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Journal articles on the topic 'Pancreatic beta cell function'

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Author: Grafiati

Published: 9 March 2023

Last updated: 11 March 2023

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1

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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2

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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3

Curran, Aoife M., Miriam F. Ryan, Elaine Drummond, Eileen R. Gibney, Michael J. Gibney, Helen M. Roche, and Lorraine Brennan. "Uncovering Factors Related to Pancreatic Beta-Cell Function." PLOS ONE 11, no. 8 (August 18, 2016): e0161350. http://dx.doi.org/10.1371/journal.pone.0161350.

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4

Fu, Accalia, Chandra E. Eberhard, and Robert A. Screaton. "Role of AMPK in pancreatic beta cell function." Molecular and Cellular Endocrinology 366, no. 2 (February 2013): 127–34. http://dx.doi.org/10.1016/j.mce.2012.06.020.

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5

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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6

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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7

Marku, Algerta, Alessandra Galli, Paola Marciani, Nevia Dule, Carla Perego, and Michela Castagna. "Iron Metabolism in Pancreatic Beta-Cell Function and Dysfunction." Cells 10, no. 11 (October 22, 2021): 2841. http://dx.doi.org/10.3390/cells10112841.

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Iron is an essential element involved in a variety of physiological functions. In the pancreatic beta-cells, being part of Fe-S cluster proteins, it is necessary for the correct insulin synthesis and processing. In the mitochondria, as a component of the respiratory chain, it allows the production of ATP and reactive oxygen species (ROS) that trigger beta-cell depolarization and potentiate the calcium-dependent insulin release. Iron cellular content must be finely tuned to ensure the normal supply but also to prevent overloading. Indeed, due to the high reactivity with oxygen and the formation of free radicals, iron excess may cause oxidative damage of cells that are extremely vulnerable to this condition because the normal elevated ROS production and the paucity in antioxidant enzyme activities. The aim of the present review is to provide insights into the mechanisms responsible for iron homeostasis in beta-cells, describing how alteration of these processes has been related to beta-cell damage and failure. Defects in iron-storing or -chaperoning proteins have been detected in diabetic conditions; therefore, the control of iron metabolism in these cells deserves further investigation as a promising target for the development of new disease treatments.

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8

Larsen, S., J. Hilsted, B. Tronier, and H. Worning. "Pancreatic hormone secretion in chronic pancreatitis without residual beta-cell function." Acta Endocrinologica 118, no. 3 (July 1988): 357–64. http://dx.doi.org/10.1530/acta.0.1180357.

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Abstract. Hormonal responses (glucagon, pancreatic polypeptide and somatostatin) to iv glucagon, iv arginine, and ingestion of a mixed meal were investigated in 6 patients with insulin-dependent diabetes secondary to chronic pancreatitis without beta-cell function, in 8 Type I (insulin-dependent) diabetics without beta-cell function, and 8 healthy subjects. No significant differences were found between the two diabetic groups regarding glucagon responses to arginine and meal ingestion. In the patients with diabetes secondary to chronic pancreatitis compared with Type I diabetics and normal controls, the pancreatic polypeptide concentrations were significantly lower and somatostatin concentrations were significantly higher after glucagon, arginine and a mixed meal. Thus, pancreatic glucagon secretion was preserved in patients with insulin-dependent diabetes secondary to chronic pancreatitis, having no residual beta-cell function. These findings suggest that pancreatic glucagon deficiency is not absolute in insulin-dependent diabetes secondary to chronic pancreatitis. A high level of somatostatin may contribute to a lower blood glucose level in patients with chronic pancreatitis.

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9

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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10

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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11

Savari, O., K. Golab, L. Schenck, R. Grose, M. Tibudan, S. Ramachandran, Z. Tekin, et al. "Preservation of Beta Cell Function Following Pancreatic Islet Autotransplantation." Transplantation 98 (July 2014): 685–86. http://dx.doi.org/10.1097/00007890-201407151-02331.

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12

Curran, Aoife M., Marie Pier Scott-Boyer, Jim Kaput, Miriam F. Ryan, Elaine Drummond, Eileen R. Gibney, Michael J. Gibney, Helen M. Roche, and Lorraine Brennan. "A proteomic signature that reflects pancreatic beta-cell function." PLOS ONE 13, no. 8 (August 30, 2018): e0202727. http://dx.doi.org/10.1371/journal.pone.0202727.

