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

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Published: 3 June 2025

Last updated: 31 July 2025

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1

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

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Type 1 diabetes is characterized by autoimmune destruction of β cells located in pancreatic islets. However, tractable in vivo models of human pancreatic β cells have been limited. Here, we generated xenogeneic human pancreatic β-like cells in the mouse pancreas by orthotopic transplantation of stem cell-derived β (SC-β) cells into the pancreas of neonatal mice. The engrafted β-like cells expressed β cell transcription factors and markers associated with functional maturity. Engrafted human cells recruited mouse endothelial cells, suggesting functional integration. Human insulin was detected i

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Beamish, Christine A., Sofia Mehta, Brenda J. Strutt, Subrata Chakrabarti, Manami Hara та David J. Hill. "Decrease in Ins+Glut2LO β-cells with advancing age in mouse and human pancreas". Journal of Endocrinology 233, № 3 (2017): 229–41. http://dx.doi.org/10.1530/joe-16-0475.

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The presence and location of resident pancreatic β-cell progenitors is controversial. A subpopulation of insulin-expressing but glucose transporter-2-low (Ins+Glut2LO) cells may represent multipotent pancreatic progenitors in adult mouse and in human islets, and they are enriched in small, extra-islet β-cell clusters (<5 β cells) in mice. Here, we sought to identify and compare the ontogeny of these cells in mouse and human pancreata throughout life. Mouse pancreata were collected at postnatal days 7, 14, 21, 28, and at 3, 6, 12, and 18 months of age, and in the first 28 days after β-cell m

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3

Butler, Alexandra E., Sangeeta Dhawan, Jonathan Hoang та ін. "β-Cell Deficit in Obese Type 2 Diabetes, a Minor Role of β-Cell Dedifferentiation and Degranulation". Journal of Clinical Endocrinology & Metabolism 101, № 2 (2016): 523–32. http://dx.doi.org/10.1210/jc.2015-3566.

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Abstract Context: Type 2 diabetes is characterized by a β-cell deficit and a progressive defect in β-cell function. It has been proposed that the deficit in β-cells may be due to β-cell degranulation and transdifferentiation to other endocrine cell types. Objective: The objective of the study was to establish the potential impact of β-cell dedifferentiation and transdifferentiation on β-cell deficit in type 2 diabetes and to consider the alternative that cells with an incomplete identity may be newly forming rather than dedifferentiated. Design, Setting, and Participants: Pancreata obtained at

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Bohuslavova, Romana, Ondrej Smolik, Jessica Malfatti та ін. "NEUROD1 Is Required for the Early α and β Endocrine Differentiation in the Pancreas". International Journal of Molecular Sciences 22, № 13 (2021): 6713. http://dx.doi.org/10.3390/ijms22136713.

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Diabetes is a metabolic disease that involves the death or dysfunction of the insulin-secreting β cells in the pancreas. Consequently, most diabetes research is aimed at understanding the molecular and cellular bases of pancreatic development, islet formation, β-cell survival, and insulin secretion. Complex interactions of signaling pathways and transcription factor networks regulate the specification, growth, and differentiation of cell types in the developing pancreas. Many of the same regulators continue to modulate gene expression and cell fate of the adult pancreas. The transcription fact

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Mwangi, Simon M., Yousef Usta, Shreya M. Raja та ін. "Glial cell line-derived neurotrophic factor enhances neurogenin3 gene expression and β-cell proliferation in the developing mouse pancreas". American Journal of Physiology-Gastrointestinal and Liver Physiology 299, № 1 (2010): G283—G292. http://dx.doi.org/10.1152/ajpgi.00096.2010.

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Glial cell line-derived neurotrophic factor (GDNF) is a factor produced by glial cells that is required for the development of the enteric nervous system. In transgenic mice that overexpress GDNF in the pancreas, GDNF has been shown to enhance β-cell mass and improve glucose control, but the transcriptional and cellular processes involved are not known. In this study we examined the influence of GDNF on the expression of neurogenin3 (Ngn3) and other transcription factors implicated in early β-cell development, as well as on β-cell proliferation during embryonic and early postnatal mouse pancre

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Garcia, Cathy, Aarthi Venkat, Daniel McQuaid, et al. "Abstract PR-05: Endocrine beta-cell stress promotes pancreatic ductal adenocarcinoma through endocrine-exocrine cell crosstalk." Cancer Research 84, no. 17_Supplement_2 (2024): PR—05—PR—05. http://dx.doi.org/10.1158/1538-7445.pancreatic24-pr-05.

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Abstract For a long time, the pancreas was thought to have separate cellular compartments that functioned distinctly from one another. The endocrine pancreas (islets of Langerhans) regulates glucose homeostasis, while the exocrine pancreas (acini and ducts) produces and secretes digestive enzymes. However, it has recently become clear that the endocrine and exocrine compartments communicate with one another, and dysfunction in one leads to dysfunction in the other, resulting in diabetes or pancreatitis. However, whether and how the endocrine pancreas drives the development of pancreatic ductal

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Kobayashi, Masaki, Osamu Kikuchi, Tsutomu Sasaki та ін. "FoxO1 as a double-edged sword in the pancreas: analysis of pancreas- and β-cell-specific FoxO1 knockout mice". American Journal of Physiology-Endocrinology and Metabolism 302, № 5 (2012): E603—E613. http://dx.doi.org/10.1152/ajpendo.00469.2011.

