta cell proliferation." Proceedings of the National Academy of Sciences 104, no. 15 (April 2, 2007): 6247–52. http://dx.doi.org/10.1073/pnas.0701509104.

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25

Wu, Zonggui, John Luo, and Luguang Luo. "American ginseng modulates pancreatic beta cell activities." Chinese Medicine 2, no. 1 (2007): 11. http://dx.doi.org/10.1186/1749-8546-2-11.

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26

Park, Kris E., Keri Chambers, Carol Ting, and Steven C. Boyages. "Stress hyperglycemia reflects pancreatic beta-cell failure." Heart, Lung and Circulation 12, no. 2 (January 2003): A65. http://dx.doi.org/10.1046/j.1443-9506.2003.02599.x.

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27

Georgiou, Pantelis, and Christopher Toumazou. "A Silicon Pancreatic Beta Cell for Diabetes." IEEE Transactions on Biomedical Circuits and Systems 1, no. 1 (March 2007): 39–49. http://dx.doi.org/10.1109/tbcas.2007.893178.

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28

Poitout, V., I. Briaud, C. Kelpe, and D. Hagman. "Gluco-lipotoxicity of the pancreatic beta cell." Annales d'Endocrinologie 65, no. 1 (February 2004): 37–41. http://dx.doi.org/10.1016/s0003-4266(04)95628-4.

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29

Hembree, Mark, Kok-Hooi Yew, Krishna Prasadan, Barry Preuett, Christina Cantu, Christopher McFall, Amanda Crowley, Susan Sharp, Charles Snyder, and George Gittes. "TGF-beta signaling in pancreatic cell differentiation." Journal of the American College of Surgeons 199, no. 3 (September 2004): 85. http://dx.doi.org/10.1016/j.jamcollsurg.2004.05.183.

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30

Swenne, I. "Pancreatic Beta-cell growth and diabetes mellitus." Diabetologia 35, no. 3 (March 1992): 193–201. http://dx.doi.org/10.1007/bf00400917.

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31

Khin, Phyu Phyu, Jong Han Lee, and Hee-Sook Jun. "Pancreatic Beta-cell Dysfunction in Type 2 Diabetes." European Journal of Inflammation 21 (January 30, 2023): 1721727X2311541. http://dx.doi.org/10.1177/1721727x231154152.

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Pancreatic β-cells produce and secrete insulin to maintain blood glucose levels within a narrow range. Defects in the function and mass of β-cells play a significant role in the development and progression of diabetes. Increased β-cell deficiency and β-cell apoptosis are observed in the pancreatic islets of patients with type 2 diabetes. At an early stage, β-cells adapt to insulin resistance, and their insulin secretion increases, but they eventually become exhausted, and the β-cell mass decreases. Various causal factors, such as high glucose, free fatty acids, inflammatory cytokines, and islet amyloid polypeptides, contribute to the impairment of β-cell function. Therefore, the maintenance of β-cell function is a logical approach for the treatment and prevention of diabetes. In this review, we provide an overview of the role of these risk factors in pancreatic β-cell loss and the associated mechanisms. A better understanding of the molecular mechanisms underlying pancreatic β-cell loss will provide an opportunity to identify novel therapeutic targets for type 2 diabetes.

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32

Gagliardino, JJ, H. Del Zotto, L. Massa, LE Flores, and MI Borelli. "Pancreatic duodenal homeobox-1 and islet neogenesis-associated protein: a possible combined marker of activateable pancreatic cell precursors." Journal of Endocrinology 177, no. 2 (May 1, 2003): 249–59. http://dx.doi.org/10.1677/joe.0.1770249.