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13

Servitja, J. M., and J. Ferrer. "Transcriptional networks controlling pancreatic development and beta cell function." Diabetologia 47, no. 4 (April 1, 2004): 597–613. http://dx.doi.org/10.1007/s00125-004-1368-9.

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14

Sasson, Shlomo. "Nutrient overload, lipid peroxidation and pancreatic beta cell function." Free Radical Biology and Medicine 111 (October 2017): 102–9. http://dx.doi.org/10.1016/j.freeradbiomed.2016.09.003.

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15

Koiter, Tjardus R., Sonja Wijkstra, Gerda C. J. Van Der Schaaf-verdonk, Henk Moes, and Gerard A. Schuiling. "Pancreatic beta-cell function and islet-cell proliferation: Effect of hyperinsulinaemia." Physiology & Behavior 57, no. 4 (April 1995): 717–21. http://dx.doi.org/10.1016/0031-9384(94)00290-8.

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16

Johansson, Å., J. Lau, M. Sandberg, L. A. H. Borg, P. U. Magnusson, and P. O. Carlsson. "Endothelial cell signalling supports pancreatic beta cell function in the rat." Diabetologia 52, no. 11 (August 11, 2009): 2385–94. http://dx.doi.org/10.1007/s00125-009-1485-6.

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17

Gannon, M., M. K. Ray, K. Van Zee, F. Rausa, R. H. Costa, and C. V. Wright. "Persistent expression of HNF6 in islet endocrine cells causes disrupted islet architecture and loss of beta cell function." Development 127, no. 13 (July 1, 2000): 2883–95. http://dx.doi.org/10.1242/dev.127.13.2883.

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We used transgenesis to explore the requirement for downregulation of hepatocyte nuclear factor 6 (HNF6) expression in the assembly, differentiation, and function of pancreatic islets. In vivo, HNF6 expression becomes downregulated in pancreatic endocrine cells at 18. 5 days post coitum (d.p.c.), when definitive islets first begin to organize. We used an islet-specific regulatory element (pdx1(PB)) from pancreatic/duodenal homeobox (pdx1) gene to maintain HNF6 expression in endocrine cells beyond 18.5 d.p.c. Transgenic animals were diabetic. HNF6-overexpressing islets were hyperplastic and remained very close to the pancreatic ducts. Strikingly, alpha, delta, and PP cells were increased in number and abnormally intermingled with islet beta cells. Although several mature beta cell markers were expressed in beta cells of transgenic islets, the glucose transporter GLUT2 was absent or severely reduced. As glucose uptake/metabolism is essential for insulin secretion, decreased GLUT2 may contribute to the etiology of diabetes in pdx1(PB)-HNF6 transgenics. Concordantly, blood insulin was not raised by glucose challenge, suggesting profound beta cell dysfunction. Thus, we have shown that HNF6 downregulation during islet ontogeny is critical to normal pancreas formation and function: continued expression impairs the clustering of endocrine cells and their separation from the ductal epithelium, disrupts the spatial organization of endocrine cell types within the islet, and severely compromises beta cell physiology, leading to overt diabetes.

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18

Juan-Mateu, Jonàs, Tatiana H. Rech, Olatz Villate, Esther Lizarraga-Mollinedo, Anna Wendt, Jean-Valery Turatsinze, Letícia A. Brondani, et al. "Neuron-enriched RNA-binding Proteins Regulate Pancreatic Beta Cell Function and Survival." Journal of Biological Chemistry 292, no. 8 (January 11, 2017): 3466–80. http://dx.doi.org/10.1074/jbc.m116.748335.

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Pancreatic beta cell failure is the central event leading to diabetes. Beta cells share many phenotypic traits with neurons, and proper beta cell function relies on the activation of several neuron-like transcription programs. Regulation of gene expression by alternative splicing plays a pivotal role in brain, where it affects neuronal development, function, and disease. The role of alternative splicing in beta cells remains unclear, but recent data indicate that splicing alterations modulated by both inflammation and susceptibility genes for diabetes contribute to beta cell dysfunction and death. Here we used RNA sequencing to compare the expression of splicing-regulatory RNA-binding proteins in human islets, brain, and other human tissues, and we identified a cluster of splicing regulators that are expressed in both beta cells and brain. Four of them, namely Elavl4, Nova2, Rbox1, and Rbfox2, were selected for subsequent functional studies in insulin-producing rat INS-1E, human EndoC-βH1 cells, and in primary rat beta cells. Silencing of Elavl4 and Nova2 increased beta cell apoptosis, whereas silencing of Rbfox1 and Rbfox2 increased insulin content and secretion. Interestingly, Rbfox1 silencing modulates the splicing of the actin-remodeling protein gelsolin, increasing gelsolin expression and leading to faster glucose-induced actin depolymerization and increased insulin release. Taken together, these findings indicate that beta cells share common splicing regulators and programs with neurons. These splicing regulators play key roles in insulin release and beta cell survival, and their dysfunction may contribute to the loss of functional beta cell mass in diabetes.