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Diabetes is characterized by an absolute or relative deficiency of pancreatic β-cells. New strategies to accelerate β-cell neogenesis or maintain existing β-cells are desired for future therapies against diabetes. We previously reported that forkhead box O1 (FoxO1) inhibits β-cell growth through a Pdx1-mediated mechanism. However, we also reported that FoxO1 protects against β-cell failure via the induction of NeuroD and MafA. Here, we investigate the physiological roles of FoxO1 in the pancreas by generating the mice with deletion of FoxO1 in the domains of the Pdx1 promoter (P-FoxO1-KO) or t

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8

Riz, Michela, Morten Gram Pedersen, Gianna Maria Toffolo, et al. "Minimal modeling of insulin secretion in the perfused rat pancreas: a drug effect case study." American Journal of Physiology-Endocrinology and Metabolism 306, no. 6 (2014): E627—E634. http://dx.doi.org/10.1152/ajpendo.00603.2013.

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The experimental protocol of the perfused rat pancreas is commonly used to evaluate β-cell function. In this context, mathematical models become useful tools through the determination of indexes that allow the assessment of β-cell function in different experimental groups and the quantification of the effects of antidiabetic drugs, secretagogues, or treatments. However, a minimal model applicable to the isolated perfused rat pancreas has so far been unavailable. In this work, we adapt the C-peptide minimal model applied previously to the intravenous glucose tolerance test to obtain a specific

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9

Perfetti, Riccardo, Jie Zhou, Máire E. Doyle, and Josephine M. Egan. "Glucagon-Like Peptide-1 Induces Cell Proliferation and Pancreatic-Duodenum Homeobox-1 Expression and Increases Endocrine Cell Mass in the Pancreas of Old, Glucose-Intolerant Rats." Endocrinology 141, no. 12 (2000): 4600–4605. http://dx.doi.org/10.1210/endo.141.12.7806.

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Abstract Glucose homeostasis in mammals is maintained by insulin secretion from the β-cells of the islets of Langerhans. Type 2 diabetes results either from primary β-cell failure alone and/or a failure to secrete enough insulin to overcome insulin resistance. Here, we show that continuous infusion of glucagon-like peptide-1 (7–36) (GLP-1; an insulinotropic agent), to young and old animals, had effects on the β-cell of the pancreas other than simply on the insulin secretory apparatus. Our previous studies on a rodent model of glucose intolerance, the aging Wistar rat, show that a plateau in is

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Wiebe, Peter O., Jay D. Kormish, Venus T. Roper, et al. "Ptf1a Binds to and Activates Area III, a Highly Conserved Region of the Pdx1 Promoter That Mediates Early Pancreas-Wide Pdx1 Expression." Molecular and Cellular Biology 27, no. 11 (2007): 4093–104. http://dx.doi.org/10.1128/mcb.01978-06.

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

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11

Wong, Wilson K. M., Anja E. Sørensen, Mugdha V. Joglekar, Anand A. Hardikar та Louise T. Dalgaard. "Non-Coding RNA in Pancreas and β-Cell Development". Non-Coding RNA 4, № 4 (2018): 41. http://dx.doi.org/10.3390/ncrna4040041.

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In this review, we provide an overview of the current knowledge on the role of different classes of non-coding RNAs for islet and β-cell development, maturation and function. MicroRNAs (miRNAs), a prominent class of small RNAs, have been investigated for more than two decades and patterns of the roles of different miRNAs in pancreatic fetal development, islet and β-cell maturation and function are now emerging. Specific miRNAs are dynamically regulated throughout the period of pancreas development, during islet and β-cell differentiation as well as in the perinatal period, where a burst of β-c

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Hara, Manami, Restituto F. Dizon, Benjamin S. Glick та ін. "Imaging pancreatic β-cells in the intact pancreas". American Journal of Physiology-Endocrinology and Metabolism 290, № 5 (2006): E1041—E1047. http://dx.doi.org/10.1152/ajpendo.00365.2005.

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We have developed a method to visualize fluorescent protein-labeled β-cells in the intact pancreas through combined reflection and confocal imaging. This method provides a 3-D view of the β-cells in situ. Imaging of the pancreas from mouse insulin I promoter (MIP)-green (GFP) and red fluorescent protein (RFP) transgenic mice shows that islets, β-cell clusters, and single β-cells are not evenly distributed but are aligned along the large blood vessels. We also observe the solitary β-cells in both fetal and adult mice and along the pancreatic and common bile ducts. We have imaged the developing

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13

Köhler, Christina U., Marvin Olewinski, Andrea Tannapfel, Wolfgang E. Schmidt, Helga Fritsch та Juris J. Meier. "Cell cycle control of β-cell replication in the prenatal and postnatal human pancreas". American Journal of Physiology-Endocrinology and Metabolism 300, № 1 (2011): E221—E230. http://dx.doi.org/10.1152/ajpendo.00496.2010.

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β-Cell regeneration declines with aging, but the molecular mechanisms controlling β-cell replication in humans are not well understood. We compared the expression of selected cell cycle proteins in prenatal and adult tissue and examined the association of these proteins with β-cell replication. Pancreatic tissue from a total of 20 human fetuses and adults was stained for Ki67, cyclin D3, p16 and p27, and insulin. The β-cellular expression of these cell cycle proteins was determined. The frequency of β-cell replication was lower in adult compared with prenatal β-cells (<0.5 vs. 3.4 ± 0.5%, r

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14

Meier, Juris J., Christina U. Köhler, Bacel Alkhatib та ін. "β-cell development and turnover during prenatal life in humans". European Journal of Endocrinology 162, № 3 (2010): 559–68. http://dx.doi.org/10.1530/eje-09-1053.