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The aim of this work was to study the possible relationship between pancreatic duodenal homeobox-1 (Pdx-1) and islet neogenesis-associated protein (INGAP) during induced islet neogenesis. Pregnant hamsters were fed with (S) and without (C) sucrose, and glycemia, insulin secretion in vitro, and pancreas immunomorphometric parameters were measured in their 7-day-old offspring. S offspring had significantly lower glycemic levels than C animals. Insulin release in response to increasing glucose concentrations in the incubation medium (2-16 mM glucose) did not increase in pancreata from either C or S offspring. However, pancreata from S offspring released more insulin than those from C animals. In S offspring, beta-cell mass, beta-cell replication rate and islet neogenesis increased significantly, with a simultaneous decrease in beta-cell apoptotic rate. INGAP- and Pdx-1-positive cell mass also increased in the islets and among acinar and duct cells. We found two subpopulations of Pdx-1 cells: INGAP-positive and INGAP-negative. Pdx-1/INGAP-positive cells did not stain with insulin, glucagon, somatostatin, pancreatic polypeptide, or neurogenin 3 antibodies. The increment of Pdx-1/INGAP-positive cells represented the major contribution to the Pdx-1 cell mass increase. Such increments varied among pancreas subsectors: ductal>insular>extrainsular. Our results suggested that INGAP participates in the regulation of islet neogenesis, and Pdx-1/INGAP-positive cells represent a new stem cell subpopulation at an early stage of development, highly activateable in neogenesis.

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33

Dahl, U., A. Sjodin, and H. Semb. "Cadherins regulate aggregation of pancreatic beta-cells in vivo." Development 122, no. 9 (September 1, 1996): 2895–902. http://dx.doi.org/10.1242/dev.122.9.2895.

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It is thought that the cadherin protein family of cell adhesion molecules regulates morphogenetic events in multicellular organisms. In this study we have investigated the importance of beta-cell cadherins for cell-cell interactions mediating the organization of endocrine cells into pancreatic islets of Langerhans. To interfere with endogenous cadherin activity in beta-cells during pancreatic development, we overexpressed a dominant negative mutant of mouse E-cadherin, lacking nearly all extracellular amino acids, in pancreatic beta-cells in transgenic mice. Expression of the truncated E-cadherin receptor displaced both E- and N-cadherin from pancreatic beta-cells. As a result, the initial clustering of beta-cells, which normally begins at 13.5-14.5 days postcoitum, was perturbed. Consequently, the clustering of endocrine cells into islets, which normally begins at 17.5-18 days postcoitum, was abrogated. Instead, transgenic beta-cells were found dispersed in the tissue as individual cells, while alpha-cells selectively aggregated into islet-like clusters devoid of beta-cells. Furthermore, expression of truncated E-cadherin in beta-cells resulted in an accumulation of beta-catenin in the cytoplasm. Thus, we have for the first time shown in vivo that cadherins regulate adhesive properties of beta-cells which are essential for the aggregation of endocrine cells into islets.

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34

Shannon, V. R., S. Ramanadham, J. Turk, and M. J. Holtzman. "Selective expression of an arachidonate 12-lipoxygenase by pancreatic islet beta-cells." American Journal of Physiology-Endocrinology and Metabolism 263, no. 5 (November 1, 1992): E828—E836. http://dx.doi.org/10.1152/ajpendo.1992.263.5.e828.