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19

Rahman, Miftakh Nur, Indriyanti Rafi Sukmawati, Irma Melyani Puspitasari, and Miswar Fattah. "Serum Free Zinc as A Predictor for Excessive Function of Pancreatic Beta-Cells in Central-Obese Men." Indonesian Biomedical Journal 11, no. 3 (December 3, 2019): 262–6. http://dx.doi.org/10.18585/inabj.v11i3.618.

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BACKGROUND: Central obesity is known as a risk factor for type 2 diabetes mellitus (T2DM). Its development is influenced by many factors such as a progressive failure of pancreatic beta cell function. The beta cells increase their function to secret insulin along T2DM development to compensate before it becomes exhausted. Zinc (Zn) plays a crucial role in beta cell function and insulin secretion. The majority of Zn in serum are bound to protein which is not readily available interact with cells. The free Zn in serum has been suggested as being more representative than total Zn in beta cell function. This research aimed to investigate the correlation between serum free Zn and homeostasis model assessment for beta cell function (HOMA-B) and to predict the pancreatic beta cell function in the development of T2DM.METHODS: This study was designed as an observational with a cross-sectional approach. The subjects were centrally obese men aged 30-50 years and who had met the inclusion and exclusion criteria from the screening tests. Control subjects were lean men without T2DM. Serum free Zn and serum total Zn were measured by using inductively coupled plasma-mass spectrometry (ICP-MS).RESULTS: There was positive correlation between serum free Zn and HOMA-B (R=0.361, p-value<0.001) but there was no correlation between serum total Zn and HOMA-B (R=-0.062, p-value=0.563). This study found that if the concentration of serum free Zn >1.7 ug/dL in central obese men was suggested as an excessive function of pancreatic beta cell and as an early warning before its exhausted.CONCLUSION: This study suggested that serum free Zn had a correlation with beta cell function and had a predictive ability for beta cell excessive function before its exhausted.KEYWORDS: Type 2 diabetes mellitus, HOMA-B, serum free zinc, central obesity

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20

WU, Jie, and Da-jin ZOU. "The role of autophagy in maintaining pancreatic beta-cell function." Academic Journal of Second Military Medical University 29, no. 12 (January 27, 2010): 1413–15. http://dx.doi.org/10.3724/sp.j.1008.2009.01413.

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21

Pérez-Armendariz, E. Martha. "Connexin 36, a key element in pancreatic beta cell function." Neuropharmacology 75 (December 2013): 557–66. http://dx.doi.org/10.1016/j.neuropharm.2013.08.015.

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22

Sarri, Yolanda, Carles Conill, Eugenia Verger, Clara Tomas, and Ramon Gomis. "Effects of single dose irradiation on pancreatic beta-cell function." Radiotherapy and Oncology 22, no. 2 (October 1991): 143–44. http://dx.doi.org/10.1016/0167-8140(91)90011-5.

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23

Nagaoka, Hideo, Ryuichi Innami, Masazumi Watanabe, Motoaki Satoh, Fumio Murayama, and Naoya Funakoshi. "Preservation of pancreatic beta cell function with pulsatile cardiopulmonary bypass." Annals of Thoracic Surgery 48, no. 6 (December 1989): 798–802. http://dx.doi.org/10.1016/0003-4975(89)90673-5.

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24

Amemiya, Shin, Kohsuke Higashida, Masatoshi Fujimoto, Kohtaro Asayama, Kazuyoshi Ichimura, Shoichi Kusano, Kenji Ohyama, and Kiyohiko Kato. "Residual Pancreatic Beta-Cell Function in Insulin-Dependent Diabetes Mellitus." Pediatrics International 29, no. 3 (June 1987): 408–13. http://dx.doi.org/10.1111/j.1442-200x.1987.tb00338.x.

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25

Malaisse, Willy J. "Role of glycogen metabolism in pancreatic islet beta cell function." Diabetologia 59, no. 11 (August 27, 2016): 2489–91. http://dx.doi.org/10.1007/s00125-016-4092-3.