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Introductionβ-cell regeneration is an area under active investigation for the future treatment of diabetes, but little is known about the patterns and dynamics of prenatal β-cell development in humans. In particular, the quantitative changes in β-cell mass in the developing pancreas have not been elucidated in detail. We addressed the following questions in prenatal humans: i) what is the timing of β-cell occurrence and islet growth? ii) What are the dynamics of β-cell replication and apoptosis?MethodsPancreatic tissue was obtained from 65 human embryos and foetuses aged between 8 weeks post c

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Aye, Tandy, Elena Toschi, Arun Sharma, Dennis Sgroi та Susan Bonner-Weir. "Identification of Markers for Newly Formed β-Cells in the Perinatal Period: A Time of Recognized β-Cell Immaturity". Journal of Histochemistry & Cytochemistry 58, № 4 (2010): 369–76. http://dx.doi.org/10.1369/jhc.2009.954909.

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Markers of β-cell maturity would be useful in staging the differentiation of stem/progenitor cells to β-cells whether in vivo or in vitro. We previously identified markers for newly formed β-cells in regenerating rat pancreases after 90% partial pancreatectomy. To test the generality of these markers of newly formed β-cells, we examined their expression during the perinatal period, a time of recognized β-cell immaturity. We show by semiquantitative RT-PCR and immunostaining over the time course from embryonic day 18/20 to birth, 1 day, 2 days, 3 days, 7 days, and adult that MMP-2, CK-19, and S

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Trivedi, N., J. Hollister-Lock, M. D. Lopez-Avalos та ін. "Increase in β-Cell Mass in Transplanted Porcine Neonatal Pancreatic Cell Clusters Is Due to Proliferation of β-Cells and Differentiation of Duct Cells*". Endocrinology 142, № 5 (2001): 2115–22. http://dx.doi.org/10.1210/endo.142.5.8162.

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Abstract A 20-fold increase in β-cell mass has been found after transplantation of porcine neonatal pancreatic cell clusters (NPCCs). Here the mechanisms leading to this increased β-cell mass were studied. NPCCs (4000 islet equivalents) generated after 8 days culture of digested neonatal pig pancreas were transplanted beneath the renal capsule of streptozotocin (STZ) diabetic and normoglycemic nude mice. Grafts were removed at 10 days, 6 weeks, and 20 weeks after transplantation for immunostaining and insulin content. Proliferation of β-cells and duct cells was assessed morphometrically using

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Butler, Alexandra E., Wendy Sacks, Robert A. Rizza та Peter C. Butler. "Down Syndrome-Associated Diabetes Is Not Due To a Congenital Deficiency in β Cells". Journal of the Endocrine Society 1, № 1 (2017): 39–45. http://dx.doi.org/10.1210/js.2016-1042.

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Abstract Aims/Hypothesis: We sought to establish whether the increased incidence of diabetes associated with Down syndrome was due to a congenital deficit in β cells. Methods: The pancreas was obtained at autopsy from nondiabetic subjects with Down syndrome (n = 29) and age-matched nondiabetic control subjects without Down syndrome (n = 28). The pancreas sections were evaluated for the fractional β-cell area. Results: No difference was found in the fractional β-cell area between the subjects with Down syndrome and the control subjects. Conclusions/Interpretations: The increased incidence and p

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18

Da Silva Xavier, Gabriela. "The Cells of the Islets of Langerhans." Journal of Clinical Medicine 7, no. 3 (2018): 54. http://dx.doi.org/10.3390/jcm7030054.

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Islets of Langerhans are islands of endocrine cells scattered throughout the pancreas. A number of new studies have pointed to the potential for conversion of non-β islet cells in to insulin-producing β-cells to replenish β-cell mass as a means to treat diabetes. Understanding normal islet cell mass and function is important to help advance such treatment modalities: what should be the target islet/β-cell mass, does islet architecture matter to energy homeostasis, and what may happen if we lose a particular population of islet cells in favour of β-cells? These are all questions to which we wil

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Arrojo e Drigo, Rafael. "Probing β-Cell Biology in Space and Time". Diabetes 70, № 10 (2021): 2163–73. http://dx.doi.org/10.2337/dbi21-0008.

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β-Cells in the islet of Langerhans have a central role in maintaining energy homeostasis. Understanding the physiology of β-cells and other islet cells requires a deep understanding of their structural and functional organization, their interaction with vessels and nerves, the layout of paracrine interactions, and the relationship between subcellular compartments and protein complexes inside each cell. These elements are not static; they are dynamic and exert their biological actions at different scales of time. Therefore, scientists must be able to investigate (and visualize) short- and long-

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Chuang, Jen-Chieh, Ji-Young Cha, James C. Garmey, Raghavendra G. Mirmira, and Joyce J. Joyce J. "Research Resource: Nuclear Hormone Receptor Expression in the Endocrine Pancreas." Molecular Endocrinology 22, no. 10 (2008): 2353–63. http://dx.doi.org/10.1210/me.2007-0568.