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The immunohistochemical distribution of arachidonate lipoxygenases in rat pancreas was characterized with specific polyclonal anti-5-lipoxygenase and anti-12-lipoxygenase antibodies. Immunohistochemical analysis of formaldehyde-fixed paraffin-embedded rat pancreas using anti-12-lipoxygenase antibody and biotin-avidin-peroxidase detection demonstrated specific staining of islets and no staining of pancreatic exocrine tissue. Less intense staining of pancreatic vascular myocytes and endothelial cells was also observed. Immunoblotting of isolated pancreatic islet extracts with the anti-12-lipoxygenase antibody demonstrated immunoperoxidase staining of a single protein band which comigrated with purified 12-lipoxygenase (relative molecular weight = 72,000) on sodium dodecyl sulfate-polyacrylamide gel electrophoresis analysis. Dispersed cells prepared from isolated islets and then subjected to fluorescence-activated cell sorting and immunostaining exhibited 12-lipoxygenase antigen in beta-cell populations but not in non-beta-cell (predominantly alpha-cell) populations. Assays of enzymatic activity confirmed that the 12-lipoxygenase-catalyzed conversion of arachidonic acid to 12-hydroxyeicosatetraenoic acid methyl ester occurred only with purified beta-cells and not with islet non-beta-cells. No evidence of 5-lipoxygenase antigen or enzymatic activity was found in purified beta-cells or in islet non-beta-cells. We conclude that rat pancreatic islet beta-cells contain an arachidonate 12-lipoxygenase which shares antigenic epitopes with the homologous enzyme contained in tissues from other species. In addition, the selective localization of the 12-lipoxygenase to pancreatic beta-cells and its absence in pancreatic acinar cells and in islet non-beta-cells support observations suggesting that 12-lipoxygenase products may participate in glucose-induced insulin secretion from beta-cells.

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35

Kim, Mi-Kyung, Hye-Soon Kim, In-Kyu Lee, and Keun-Gyu Park. "Endoplasmic Reticulum Stress and Insulin Biosynthesis: A Review." Experimental Diabetes Research 2012 (2012): 1–7. http://dx.doi.org/10.1155/2012/509437.

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Insulin resistance and pancreatic beta cell dysfunction are major contributors to the pathogenesis of diabetes. Various conditions play a role in the pathogenesis of pancreatic beta cell dysfunction and are correlated with endoplasmic reticulum (ER) stress. Pancreatic beta cells are susceptible to ER stress. Many studies have shown that increased ER stress induces pancreatic beta cell dysfunction and diabetes mellitus using genetic models of ER stress and by various stimuli. There are many reports indicating that ER stress plays an important role in the impairment of insulin biosynthesis, suggesting that reduction of ER stress could be a therapeutic target for diabetes. In this paper, we reviewed the relationship between ER stress and diabetes and how ER stress controls insulin biosynthesis.

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36

Zhou, Yu, Min Gong, Yingfei Lu, Jianquan Chen, and Rong Ju. "Prenatal androgen excess impairs beta-cell function by decreased sirtuin 3 expression." Journal of Endocrinology 251, no. 1 (October 1, 2021): 69–81. http://dx.doi.org/10.1530/joe-21-0129.

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Prenatal androgen exposure induces metabolic disorders in female offspring. However, the long-term effect of maternal testosterone excess on glucose metabolism, especially on pancreatic beta-cell function, is rarely investigated. Our current study mainly focused on the effects of prenatal testosterone exposure on glucose metabolism and pancreatic beta- cell function in aged female offspring. By using maternal mice and their female offspring as animal models, we found that prenatal androgen treatment induced obesity and glucose intolerance in aged offspring. These influences were accompanied by decreased fasting serum insulin concentration, elevated serum triglyceride, and testosterone concentrations. Glucose stimulated insulin secretion in pancreatic beta cells of aged female offspring was also affected by prenatal testosterone exposure. We further confirmed that increased serum testosterone contributed to downregulation of sirtuin 3 expression, activated oxidative stress, and impaired pancreatic beta-cell function in aged female offspring. Moreover, over-expression of sirtuin 3 in islets isolated from female offspring treated with prenatal testosterone normalized the oxidative stress level, restored cyclic AMP, and ATP generation, which finally improved glucose-stimulated insulin secretion in beta cells. Taken together, these results demonstrated that prenatal testosterone exposure caused a metabolic disturbance in aged female offspring via suppression of sirtuin 3 expression and activation of oxidative stress in pancreatic beta cells.

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37

Piper, K., S. Brickwood, LW Turnpenny, IT Cameron, SG Ball, DI Wilson, and NA Hanley. "Beta cell differentiation during early human pancreas development." Journal of Endocrinology 181, no. 1 (April 1, 2004): 11–23. http://dx.doi.org/10.1677/joe.0.1810011.