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26

Prentki, Marc, Barbara E. Corkey, and S. R. Murthy Madiraju. "Lipid-associated metabolic signalling networks in pancreatic beta cell function." Diabetologia 63, no. 1 (August 19, 2019): 10–20. http://dx.doi.org/10.1007/s00125-019-04976-w.

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27

Miki, T., K. Nagashima, and S. Seino. "The structure and function of the ATP-sensitive K+ channel in insulin-secreting pancreatic beta-cells." Journal of Molecular Endocrinology 22, no. 2 (April 1, 1999): 113–23. http://dx.doi.org/10.1677/jme.0.0220113.

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ATP-sensitive K+ channels (KATP channels) play important roles in many cellular functions by coupling cell metabolism to electrical activity. The KATP channels in pancreatic beta-cells are thought to be critical in the regulation of glucose-induced and sulfonylurea-induced insulin secretion. Until recently, however, the molecular structure of the KATP channel was not known. Cloning members of the novel inwardly rectifying K+ channel subfamily Kir6.0 (Kir6.1 and Kir6.2) and the sulfonylurea receptors (SUR1 and SUR2) has clarified the molecular structure of KATP channels. The pancreatic beta-cell KATP channel comprises two subunits: a Kir6.2 subunit and an SUR1 subunit. Molecular biological and molecular genetic studies have provided insights into the physiological and pathophysiological roles of the pancreatic beta-cell KATP channel in insulin secretion.

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28

Meda, Paolo. "Protein-Mediated Interactions of Pancreatic Islet Cells." Scientifica 2013 (2013): 1–22. http://dx.doi.org/10.1155/2013/621249.

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The islets of Langerhans collectively form the endocrine pancreas, the organ that is soley responsible for insulin secretion in mammals, and which plays a prominent role in the control of circulating glucose and metabolism. Normal function of these islets implies the coordination of different types of endocrine cells, noticeably of the beta cells which produce insulin. Given that an appropriate secretion of this hormone is vital to the organism, a number of mechanisms have been selected during evolution, which now converge to coordinate beta cell functions. Among these, several mechanisms depend on different families of integral membrane proteins, which ensure direct (cadherins, N-CAM, occludin, and claudins) and paracrine communications (pannexins) between beta cells, and between these cells and the other islet cell types. Also, other proteins (integrins) provide communication of the different islet cell types with the materials that form the islet basal laminae and extracellular matrix. Here, we review what is known about these proteins and their signaling in pancreaticβ-cells, with particular emphasis on the signaling provided by Cx36, given that this is the integral membrane protein involved in cell-to-cell communication, which has so far been mostly investigated for effects on beta cell functions.

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29

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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30

So, Wing Yan, Wai Nam Liu, Adrian Kee Keong Teo, Guy A. Rutter, and Weiping Han. "Paired box 6 programs essential exocytotic genes in the regulation of glucose-stimulated insulin secretion and glucose homeostasis." Science Translational Medicine 13, no. 600 (June 30, 2021): eabb1038. http://dx.doi.org/10.1126/scitranslmed.abb1038.

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The paired box 6 (PAX6) transcription factor is crucial for normal pancreatic islet development and function. Heterozygous mutations of PAX6 are associated with impaired insulin secretion and early-onset diabetes mellitus in humans. However, the molecular mechanism of PAX6 in controlling insulin secretion in human beta cells and its pathophysiological role in type 2 diabetes (T2D) remain ambiguous. We investigated the molecular pathway of PAX6 in the regulation of insulin secretion and the potential therapeutic value of PAX6 in T2D by using human pancreatic beta cell line EndoC-βH1, the db/db mouse model, and primary human pancreatic islets. Through loss- and gain-of-function approaches, we uncovered a mechanism by which PAX6 modulates glucose-stimulated insulin secretion (GSIS) through a cAMP response element–binding protein (CREB)/Munc18-1/2 pathway. Moreover, under diabetic conditions, beta cells and pancreatic islets displayed dampened PAX6/CREB/Munc18-1/2 pathway activity and impaired GSIS, which were reversed by PAX6 replenishment. Adeno-associated virus–mediated PAX6 overexpression in db/db mouse pancreatic beta cells led to a sustained amelioration of glycemic perturbation in vivo but did not affect insulin resistance. Our study highlights the pathophysiological role of PAX6 in T2D-associated beta cell dysfunction in humans and suggests the potential of PAX6 gene transfer in preserving and restoring beta cell function.