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Abstract The endocrine pancreas comprises the islets of Langerhans, tiny clusters of cells that contribute only about 2% to the total pancreas mass. However, this little endocrine organ plays a critical role in maintaining glucose homeostasis by the regulated secretion of insulin (by β-cells) and glucagon (by α-cells). The rapid increase in the incidence of diabetes worldwide has spurred renewed interest in islet cell biology. Some of the most widely prescribed oral drugs for treating type 2 diabetes include agents that bind and activate the nuclear hormone receptor, peroxisome proliferator-ac

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Alvarsson, Alexandra, Maria Jimenez-Gonzalez, Rosemary Li, et al. "A 3D atlas of the dynamic and regional variation of pancreatic innervation in diabetes." Science Advances 6, no. 41 (2020): eaaz9124. http://dx.doi.org/10.1126/sciadv.aaz9124.

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Understanding the detailed anatomy of the endocrine pancreas, its innervation, and the remodeling that occurs in diabetes can provide new insights into metabolic disease. Using tissue clearing and whole-organ imaging, we identified the 3D associations between islets and innervation. This technique provided detailed quantification of α and β cell volumes and pancreatic nerve fibers, their distribution and heterogeneity in healthy tissue, canonical mouse models of diabetes, and samples from normal and diabetic human pancreata. Innervation was highly enriched in the mouse endocrine pancreas, with

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Movassat, Jamileh, та Bernard Portha. "Early administration of keratinocyte growth factor improves β-cell regeneration in rat with streptozotocin-induced diabetes". Journal of Endocrinology 195, № 2 (2007): 333–40. http://dx.doi.org/10.1677/joe-07-0098.

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The aim of our study was to investigate the ability of keratinocyte growth factor (KGF; palifermin) in regulating β-cell growth in normal newborn rats and in rats with neonatal diabetes. Wistar rats were injected with streptozotocin (STZ) to induce diabetes on the dayof birth. From days 2 to 6 after birth, animals received a daily s.c. injection of KGF (STZ/KGF group) and at the dose of 3 mg/kg body weight or saline solution (STZ groups). A group of non-diabetic Wistar rats was treated either with saline (Wistar group) or with KGF from days 2 to 6 after birth at the dose of 3 mg/kg body weight

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Parajuli, Sandesh, Riccardo Tamburrini, Fahad Aziz, et al. "Simultaneous Pancreas-Kidney Transplant Outcomes Stratified by Autoantibodies Status and Pretransplant Fasting C-peptide." Transplantation Direct 10, no. 11 (2024): e1721. http://dx.doi.org/10.1097/txd.0000000000001721.

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Backgrounds. Pancreatic beta cell function and islet autoantibodies classically distinguish types of diabetes (type 1 diabetes mellitus [DM] or type 2 DM). Here, we sought to evaluate simultaneous pancreas-kidney (SPK) transplant outcomes stratified by the presence or absence of beta cell function and autoantibodies. Methods. SPK recipients were eligible if pretransplant autoantibodies were measured against insulin, islet cell, or glutamic acid decarboxylase 65-kD isoform. Recipients were categorized as A+ or A– based on the detection of ≥1 autoantibodies. Recipients were similarly categorized

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Carvalho, C. P. F., R. B. Oliveira, A. Britan та ін. "Impaired β-cell-β-cell coupling mediated by Cx36 gap junctions in prediabetic mice". American Journal of Physiology-Endocrinology and Metabolism 303, № 1 (2012): E144—E151. http://dx.doi.org/10.1152/ajpendo.00489.2011.

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Gap junctional intercellular communication between β-cells is crucial for proper insulin biosynthesis and secretion. The aim of this work was to investigate the expression of connexin (Cx)36 at the protein level as well as the function and structure of gap junctions (GJ) made by this protein in the endocrine pancreas of prediabetic mice. C57BL/6 mice were fed a high-fat (HF) or regular chow diet for 60 days. HF-fed mice became obese and prediabetic, as shown by peripheral insulin resistance, moderate hyperglycemia, hyperinsulinemia, and compensatory increase in endocrine pancreas mass. Compare

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Simeone, Diane M., Lizhi Zhang, Mary K. Treutelaar, et al. "Islet hypertrophy following pancreatic disruption of Smad4 signaling." American Journal of Physiology-Endocrinology and Metabolism 291, no. 6 (2006): E1305—E1316. http://dx.doi.org/10.1152/ajpendo.00561.2005.

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To investigate the role of transforming growth factor (TGF)-β family signaling in the adult pancreas, a transgenic mouse (E-dnSmad4) was created that expresses a dominant-negative Smad4 protein driven by a fragment of the elastase promoter. Although E-dnSmad4 mice have normal growth, pancreas weight, and pancreatic exocrine and ductal histology, beginning at 4–6 wk of age, E-dnSmad4 mice show an age-dependent increase in the size of islets. In parallel, an expanded population of replicating cells expressing the E-dnSmad4 transgene is found in the stroma between the enlarged islets and pancreat

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Grzesik, Wojciech J., Joseph L. Nadler, Yui Machida, Jerry L. Nadler, Yumi Imai, and Margaret A. Morris. "Expression Pattern of 12-Lipoxygenase in Human Islets With Type 1 Diabetes and Type 2 Diabetes." Journal of Clinical Endocrinology & Metabolism 100, no. 3 (2015): E387—E395. http://dx.doi.org/10.1210/jc.2014-3630.