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Understanding gene expression profiles during early human pancreas development is limited by comparison to studies in rodents. In this study, from the inception of pancreatic formation, embryonic pancreatic epithelial cells, approximately half of which were proliferative, expressed nuclear PDX1 and cytoplasmic CK19. Later, in the fetal pancreas, insulin was the most abundant hormone detected during the first trimester in largely non-proliferative cells. At sequential stages of early fetal development, as the number of insulin-positive cell clusters increased, the detection of CK19 in these cells diminished. PDX1 remained expressed in fetal beta cells. Vascular structures were present within the loose stroma surrounding pancreatic epithelial cells during embryogenesis. At 10 weeks post-conception (w.p.c.), all clusters containing more than ten insulin-positive cells had developed an intimate relationship with these vessels, compared with the remainder of the developing pancreas. At 12-13 w.p.c., human fetal islets, penetrated by vasculature, contained cells independently immunoreactive for insulin, glucagon, somatostatin and pancreatic polypeptide (PP), coincident with the expression of maturity markers prohormone convertase 1/3 (PC1/3), islet amyloid polypeptide, Chromogranin A and, more weakly, GLUT2. These data support the function of fetal beta cells as true endocrine cells by the end of the first trimester of human pregnancy.

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38

Memon, Bushra, and Essam M. Abdelalim. "Stem Cell Therapy for Diabetes: Beta Cells versus Pancreatic Progenitors." Cells 9, no. 2 (January 23, 2020): 283. http://dx.doi.org/10.3390/cells9020283.

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Diabetes mellitus (DM) is one of the most prevalent metabolic disorders. In order to replace the function of the destroyed pancreatic beta cells in diabetes, islet transplantation is the most widely practiced treatment. However, it has several limitations. As an alternative approach, human pluripotent stem cells (hPSCs) can provide an unlimited source of pancreatic cells that have the ability to secrete insulin in response to a high blood glucose level. However, the determination of the appropriate pancreatic lineage candidate for the purpose of cell therapy for the treatment of diabetes is still debated. While hPSC-derived beta cells are perceived as the ultimate candidate, their efficiency needs further improvement in order to obtain a sufficient number of glucose responsive beta cells for transplantation therapy. On the other hand, hPSC-derived pancreatic progenitors can be efficiently generated in vitro and can further mature into glucose responsive beta cells in vivo after transplantation. Herein, we discuss the advantages and predicted challenges associated with the use of each of the two pancreatic lineage products for diabetes cell therapy. Furthermore, we address the co-generation of functionally relevant islet cell subpopulations and structural properties contributing to the glucose responsiveness of beta cells, as well as the available encapsulation technology for these cells.

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Deshmukh, Harshal A., Anne Lundager Madsen, Ana Viñuela, Christian Theil Have, Niels Grarup, Andrea Tura, Anubha Mahajan, et al. "Genome-Wide Association Analysis of Pancreatic Beta-Cell Glucose Sensitivity." Journal of Clinical Endocrinology & Metabolism 106, no. 1 (September 18, 2020): 80–90. http://dx.doi.org/10.1210/clinem/dgaa653.