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31

Yu, Haoyong, Ruixia Li, Lei Zhang, Haibing Chen, Yuqian Bao, and Weiping Jia. "Serum CA19-9 Level Associated with Metabolic Control and Pancreatic Beta Cell Function in Diabetic Patients." Experimental Diabetes Research 2012 (2012): 1–5. http://dx.doi.org/10.1155/2012/745189.

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CA19-9 is a tumor-associated antigen. It is also a marker of pancreatic tissue damage that might be caused by diabetes. Long-term poor glycemic control may lead to pancreatic beta cell dysfunction which is reflected by elevated serum CA19-9 level. Intracellular cholesterol accumulation leads to islet dysfunction and impaired insulin secretion which provide a new lipotoxic model. This study firstly found total cholesterol was one of the independent contributors to CA19-9. Elevated serum CA19-9 level in diabetic patients may indicate further investigations of glycemic control, pancreatic beta cell function, and total cholesterol level.

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32

Chen, Shiau-Mei, Siow-Wey Hee, Shih-Yun Chou, Meng-Wei Liu, Che-Hong Chen, Daria Mochly-Rosen, Tien-Jyun Chang, and Lee-Ming Chuang. "Activation of Aldehyde Dehydrogenase 2 Ameliorates Glucolipotoxicity of Pancreatic Beta Cells." Biomolecules 11, no. 10 (October 6, 2021): 1474. http://dx.doi.org/10.3390/biom11101474.

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Chronic hyperglycemia and hyperlipidemia hamper beta cell function, leading to glucolipotoxicity. Mitochondrial aldehyde dehydrogenase 2 (ALDH2) detoxifies reactive aldehydes, such as methylglyoxal (MG) and 4-hydroxynonenal (4-HNE), derived from glucose and lipids, respectively. We aimed to investigate whether ALDH2 activators ameliorated beta cell dysfunction and apoptosis induced by glucolipotoxicity, and its potential mechanisms of action. Glucose-stimulated insulin secretion (GSIS) in MIN6 cells and insulin secretion from isolated islets in perifusion experiments were measured. The intracellular ATP concentrations and oxygen consumption rates of MIN6 cells were assessed. Furthermore, the cell viability, apoptosis, and mitochondrial and intracellular reactive oxygen species (ROS) levels were determined. Additionally, the pro-apoptotic, apoptotic, and anti-apoptotic signaling pathways were investigated. We found that Alda-1 enhanced GSIS by improving the mitochondrial function of pancreatic beta cells. Alda-1 rescued MIN6 cells from MG- and 4-HNE-induced beta cell death, apoptosis, mitochondrial dysfunction, and ROS production. However, the above effects of Alda-1 were abolished in Aldh2 knockdown MIN6 cells. In conclusion, we reported that the activator of ALDH2 not only enhanced GSIS, but also ameliorated the glucolipotoxicity of beta cells by reducing both the mitochondrial and intracellular ROS levels, thereby improving mitochondrial function, restoring beta cell function, and protecting beta cells from apoptosis and death.

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33

Paulsen, Sarah Juel, Niels Vrang, Leif Kongskov Larsen, Philip Just Larsen, and Jacob Jelsing. "Stereological assessment of pancreatic beta-cell mass development in male Zucker Diabetic Fatty (ZDF) rats: correlation with pancreatic beta-cell function." Journal of Anatomy 217, no. 5 (August 30, 2010): 624–30. http://dx.doi.org/10.1111/j.1469-7580.2010.01285.x.

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34

Xi, Yannan, Siming Liu, Ahmed Bettaieb, Kosuke Matsuo, Izumi Matsuo, Ellen Hosein, Samah Chahed, et al. "Pancreatic T cell protein–tyrosine phosphatase deficiency affects beta cell function in mice." Diabetologia 58, no. 1 (October 23, 2014): 122–31. http://dx.doi.org/10.1007/s00125-014-3413-7.

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35

Ghosal, Abhisek, Thillai V. Sekar, and Hamid M. Said. "Biotin uptake by mouse and human pancreatic beta cells/islets: a regulated, lipopolysaccharide-sensitive carrier-mediated process." American Journal of Physiology-Gastrointestinal and Liver Physiology 307, no. 3 (August 1, 2014): G365—G373. http://dx.doi.org/10.1152/ajpgi.00157.2014.