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Context: Inflammation in the pancreas can cause β-cell stress, leading to diabetes development. Access to human pancreas tissues via the Network for Pancreatic Organ Donors with Diabetes (nPOD) has allowed characterization of pathways leading to this inflammation. Objective: 12-Lipoxygenase (12-LO) induces inflammation and has been implicated in diabetes development. Our goal was to determine expression of 12-LO in human islets from control, autoantibody-positive, type 1 diabetic, and type 2 diabetic nPOD pancreas donors. Design: Pancreas tissues from nPOD donors were examined by immunohistoch

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Zhang, Mingfeng, Qing Lin, Tong Qi та ін. "Growth factors and medium hyperglycemia induce Sox9+ ductal cell differentiation into β cells in mice with reversal of diabetes". Proceedings of the National Academy of Sciences 113, № 3 (2016): 650–55. http://dx.doi.org/10.1073/pnas.1524200113.

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We previously reported that long-term administration of a low dose of gastrin and epidermal growth factor (GE) augments β-cell neogenesis in late-stage diabetic autoimmune mice after eliminating insulitis by induction of mixed chimerism. However, the source of β-cell neogenesis is still unknown. SRY (sex-determining region Y)-box 9+ (Sox9+) ductal cells in the adult pancreas are clonogenic and can give rise to insulin-producing β cells in an in vitro culture. Whether Sox9+ ductal cells in the adult pancreas can give rise to β cells in vivo remains controversial. Here, using lineage-tracing wit

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Hara, Manami, Xiaoyu Wang, Toshihiko Kawamura та ін. "Transgenic mice with green fluorescent protein-labeled pancreatic β-cells". American Journal of Physiology-Endocrinology and Metabolism 284, № 1 (2003): E177—E183. http://dx.doi.org/10.1152/ajpendo.00321.2002.

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We have generated transgenic mice that express green fluorescent protein (GFP) under the control of the mouse insulin I gene promoter (MIP). The MIP-GFP mice develop normally and are indistinguishable from control animals with respect to glucose tolerance and pancreatic insulin content. Histological studies showed that the MIP-GFP mice had normal islet architecture with coexpression of insulin and GFP in the β-cells of all islets. We observed GFP expression in islets from embryonic day E13.5 through adulthood. Studies of β-cell function revealed no difference in glucose-induced intracellular c

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Foster, Timothy P., Brittany Bruggeman, Martha Campbell-Thompson, Mark A. Atkinson, Michael J. Haller, and Desmond A. Schatz. "EXOCRINE PANCREAS DYSFUNCTION IN TYPE 1 DIABETES." Endocrine Practice 26, no. 12 (2020): 1505–13. http://dx.doi.org/10.4158/ep-2020-0295.

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Objective: Type 1 diabetes (T1D) is characterized by autoimmune β-cell destruction, but exocrine pancreas abnormalities may also play a role in the disease pathophysiology. Herein, we review the current evidence of exocrine damage in T1D and discuss its underlying pathophysiology, clinical evaluation, and treatment. Method: Extensive literature search was performed for “type 1 diabetes” and “exocrine dysfunction” on PubMed and Google Scholar databases. Results: T1D pancreata are significantly smaller than controls, both in weight and volume. T cells, dendritic cells, neutrophils, and products

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Xie, Tao, Min Chen та Lee S. Weinstein. "Pancreas-specific Gsα deficiency has divergent effects on pancreatic α- and β-cell proliferation". Journal of Endocrinology 206, № 3 (2010): 261–69. http://dx.doi.org/10.1677/joe-10-0030.

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The ubiquitously expressed G protein α-subunit Gsα mediates the intracellular cAMP response to glucagon-like peptide 1 (GLP1) and other incretin hormones in pancreatic islet cells. We have shown previously that mice with β-cell-specific Gsα deficiency (βGsKO) develop severe early-onset insulin-deficient diabetes with a severe defect in β-cell proliferation. We have now generated mice with Gsα deficiency throughout the whole pancreas by mating Gsα-floxed mice with Pdx1-cre transgenic mice (PGsKO). PGsKO mice also developed severe insulin-deficient diabetes at a young age, confirming the importa

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Guillen, C., P. Navarro, M. Robledo, A. M. Valverde та M. Benito. "Differential Mitogenic Signaling in Insulin Receptor-Deficient Fetal Pancreatic β-Cells". Endocrinology 147, № 4 (2006): 1959–68. http://dx.doi.org/10.1210/en.2005-0831.

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Insulin receptor (IR) may play an essential role in the development of β-cell mass in the mouse pancreas. To further define the function of this signaling system in β-cell development, we generated IR-deficient β-cell lines. Fetal pancreata were dissected from mice harboring a floxed allele of the insulin receptor (IRLoxP) and used to isolate islets. These islets were infected with a retrovirus to express simian virus 40 large T antigen, a strategy for establishing β-cell lines (β-IRLoxP). Subsequently, these cells were infected with adenovirus encoding cre recombinase to delete insulin recept

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White, Michael G., Hussain R. Al-Turaifi, Graham N. Holliman, Ali Aldibbiat, Aiman Mahmoud, and James A. M. Shaw. "Pluripotency-associated stem cell marker expression in proliferative cell cultures derived from adult human pancreas." Journal of Endocrinology 211, no. 2 (2011): 169–76. http://dx.doi.org/10.1530/joe-11-0123.