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Abstract Context Pancreatic beta-cell glucose sensitivity is the slope of the plasma glucose-insulin secretion relationship and is a key predictor of deteriorating glucose tolerance and development of type 2 diabetes. However, there are no large-scale studies looking at the genetic determinants of beta-cell glucose sensitivity. Objective To understand the genetic determinants of pancreatic beta-cell glucose sensitivity using genome-wide meta-analysis and candidate gene studies. Design We performed a genome-wide meta-analysis for beta-cell glucose sensitivity in subjects with type 2 diabetes and nondiabetic subjects from 6 independent cohorts (n = 5706). Beta-cell glucose sensitivity was calculated from mixed meal and oral glucose tolerance tests, and its associations between known glycemia-related single nucleotide polymorphisms (SNPs) and genome-wide association study (GWAS) SNPs were estimated using linear regression models. Results Beta-cell glucose sensitivity was moderately heritable (h2 ranged from 34% to 55%) using SNP and family-based analyses. GWAS meta-analysis identified multiple correlated SNPs in the CDKAL1 gene and GIPR-QPCTL gene loci that reached genome-wide significance, with SNP rs2238691 in GIPR-QPCTL (P value = 2.64 × 10−9) and rs9368219 in the CDKAL1 (P value = 3.15 × 10−9) showing the strongest association with beta-cell glucose sensitivity. These loci surpassed genome-wide significance when the GWAS meta-analysis was repeated after exclusion of the diabetic subjects. After correction for multiple testing, glycemia-associated SNPs in or near the HHEX and IGF2B2 loci were also associated with beta-cell glucose sensitivity. Conclusion We show that, variation at the GIPR-QPCTL and CDKAL1 loci are key determinants of pancreatic beta-cell glucose sensitivity.

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Korbutt, Gregory S., and Daniel G. Pipeleers. "Cold-Preservation of Pancreatic Beta Cells." Cell Transplantation 3, no. 4 (July 1994): 291–97. http://dx.doi.org/10.1177/096368979400300405.

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Clinical islet transplantation requires graft preservation conditions with a minimal loss in viable beta cells. The present study examines whether rat pancreatic beta cells survive a 96 h storage period at 4°C. In a single cell viability assay, less than 20% viable cells were counted after 48 h storage in physiological HAM's F10 medium; cell survival was better in the high potassium solutions UW or Collins and further improved by supplementing Collins with albumin and benzamidine (CAB - 77% viability after 96 h). Suspended beta cell aggregates were also well preserved during 4 days in CAB-4°C as judged from DNA recovery and electron microscopy. After cold-storage in CAB, beta cells exhibited a higher insulin content than after culture in HAM's F10 at 20° or 37°C, but their capacity for subsequent insulin synthesis and release was comparable. When isolated islets were stored in CAB-4°C for 96 h, they yielded slightly higher numbers of dissociated cells than after culture in HAM's F10 at 20°C. Implantation of cold stored islets from 2 donor pancreata corrected hyperglycemia in streptozotocin-diabetic rats. It is concluded that rat beta cells can be stored in a supplemented Collins solution for at least 4 days at 4°C, with preservation of initial cell number, hormone content and glucose responsiveness. During short-term periods, this new storage condition is at least equivalent to cultures at 20° or 37°C. Further studies are needed to assess any advantage for long-term storage of islet cell grafts.

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Herrera, P. L. "Adult insulin- and glucagon-producing cells differentiate from two independent cell lineages." Development 127, no. 11 (June 1, 2000): 2317–22. http://dx.doi.org/10.1242/dev.127.11.2317.

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To analyze cell lineage in the pancreatic islets, we have irreversibly tagged all the progeny of cells through the activity of Cre recombinase. Adult glucagon alpha and insulin beta cells are shown to derive from cells that have never transcribed insulin or glucagon, respectively. Also, the beta-cell progenitors, but not alpha-cell progenitors, transcribe the pancreatic polypeptide (PP) gene. Finally, the homeodomain gene PDX1, which is expressed by adult beta-cells, is also expressed by alpha-cell progenitors. Thus the islet alpha- and beta-cell lineages appear to arise independently during ontogeny, probably from a common precursor.

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Prause, Michala, Signe Schultz Pedersen, Violeta Tsonkova, Min Qiao, and Nils Billestrup. "Butyrate Protects Pancreatic Beta Cells from Cytokine-Induced Dysfunction." International Journal of Molecular Sciences 22, no. 19 (September 27, 2021): 10427. http://dx.doi.org/10.3390/ijms221910427.