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Biotin is essential for the normal function of pancreatic beta cells. These cells obtain biotin from their surroundings via transport across their cell membrane. Little is known about the uptake mechanism involved, how it is regulated, and how it is affected by internal and external factors. We addressed these issues using the mouse-derived pancreatic beta-TC-6 cells and freshly isolated mouse and human primary pancreatic beta cells as models. The results showed biotin uptake by pancreatic beta-TC-6 cells occurs via a Na+-dependent, carrier-mediated process, that is sensitive to desthiobiotin, as well as to pantothenic acid and lipoate; the process is also saturable as a function of concentration (apparent Km = 22.24 ± 5.5 μM). These cells express the sodium-dependent multivitamin transporter (SMVT), whose knockdown (with doxycycline-inducible shRNA) led to a sever inhibition in biotin uptake. Similarly, uptake of biotin by mouse and human primary pancreatic islets is Na+-dependent and carrier-mediated, and both cell types express SMVT. Biotin uptake by pancreatic beta-TC-6 cells is also adaptively regulated (via transcriptional mechanism) by extracellular substrate level. Chronic treatment of pancreatic beta-TC-6 cells with bacterial lipopolysaccharides (LPS) leads to inhibition in biotin uptake. This inhibition is mediated via a Toll-Like receptor 4-mediated process and involves a decrease in membrane expression of SMVT. These findings show, for the first time, that pancreatic beta cells/islets take up biotin via a specific and regulated carrier-mediated process, and that the process is sensitive to the effect of LPS.

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36

Schumann, D. M., K. Maedler, I. Franklin, D. Konrad, J. Storling, M. Boni-Schnetzler, A. Gjinovci, et al. "The Fas pathway is involved in pancreatic beta cell secretory function." Proceedings of the National Academy of Sciences 104, no. 8 (February 13, 2007): 2861–66. http://dx.doi.org/10.1073/pnas.0611487104.

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37

Pi, Jingbo, Qiang Zhang, Jingqi Fu, Courtney G. Woods, Yongyong Hou, Barbara E. Corkey, Sheila Collins, and Melvin E. Andersen. "ROS signaling, oxidative stress and Nrf2 in pancreatic beta-cell function." Toxicology and Applied Pharmacology 244, no. 1 (April 2010): 77–83. http://dx.doi.org/10.1016/j.taap.2009.05.025.

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Woynillowicz, Amanda K., Sandeep Raha, Catherine J. Nicholson, and Alison C. Holloway. "The effect of smoking cessation pharmacotherapies on pancreatic beta cell function." Toxicology and Applied Pharmacology 265, no. 1 (November 2012): 122–27. http://dx.doi.org/10.1016/j.taap.2012.08.020.

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39

Campbell, Susan C., Ali Aldibbiat, Claire E. Marriott, Caroline Landy, Tomader Ali, William F. Ferris, Clive S. Butler, James A. Shaw, and Wendy M. Macfarlane. "Selenium stimulates pancreatic beta-cell gene expression and enhances islet function." FEBS Letters 582, no. 15 (June 4, 2008): 2333–37. http://dx.doi.org/10.1016/j.febslet.2008.05.038.

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40

Sturis, J., I. J. Kurland, M. M. Byrne, E. Mosekilde, P. Froguel, S. J. Pilkis, G. I. Bell, and K. S. Polonsky. "Compensation in pancreatic beta-cell function in subjects with glucokinase mutations." Diabetes 43, no. 5 (May 1, 1994): 718–23. http://dx.doi.org/10.2337/diabetes.43.5.718.

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41

Henaoui, Imène Sarah, Cécile Jacovetti, Inês Guerra Mollet, Claudiane Guay, Jonathan Sobel, Lena Eliasson, and Romano Regazzi. "PIWI-interacting RNAs as novel regulators of pancreatic beta cell function." Diabetologia 60, no. 10 (July 16, 2017): 1977–86. http://dx.doi.org/10.1007/s00125-017-4368-2.

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42

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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Retnakaran, Ravi. "JOE DOUPE LECTURE: Emerging Strategies for the Preservation of Pancreatic Beta-cell Function in early Type 2 Diabetes." Clinical & Investigative Medicine 37, no. 6 (December 1, 2014): 414. http://dx.doi.org/10.25011/cim.v37i6.22247.