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The source of new β-cells in adult human pancreas remains incompletely elucidated with recent studies on rodents providing evidence for neogenesis from progenitor cells in addition to self-replication. The aim of this study was to investigate the expression of pluripotency-associated stem cell markers in proliferative cultures derived from adult human pancreas. Human pancreatic tissue was obtained from deceased donors following ethical approval and relative consent. Islet-enriched fraction was separated from the retrieved organ by digestion and density gradient centrifugation. Dissociated cell

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Wong, Alicia, Brian Akhaphong, Daniel Baumann та Emilyn U. Alejandro. "Genetic Ablation of the Nutrient Sensor Ogt in Endocrine Progenitors Is Dispensable for β-Cell Development but Essential for Maintenance of β-Cell Mass". Biomedicines 11, № 1 (2022): 105. http://dx.doi.org/10.3390/biomedicines11010105.

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Previously we utilized a murine model to demonstrate that Ogt deletion in pancreatic progenitors (OgtKOPanc) causes pancreatic hypoplasia, partly mediated by a reduction in the Pdx1-expressing pancreatic progenitor pool. Here, we continue to explore the role of Ogt in pancreas development by deletion of Ogt in the endocrine progenitors (OgtKOEndo). At birth OgtKOEndo, were normoglycemic and had comparable pancreas weight and α-cell, and β-cell mass to littermate controls. At postnatal day 23, OgtKOEndo displayed wide ranging but generally elevated blood glucose levels, with histological analys

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Finegood, Diane T., Gordon C. Weir, and Susan Bonner-Weir. "Prior streptozotocin treatment does not inhibit pancreas regeneration after 90% pancreatectomy in rats." American Journal of Physiology-Endocrinology and Metabolism 276, no. 5 (1999): E822—E827. http://dx.doi.org/10.1152/ajpendo.1999.276.5.e822.

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The effects of residual β-cell mass and glycemia on regeneration of endocrine pancreas after 90% pancreatectomy were investigated. Streptozotocin or buffer alone was injected into 4-wk-old male Lewis rats ( day 0). On day 7, varying numbers of syngeneic islets were transplanted under the kidney capsule to achieve varying degrees of glucose normalization. On day 14, a 90% pancreatectomy or sham pancreatectomy was performed. On day 19, rats were killed and the pancreas was fixed for quantitative morphometric determination of β-cell mass. Focal areas of regenerating pancreas were observed in all

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de Miguel-Santos, Laura, Elisa Fernández-Millán, María Ángeles Martín, Fernando Escrivá та Carmen Álvarez. "Maternal undernutrition increases pancreatic IGF-2 and partially suppresses the physiological wave of β-cell apoptosis during the neonatal period". Journal of Molecular Endocrinology 44, № 1 (2009): 25–36. http://dx.doi.org/10.1677/jme-09-0045.

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Replication, neogenesis, and apoptosis play a main role in neonatal endocrine pancreas remodeling. IGFs are major contributors to β-cell growth and function and are highly sensitive to nutritional status. We previously showed that maternal malnutrition caused an increase in β-cell mass in fetuses related to the stimulation of β-cell proliferation due to increased pancreatic IGF-1. At 4 days of life, the β-cell mass was decreased in undernourished neonates and persisted until adult age. To clarify whether undernutrition disrupts islet remodeling, we quantified β-cell mass, neogenesis, replicati

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Elvira, Bernat, Valerie Vandenbempt, Julia Bauzá-Martinez та ін. "PTPN2 Regulates the Interferon Signaling and Endoplasmic Reticulum Stress Response in Pancreatic β-Cells in Autoimmune Diabetes". Diabetes 71, № 4 (2022): 653–68. http://dx.doi.org/10.2337/db21-0443.

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Type 1 diabetes (T1D) results from autoimmune destruction of β-cells in the pancreas. Protein tyrosine phosphatases (PTPs) are candidate genes for T1D and play a key role in autoimmune disease development and β-cell dysfunction. Here, we assessed the global protein and individual PTP profiles in the pancreas from nonobese mice with early-onset diabetes (NOD) mice treated with an anti-CD3 monoclonal antibody and interleukin-1 receptor antagonist. The treatment reversed hyperglycemia, and we observed enhanced expression of PTPN2, a PTP family member and T1D candidate gene, and endoplasmic reticu

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Bellofatto, Kevin, Beat Moeckli, Charles-Henri Wassmer, et al. "Bioengineered Islet Cell Transplantation." Current Transplantation Reports 8, no. 2 (2021): 57–66. http://dx.doi.org/10.1007/s40472-021-00318-1.

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Abstract Purpose of Review β cell replacement via whole pancreas or islet transplantation has greatly evolved for the cure of type 1 diabetes. Both these strategies are however still affected by several limitations. Pancreas bioengineering holds the potential to overcome these hurdles aiming to repair and regenerate β cell compartment. In this review, we detail the state-of-the-art and recent progress in the bioengineering field applied to diabetes research. Recent Findings The primary target of pancreatic bioengineering is to manufacture a construct supporting insulin activity in vivo. Scaffo

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Shi, Kerong, Vaishali I. Parekh, Swarnava Roy, Shruti S. Desai та Sunita K. Agarwal. "The embryonic transcription factor Hlxb9 is a menin interacting partner that controls pancreatic β-cell proliferation and the expression of insulin regulators". Endocrine-Related Cancer 20, № 1 (2013): 111–22. http://dx.doi.org/10.1530/erc-12-0077.