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Pancreatic beta cell dysfunction caused by metabolic and inflammatory stress contributes to the development of type 2 diabetes (T2D). Butyrate, produced by the gut microbiota, has shown beneficial effects on glucose metabolism in animals and humans and may directly affect beta cell function, but the mechanisms are poorly described. The aim of this study was to investigate the effect of butyrate on cytokine-induced beta cell dysfunction in vitro. Mouse islets, rat INS-1E, and human EndoC-βH1 beta cells were exposed long-term to non-cytotoxic concentrations of cytokines and/or butyrate to resemble the slow onset of inflammation in T2D. Beta cell function was assessed by glucose-stimulated insulin secretion (GSIS), gene expression by qPCR and RNA-sequencing, and proliferation by incorporation of EdU into newly synthesized DNA. Butyrate protected beta cells from cytokine-induced impairment of GSIS and insulin content in the three beta cell models. Beta cell proliferation was reduced by both cytokines and butyrate. Expressions of the beta cell specific genes Ins, MafA, and Ucn3 reduced by the cytokine IL-1β were not affected by butyrate. In contrast, butyrate upregulated the expression of secretion/transport-related genes and downregulated inflammatory genes induced by IL-1β in mouse islets. In summary, butyrate prevents pro-inflammatory cytokine-induced beta cell dysfunction.

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Verdaguer, J., J. W. Yoon, B. Anderson, N. Averill, T. Utsugi, B. J. Park, and P. Santamaria. "Acceleration of spontaneous diabetes in TCR-beta-transgenic nonobese diabetic mice by beta-cell cytotoxic CD8+ T cells expressing identical endogenous TCR-alpha chains." Journal of Immunology 157, no. 10 (November 15, 1996): 4726–35. http://dx.doi.org/10.4049/jimmunol.157.10.4726.

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Abstract The role of target cell autoantigens and their repertoire vs those of foreign Ags, superantigens, or non-Ag-specific stimuli in the activation and recruitment of effector T cells in most spontaneous models of autoimmune diseases remains elusive. Here we report on the use of single TCR-beta transgenic mice to study the mechanisms that drive the accumulation of pathogenic T cells in the pancreatic islets of nonobese diabetic (NOD) mice, a model for insulin-dependent diabetes mellitus. Expression of the V(beta)8.1+ TCR-beta rearrangement of a diabetogenic H-2Kd-restricted beta cell cytotoxic CD8+ T cell (beta-CTL) clone in NOD mice caused a 10-fold increase in the peripheral precursor frequency of beta-CTL and a selective acceleration of the recruitment of CD8+ T cells to the pancreatic islets of prediabetic animals. This resulted in an earlier onset and a faster progression of beta cell depletion, and led to a dramatic acceleration of the onset of diabetes. Most islet-derived beta-CTL from diabetic transgenic NOD mice expressed an endogenously-derived TCR-alpha sequence identical to that of the clonotype donating the TCR-beta transgene, and a TCR-alpha-CDR3 sequence homologous to those expressed by most islet-derived beta-CTL from nontransgenic NOD mice. TCR-beta transgene expression did not change the peripheral frequency of beta cell-specific CD4+ T cells, the rate at which these cells accumulated in the pancreatic islets, or the incidence of diabetes. Taken together, our data indicate that retention of CD8+ and CD4+ T cells in the pancreatic islets of NOD mice is driven by beta cell autoantigens, rather than by local superantigens or non-Ag-specific stimuli, and that beta-CTL are major effectors of beta cell damage in spontaneous insulin-dependent diabetes mellitus.

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Puddu, Alessandra, Roberta Sanguineti, François Mach, Franco Dallegri, Giorgio Luciano Viviani, and Fabrizio Montecucco. "Update on the Protective Molecular Pathways Improving Pancreatic Beta-Cell Dysfunction." Mediators of Inflammation 2013 (2013): 1–14. http://dx.doi.org/10.1155/2013/750540.