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A fundamental problem in the clinical management of type 2 diabetes is the inability to prevent the ongoing deterioration of pancreatic beta-cell function over time that underlies the chronic progressive nature of this condition. Importantly, beta-cell dysfunction has both reversible and irreversible components. Furthermore, the amelioration of reversible beta-cell dysfunction through the early institution of short-term insulin-based therapy has emerged as a strategy that can yield temporary remission of type 2 diabetes. In this context, we have forwarded a novel therapeutic paradigm consisting of initial induction therapy to improve beta-cell function early in the course of diabetes followed by maintenance therapy aimed at preserving this beneficial beta-cell effect. Ultimately, this approach may yield an optimized therapeutic strategy for the durable preservation of beta-cell function and consequent modification of the natural history of type 2 diabetes.

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Perera, Chamini, Zhihong Xu, Alpha Raj Mekapogu, S. M. Zahid Hosen, Srinivasa Pothula, Jerry Greenfield, Suresh Chari, et al. "1133 PANCREATIC STELLATE CELL AND CANCER CELL DERIVED EXOSOMES IMPAIR BETA CELL FUNCTION: IMPLICATIONS FOR PANCREATIC CANCER RELATED DIABETES." Gastroenterology 158, no. 6 (May 2020): S—221. http://dx.doi.org/10.1016/s0016-5085(20)31245-2.

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45

Rajput, Sajid Ali, Munazza Raza Mirza, and M. Iqbal Choudhary. "Bergenin protects pancreatic beta cells against cytokine-induced apoptosis in INS-1E cells." PLOS ONE 15, no. 12 (December 21, 2020): e0241349. http://dx.doi.org/10.1371/journal.pone.0241349.

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Beta cell apoptosis induced by proinflammatory cytokines is one of the hallmarks of diabetes. Small molecules which can inhibit the cytokine-induced apoptosis could lead to new drug candidates that can be used in combination with existing therapeutic interventions against diabetes. The current study evaluated several effects of bergenin, an isocoumarin derivative, in beta cells in the presence of cytokines. These included (i) increase in beta cell viability (by measuring cellular ATP levels) (ii) suppression of beta cell apoptosis (by measuring caspase activity), (iii) improvement in beta cell function (by measuring glucose-stimulated insulin secretion), and (iv) improvement of beta cells mitochondrial physiological functions. The experiments were carried out using rat beta INS-1E cell line in the presence or absence of bergenin and a cocktail of proinflammatory cytokines (interleukin-1beta, tumor necrosis factor-alpha, and interferon- gamma) for 48 hr. Bergenin significantly inhibited beta cell apoptosis, as inferred from the reduction in the caspase-3 activity (IC50 = 7.29 ± 2.45 μM), and concurrently increased cellular ATP Levels (EC50 = 1.97 ± 0.47 μM). Bergenin also significantly enhanced insulin secretion (EC50 = 6.73 ± 2.15 μM) in INS-1E cells, presumably because of the decreased nitric oxide production (IC50 = 6.82 ± 2.83 μM). Bergenin restored mitochondrial membrane potential (EC50 = 2.27 ± 0.83 μM), decreased ROS production (IC50 = 14.63 ± 3.18 μM), and improved mitochondrial dehydrogenase activity (EC50 = 1.39 ± 0.62 μM). This study shows for the first time that bergenin protected beta cells from cytokine-induced apoptosis and restored insulin secretory function by virtue of its anti-inflammatory, antioxidant and anti-apoptotic properties. To sum up, the above mentioned data highlight bergenin as a promising anti-apoptotic agent in the context of diabetes.

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

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

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Leiter, E. H., M. Prochazka, and L. D. Shultz. "Effect of immunodeficiency on diabetogenesis in genetically diabetic (db/db) mice." Journal of Immunology 138, no. 10 (May 15, 1987): 3224–29. http://dx.doi.org/10.4049/jimmunol.138.10.3224.

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Abstract The pathogenesis of diabetes in C57BL/KsJ-db/db mice has been proposed to entail autoimmune mechanisms. We have combined immunodeficiency genes with the db mutation to determine whether beta cell necrosis and establishment of severe diabetes would occur in the absence of normal T and/or B lymphocyte functions. Inbred mice carrying the recessive mutations, severe combined immunodeficiency (scid), X-linked immunodeficiency (xid), nude (nu), and the Y-linked autoimmune accelerator (Yaa), were crossed with strains congenic for the db mutation. The diabetes syndrome was studied in double homozygotes produced in the F2 generation. In another experiment, C57BL/KsJ-db/db males were made T cell function deficient by adolescent thymectomy followed by lethal irradiation and bone marrow reconstitution. None of these manipulations served to prevent the induction of a severe diabetes syndrome in any of the model systems analyzed. Thus, diabetogenesis characterized by massive necrosis of the pancreatic beta cells and atrophy of the pancreatic islets was observed in both the absence of normal T cell function (as assessed by absence of T cell mitogen response) and humoral autoimmunity against beta cell antigens (insulin, retroviral p73). In conclusion, our data indicate that anti-beta cell autoimmunity is not a primary event in the etiopathogenesis of diabetes in the db/db mouse.