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The multiple endocrine neoplasia type 1 (MEN1) syndrome is caused by germline mutations in the MEN1 gene encoding menin, with tissue-specific tumors of the parathyroids, anterior pituitary, and enteropancreatic endocrine tissues. Also, 30–40% of sporadic pancreatic endocrine tumors show somatic MEN1 gene inactivation. Although menin is expressed in all cell types of the pancreas, mouse models with loss of menin in either pancreatic α-cells, or β-cells, or total pancreas develop β-cell-specific endocrine tumors (insulinomas). Loss of widely expressed tumor suppressor genes may produce tissue-sp

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Xiao, Xiangwei, Congde Chen, Ping Guo та ін. "Forkhead Box Protein 1 (FoxO1) Inhibits Accelerated β Cell Aging in Pancreas-specific SMAD7 Mutant Mice". Journal of Biological Chemistry 292, № 8 (2017): 3456–65. http://dx.doi.org/10.1074/jbc.m116.770032.

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The mechanisms underlying the effects of exocrine dysfunction on the development of diabetes remain largely unknown. Here we show that pancreatic depletion of SMAD7 resulted in age-dependent increases in β cell dysfunction with accelerated glucose intolerance, followed by overt diabetes. The accelerated β cell dysfunction and loss of proliferation capacity, two features of β cell aging, appeared to be non-cell-autonomous, secondary to the adjacent exocrine failure as a “bystander effect.” Increased Forkhead box protein 1 (FoxO1) acetylation and nuclear retention was followed by progressive Fox

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Green, Alice S., Paul J. Rozance, and Sean W. Limesand. "Consequences of a compromised intrauterine environment on islet function." Journal of Endocrinology 205, no. 3 (2010): 211–24. http://dx.doi.org/10.1677/joe-09-0399.

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Low birth weight is an important risk factor for impaired glucose tolerance and diabetes later in life. One hypothesis is that fetal β-cells inherit a persistent defect as a developmental response to fetal malnutrition, a primary cause of intrauterine growth restriction (IUGR). Our understanding of fetal programing events in the human endocrine pancreas is limited, but several animal models of IUGR extend our knowledge of developmental programing in β-cells. Pathological outcomes such as β-cell dysfunction, impaired glucose tolerance, and diabetes are often observed in adult offspring from the

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Dong, Yuanlin, Simone Hernandez Ruano, Akansha Mishra, Kathleen A. Pennington та Chandrasekhar Yallampalli. "Adrenomedullin and its receptors are expressed in mouse pancreatic β-cells and suppresses insulin synthesis and secretion". PLOS ONE 17, № 3 (2022): e0265890. http://dx.doi.org/10.1371/journal.pone.0265890.

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Gestational diabetes mellitus (GDM) is associated with defective pancreatic β-cell adaptation in pregnancy, but the underlying mechanism remains obscure. Our previous studies demonstrated that GDM women display increased plasma adrenomedullin (ADM) levels, and non-obese GDM mice show decreased serum concentrations of insulin and the number of β-cells in pancreas islets. The aims of this study is to examine if ADM and its receptors are expressed in female mouse pancreas, and if so, whether insulin secretion is regulated by ADM in mouse β-cell line, NIT-1 cells and isolated mouse pancreatic isle

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Mukhtar, Sameen, and Muhammad Haris. "Teplizumab: an FDA- approved drug, marks milestone in treatment of type 1 diabetes." International Journal of Scientific Reports 10, no. 1 (2023): 29–30. http://dx.doi.org/10.18203/issn.2454-2156.intjscirep20233870.

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Diabetes type-1 is a chronic disease characterized by immune-mediated destruction of insulin-producing beta cells in the pancreas. It progresses through distinct stages at varying rates, with stage 1 being β-cell autoimmunity with normal blood sugar, stage 2 being β-cell autoimmunity with dysglycemia, and stage 3 being symptomatic disease onset.

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Zhou, Shutong, Dongni Yu, Shangyong Ning та ін. "Augmented Rac1 Expression and Activity are Associated with Oxidative Stress and Decline of β Cell Function in Obesity". Cellular Physiology and Biochemistry 35, № 6 (2015): 2135–48. http://dx.doi.org/10.1159/000374019.

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Background: The aim of this study was to clarify the relationship among Rac1 expression and activation, oxidative stress and β cell dysfunction in obesity. Methods: In vivo, serum levels of glucose, insulin, oxidative stress markers and Rac1 expression were compared between ob/ob mice and C57BL/6J controls. Then, these variables were rechecked after the administration of the specific Rac1 inhibitor-NSC23766 in ob/ob mice. In vitro, NIT-1 β cells were cultured in a hyperglycemic and/or hyperlipidemic state with or without NSC23766, and the differences of Rac1 expression and translocation, NADPH

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Aston-Mourney, Kathryn, Shoba L. Subramanian, Sakeneh Zraika та ін. "One year of sitagliptin treatment protects against islet amyloid-associated β-cell loss and does not induce pancreatitis or pancreatic neoplasia in mice". American Journal of Physiology-Endocrinology and Metabolism 305, № 4 (2013): E475—E484. http://dx.doi.org/10.1152/ajpendo.00025.2013.

