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Artykuły w czasopismach na temat „Pancreatic beta-cell”

Autor: Grafiati

Data publikacji: 4 czerwca 2021

Data aktualizacji: 25 lipca 2025

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1

Rastogi, D. P., A. C. Saxena, and Sunil Kumar. "Pancreatic beta-cell regeneration." British Homeopathic Journal 77, no. 03 (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-hypophys

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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 (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 soma

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3

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

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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 (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 (2004): 329–41. http://dx.doi.org/10.1007/s11938-004-0046-9.

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Bartolomé, Alberto. "The Pancreatic Beta Cell: Editorial." Biomolecules 13, no. 3 (2023): 495. http://dx.doi.org/10.3390/biom13030495.

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7

Russ, Holger A., Limor Landsman, Christopher L. Moss, et al. "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 hE

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8

Tambuwal, Umar M., Sabir A. Ahmad, Sada K. Bello, et al. "Comparing the Effect of Exercise and Metformin on Pancreatic Beta Cell Function in Nigerians with Prediabetes: A Randomized Controlled Trial." East African Scholars Journal of Medical Sciences 8, no. 04 (2025): 114–21. https://doi.org/10.36349/easms.2025.v08i04.001.

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Prediabetes is an important risk factor for the development of type 2 diabetes and is common in Nigeria. Effective intervention can reverse the underlying pathogenesis of pancreatic beta-cell dysfunction in prediabetes. Several studies have reported the prevalence of prediabetes across Nigeria, but lack information on the effect of intervention or natural outcome on pancreatic beta-cell function among Nigerians with prediabetes. The objective of this study was to determine and compare the effect of moderate exercise and metformin on pancreatic beta-cell function among participants with prediab

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9

Bouwens, Luc, and Ilse Rooman. "Regulation of Pancreatic Beta-Cell Mass." Physiological Reviews 85, no. 4 (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-repl

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10

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

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11

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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Diedisheim, Marc, Masaya Oshima, Olivier Albagli, 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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13

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 (2010): 289–98. http://dx.doi.org/10.1016/j.bbalip.2009.08.006.

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14

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 (1989): 726–28. http://dx.doi.org/10.1016/0002-9343(89)90457-9.

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15

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

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16

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

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17

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

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18

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 studie

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19

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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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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21

Ehrhart, N., S. J. Withrow, E. J. Ehrhart, and J. H. Wimsatt. "Pancreatic beta cell tumor in ferrets: 20 cases (1986–1994)." Journal of the American Veterinary Medical Association 209, no. 10 (1996): 1737–40. http://dx.doi.org/10.2460/javma.1996.209.10.1737.

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Objective— To characterize survival times, disease-free intervals, and prognostic variables in ferrets with pancreatic beta cell neoplasia. Design— Retrospective study. Animals— 20 ferrets with histologically confirmed pancreatic beta cell tumors. Procedure— Medical records of ferrets with pancreatic beta cell tumors were reviewed. Variables such as age, sex, duration of clinical signs, existence of other neoplasia, single versus multiple masses in the pancreas, benign or malignant histologic features, and the type of treatment used at redevelopment of clinical signs were examined to determine

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22

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 (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 n

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23

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 (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-lipoxyg

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24

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, sugg

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25

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 (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

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26

Dahl, U., A. Sjodin, and H. Semb. "Cadherins regulate aggregation of pancreatic beta-cells in vivo." Development 122, no. 9 (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-cadhe

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27

Verdaguer, J., J. W. Yoon, B. Anderson, et al. "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 (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 cytot

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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 (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

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29

Herrera, P. L. "Adult insulin- and glucagon-producing cells differentiate from two independent cell lineages." Development 127, no. 11 (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 o

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Zhu, Wuyun, Neil Tanday, Peter R. Flatt, and Nigel Irwin. "The Beneficial Impact of a Novel Pancreatic Polypeptide Analogue on Islet Cell Lineage." International Journal of Molecular Sciences 26, no. 9 (2025): 4215. https://doi.org/10.3390/ijms26094215.

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(Proline3)PP, or (P3)PP, is an enzymatically stable, neuropeptide Y4 receptor (NPY4R)-selective, pancreatic polypeptide (PP) analogue with established weight-lowering and pancreatic islet morphology benefits in obesity-diabetes. In the current study, we now investigate the impact of twice-daily (P3)PP administration (25 nmol/kg) for 11 days on islet cell lineage, using streptozotocin (STZ) diabetic Ins1Cre/+;Rosa26-eYFP and GluCreERT2;Rosa26-eYFP transgenic mice with enhanced yellow fluorescent protein (eYFP) labelling of beta-cell and alpha-cells, respectively. (P3)PP had no obvious impact on

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Hosseini, Azar, Reza Shafiee-Nick, and Ahmad Ghorbani. "Pancreatic beta cell protection/regeneration with phytotherapy." Brazilian Journal of Pharmaceutical Sciences 51, no. 1 (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 diab

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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 (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 pa

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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 (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 resemb

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Memon, Bushra, and Essam M. Abdelalim. "Stem Cell Therapy for Diabetes: Beta Cells versus Pancreatic Progenitors." Cells 9, no. 2 (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 st

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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 isle

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Pryke, Luke A., Ziyue Liu, Alka K. Khaitan, Emily K. Sims, and Samir K. Gupta. "Immune checkpoints and pancreatic beta cell dysfunction in HIV." AIDS 38, no. 11 (2024): 1725–27. http://dx.doi.org/10.1097/qad.0000000000003932.