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The primary function of pancreatic beta-cells is to produce and release insulin in response to increment in extracellular glucose concentrations, thus maintaining glucose homeostasis. Deficient beta-cell function can have profound metabolic consequences, leading to the development of hyperglycemia and, ultimately, diabetes mellitus. Therefore, strategies targeting the maintenance of the normal function and protecting pancreatic beta-cells from injury or death might be crucial in the treatment of diabetes. This narrative review will update evidence from the recently identified molecular regulators preserving beta-cell mass and function recovery in order to suggest potential therapeutic targets against diabetes. This review will also highlight the relevance for novel molecular pathways potentially improving beta-cell dysfunction.

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Domínguez-Bendala, Juan. "Present and future cell therapies for pancreatic beta cell replenishment." World Journal of Gastroenterology 18, no. 47 (2012): 6876. http://dx.doi.org/10.3748/wjg.v18.i47.6876.

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Sharma, A., M. Taneja, P. Rietz, J. Weitekamp, and S. Bonner-Weir. "Novel pancreatic precursor cell lines for studying beta-cell differentiation." Diabetes 50, Supplement 1 (February 1, 2001): S42—S43. http://dx.doi.org/10.2337/diabetes.50.2007.s42.

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Mohan, Shruti, Ryan Lafferty, Neil Tanday, Peter R. Flatt, R. Charlotte Moffett, and Nigel Irwin. "Beneficial impact of Ac3IV, an AVP analogue acting specifically at V1a and V1b receptors, on diabetes islet morphology and transdifferentiation of alpha- and beta-cells." PLOS ONE 16, no. 12 (December 20, 2021): e0261608. http://dx.doi.org/10.1371/journal.pone.0261608.

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Ac3IV (Ac-CYIQNCPRG-NH2) is an enzymatically stable vasopressin analogue that selectively activates Avpr1a (V1a) and Avpr1b (V1b) receptors. In the current study we have employed streptozotocin (STZ) diabetic transgenic Ins1Cre/+;Rosa26-eYFP and GluCreERT2;Rosa26-eYFP mice, to evaluate the impact of sustained Ac3IV treatment on pancreatic islet cell morphology and transdifferentiation. Twice-daily administration of Ac3IV (25 nmol/kg bw) to STZ-diabetic Ins1Cre/+;Rosa26-eYFP mice for 12 days increased pancreatic insulin (p<0.01) and significantly reversed the detrimental effects of STZ on pancreatic islet morphology. Such benefits were coupled with increased (p<0.01) beta-cell proliferation and decreased (p<0.05) beta-cell apoptosis. In terms of islet cell lineage tracing, induction of diabetes increased (p<0.001) beta- to alpha-cell differentiation in Ins1Cre/+;Rosa26-eYFP mice, with Ac3IV partially reversing (p<0.05) such transition events. Comparable benefits of Ac3IV on pancreatic islet architecture were observed in STZ-diabetic GluCreERT2;ROSA26-eYFP transgenic mice. In this model, Ac3IV provoked improvements in islet morphology which were linked to increased (p<0.05-p<0.01) transition of alpha- to beta-cells. Ac3IV also increased (p<0.05-p<0.01) CK-19 co-expression with insulin in pancreatic ductal and islet cells. Blood glucose levels were unchanged by Ac3IV in both models, reflecting the severity of diabetes induced. Taken together these data indicate that activation of islet receptors for V1a and V1b positively modulates alpha- and beta-cell turnover and endocrine cell lineage transition events to preserve beta-cell identity and islet architecture.

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Nagamine, Takahiko. "Does olanzapine impair pancreatic beta-cell function directly?" Clinical Neuropsychopharmacology and Therapeutics 5 (2014): 23–25. http://dx.doi.org/10.5234/cnpt.5.23.

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Wagner, Bridget K. "Small-molecule discovery in the pancreatic beta cell." Current Opinion in Chemical Biology 68 (June 2022): 102150. http://dx.doi.org/10.1016/j.cbpa.2022.102150.

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Wagner, Bridget K. "Small-molecule discovery in the pancreatic beta cell." Current Opinion in Chemical Biology 68 (June 2022): 102150. http://dx.doi.org/10.1016/j.cbpa.2022.102150.

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