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The dipeptidyl peptidase-4 (DPP-4) inhibitor sitagliptin is an attractive therapy for diabetes, as it increases insulin release and may preserve β-cell mass. However, sitagliptin also increases β-cell release of human islet amyloid polypeptide (hIAPP), the peptide component of islet amyloid, which is cosecreted with insulin. Thus, sitagliptin treatment may promote islet amyloid formation and its associated β-cell toxicity. Conversely, metformin treatment decreases islet amyloid formation by decreasing β-cell secretory demand and could therefore offset sitagliptin's potential proamyloidogenic e

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Wu, Wen-Jun. "Diabetes remission and nonalcoholic fatty pancreas disease." World Journal of Diabetes 15, no. 7 (2024): 1390–93. http://dx.doi.org/10.4239/wjd.v15.i7.1390.

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This editorial focuses on the relationship between nonalcoholic fatty pancreas disease (NAFPD) and the development and remission of type 2 diabetes (T2D). NAFPD is characterized by intrapancreatic fatty deposition associated with obesity and not associated with alcohol abuse, viral infections, and other factors. Ectopic fat deposition in the pancreas is associated with the development of T2D, and the underlying mechanism is lipotoxic β-cell dysfunction. However, the results on the relationship between intrapancreatic fat deposition (IPFD) and β-cell function are conflicting. Regardless of the

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Columbus, Joshua, YuTing Chiang, Weijuan Shao, et al. "Insulin treatment and high-fat diet feeding reduces the expression of three Tcf genes in rodent pancreas." Journal of Endocrinology 207, no. 1 (2010): 77–86. http://dx.doi.org/10.1677/joe-10-0044.

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Specific single-nucleotide polymorphisms in intronic regions of human TCF7L2 are associated with an elevated risk of developing type 2 diabetes. Whether Tcf7l2 is expressed in pancreatic islets of rodent species at a considerable level, however, remains controversial. We used RT-PCR and quantitative RT-PCR to examine Tcf7l2 expression in rodent gut, pancreas, isolated pancreatic islets, and cultured cell lines. The expression level of Tcf7l2 was relatively lower in the pancreas compared to the gut or the pancreatic β-cell line Ins-1. Immunostaining did not detect a Tcf7l2 signal in mouse pancr

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Kaneto, Hideaki, Tomohiko Kimura, Masashi Shimoda та ін. "Molecular Mechanism of Pancreatic β-Cell Failure in Type 2 Diabetes Mellitus". Biomedicines 10, № 4 (2022): 818. http://dx.doi.org/10.3390/biomedicines10040818.

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Various important transcription factors in the pancreas are involved in the process of pancreas development, the differentiation of endocrine progenitor cells into mature insulin-producing pancreatic β-cells and the preservation of mature β-cell function. However, when β-cells are continuously exposed to a high glucose concentration for a long period of time, the expression levels of several insulin gene transcription factors are substantially suppressed, which finally leads to pancreatic β-cell failure found in type 2 diabetes mellitus. Here we show the possible underlying pathway for β-cell

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Napolitano, Tiziana, Serena Silvano, Chaïma Ayachi, et al. "Wnt Pathway in Pancreatic Development and Pathophysiology." Cells 12, no. 4 (2023): 565. http://dx.doi.org/10.3390/cells12040565.

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The pancreas is an abdominal gland that serves 2 vital purposes: assist food processing by secreting digestive enzymes and regulate blood glucose levels by releasing endocrine hormones. During embryonic development, this gland originates from epithelial buds located on opposite sites of the foregut endoderm. Pancreatic cell specification and maturation are coordinated by a complex interplay of extrinsic and intrinsic signaling events. In the recent years, the canonical Wnt/β-catenin pathway has emerged as an important player of pancreas organogenesis, regulating pancreatic epithelium specifica

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Liu, Ye Qi, Peter W. Nevin та Jack L. Leahy. "β-Cell adaptation in 60% pancreatectomy rats that preserves normoinsulinemia and normoglycemia". American Journal of Physiology-Endocrinology and Metabolism 279, № 1 (2000): E68—E73. http://dx.doi.org/10.1152/ajpendo.2000.279.1.e68.

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Islet β-cells are the regulatory element of the glucose homeostasis system. When functioning normally, they precisely counterbalance changes in insulin sensitivity or β-cell mass to preserve normoglycemia. This understanding seems counter to the dogma that β-cells are regulated by glycemia. We studied 60% pancreatectomy rats (Px) 4 wk postsurgery to elucidate the β-cell adaptive mechanisms. Nonfasting glycemia and insulinemia were identical in Px and sham-operated controls. There was partial regeneration of the excised β-cells in the Px rats, but it was limited in scope, with the pancreas β-ce

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Cole, Lori, Miranda Anderson, Parker B. Antin та Sean W. Limesand. "One process for pancreatic β-cell coalescence into islets involves an epithelial–mesenchymal transition". Journal of Endocrinology 203, № 1 (2009): 19–31. http://dx.doi.org/10.1677/joe-09-0072.

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Islet replacement is a promising therapy for treating diabetes mellitus, but the supply of donor tissue for transplantation is limited. To overcome this limitation, endocrine tissue can be expanded, but this requires an understanding of normal developmental processes that regulate islet formation. In this study, we compare pancreas development in sheep and human, and provide evidence that an epithelial–mesenchymal transition (EMT) is involved in β-cell differentiation and islet formation. Transcription factors know to regulate pancreas formation, pancreatic duodenal homeobox factor 1, neurogen

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