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We explored the impact of immune dysregulation on pancreatic beta cell injury in HIV patients. Analyzing 105 participant samples, we observed lower IL-21 levels and elevated immune checkpoint levels (e.g. PD-1, CD27+, CD40+) in untreated HIV patients. Notably, soluble TIM-3 correlated positively with improved beta cell function and inversely with beta cell stress, suggesting its potential role in beta cell protection in untreated HIV.

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Gallardo-Villanueva, Paula, Tamara Fernández-Marcelo, Laura Villamayor, et al. "Synergistic Effect of a Flavonoid-Rich Cocoa–Carob Blend and Metformin in Preserving Pancreatic Beta Cells in Zucker Diabetic Fatty Rats." Nutrients 16, no. 2 (2024): 273. http://dx.doi.org/10.3390/nu16020273.

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The loss of functional beta-cell mass in diabetes is directly linked to the development of diabetic complications. Although dietary flavonoids have demonstrated antidiabetic properties, their potential effects on pancreatic beta-cell preservation and their synergistic benefits with antidiabetic drugs remain underexplored. We have developed a potential functional food enriched in flavonoids by combining cocoa powder and carob flour (CCB), which has shown antidiabetic effects. Here, we investigated the ability of the CCB, alone or in combination with metformin, to preserve pancreatic beta cells

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

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

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Kohler, Martin, Daniel Nyqvist, Tilo Moede, et al. "Imaging of Pancreatic Beta-Cell Signal-Transduction." Current Medicinal Chemistry-Immunology, Endocrine & Metabolic Agents 4, no. 4 (2004): 281–99. http://dx.doi.org/10.2174/1568013043357275.

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Rulifson, I. C., S. K. Karnik, P. W. Heiser, et al. "Wnt signaling regulates pancreatic beta cell proliferation." Proceedings of the National Academy of Sciences 104, no. 15 (2007): 6247–52. http://dx.doi.org/10.1073/pnas.0701509104.

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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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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 (2003): A65. http://dx.doi.org/10.1046/j.1443-9506.2003.02599.x.

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

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

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Hembree, Mark, Kok-Hooi Yew, Krishna Prasadan, et al. "TGF-beta signaling in pancreatic cell differentiation." Journal of the American College of Surgeons 199, no. 3 (2004): 85. http://dx.doi.org/10.1016/j.jamcollsurg.2004.05.183.

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

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Fan, Fan, and Xuelin Lou. "Dynamin function in pancreatic beta cell autophagy." Biophysical Journal 123, no. 3 (2024): 105a—106a. http://dx.doi.org/10.1016/j.bpj.2023.11.761.

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Guz, Y., M. R. Montminy, R. Stein, et al. "Expression of murine STF-1, a putative insulin gene transcription factor, in beta cells of pancreas, duodenal epithelium and pancreatic exocrine and endocrine progenitors during ontogeny." Development 121, no. 1 (1995): 11–18. http://dx.doi.org/10.1242/dev.121.1.11.

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The XlHbox 8 homeodomain protein of Xenopus and STF-1, its mammalian homolog, are selectively expressed by beta cells of adult mouse pancreatic islets, where they are likely to regulate insulin expression. We sought to determine whether the expression of the homeobox protein/s during mouse embryonic development was specific to beta cells or, alternatively, whether XlHbox 8/STF-1 protein/s were initially expressed by multipotential precursors and only later became restricted to the insulin-containing cells. With two antibodies, we studied the localization of STF-1 during murine pancreatic devel

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Jorns, A., R. Munday, M. Tiedge, and S. Lenzen. "Comparative toxicity of alloxan, N-alkylalloxans and ninhydrin to isolated pancreatic islets in vitro." Journal of Endocrinology 155, no. 2 (1997): 283–93. http://dx.doi.org/10.1677/joe.0.1550283.

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The in vitro toxicity of the diabetogenic agent alloxan as documented by the induction of beta cell necrosis was studied in isolated ob/ob mouse pancreatic islets. The effect of alloxan has been compared with that of a number of N-alkyl alloxan derivatives and with that of the structurally related compound, ninhydrin. Alloxan and its derivatives were selectively toxic to pancreatic beta cells, with other endocrine cells and exocrine parenchymal cells being well preserved, even at high concentration. In contrast, ninhydrin was selectively toxic to pancreatic beta cells only at comparatively low

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