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Luo, LG, and N. Yano. "Expression of thyrotropin-releasing hormone receptor in immortalized beta-cell lines and rat pancreas." Journal of Endocrinology 181, no. 3 (June 1, 2004): 401–12. http://dx.doi.org/10.1677/joe.0.1810401.

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Thyrotropin-releasing hormone (TRH), a hypothalamic tripeptide, is expressed in pancreatic islets at peak levels during the late gestation and early neonate period. TRH increases insulin production in cultured beta-cells, suggesting that it might play a role in regulating pancreatic beta-cell function. However, there is limited information on TRH receptor expression in the pancreas. The aim of the present study was to explore the distribution of the TRH receptor in the pancreas and its function in pancreatic beta-cells. TRH receptor type 1 (TRHR1) gene expression was detected by RT-PCR and verified by Northern blotting and immunoblotting in the beta-cell lines, INS-1 and betaTC-6, and the rat pancreatic organ. The absence of TRH receptor type 2 expression in the tissue and cells indicated the tissue specificity of TRH receptor expression in the pancreas. The TRHR1 signals (detected by in situ hybridization) were distributed not only in islets but also in the surrounding areas of the pancreatic ductal and vasal epithelia. The apparent dissociation constant value for the affinity of [(3)H]3-methyl-histidine TRH (MeTRH) is 4.19 in INS-1 and 3.09 nM in betaTC-6. In addition, TRH induced epidermal growth factor (EGF) receptor phosphorylation with a half-maximum concentration of approximately 50 nM, whereas the high affinity analogue of TRH, MeTRH, was 1 nM. This suggested that the affinity of TRH ligands for the TRH receptor influences the activation of EGF receptor phosphorylation in betaTC-6 cells. Our observations suggested that the biological role of TRH in pancreatic beta-cells is via the activation of TRHR1. Further research is required to identify the role of TRHR1 in the pancreas aside from the islets.

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German, M. S., L. G. Moss, J. Wang, and W. J. Rutter. "The insulin and islet amyloid polypeptide genes contain similar cell-specific promoter elements that bind identical beta-cell nuclear complexes." Molecular and Cellular Biology 12, no. 4 (April 1992): 1777–88. http://dx.doi.org/10.1128/mcb.12.4.1777-1788.1992.

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The pancreatic beta cell makes several unique gene products, including insulin, islet amyloid polypeptide (IAPP), and beta-cell-specific glucokinase (beta GK). The functions of isolated portions of the insulin, IAPP, and beta GK promoters were studied by using transient expression and DNA binding assays. A short portion (-247 to -197 bp) of the rat insulin I gene, the FF minienhancer, contains three interacting transcriptional regulatory elements. The FF minienhancer binds at least two nuclear complexes with limited tissue distribution. Sequences similar to that of the FF minienhancer are present in the 5' flanking DNA of the human IAPP and rat beta GK genes and also the rat insulin II and mouse insulin I and II genes. Similar minienhancer constructs from the insulin and IAPP genes function as cell-specific transcriptional regulatory elements and compete for binding of the same nuclear factors, while the beta GK construct competes for protein binding but functions poorly as a minienhancer. These observations suggest that the patterns of expression of the beta-cell-specific genes result in part from sharing the same transcriptional regulators.

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50

German, M. S., L. G. Moss, J. Wang, and W. J. Rutter. "The insulin and islet amyloid polypeptide genes contain similar cell-specific promoter elements that bind identical beta-cell nuclear complexes." Molecular and Cellular Biology 12, no. 4 (April 1992): 1777–88. http://dx.doi.org/10.1128/mcb.12.4.1777.

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The pancreatic beta cell makes several unique gene products, including insulin, islet amyloid polypeptide (IAPP), and beta-cell-specific glucokinase (beta GK). The functions of isolated portions of the insulin, IAPP, and beta GK promoters were studied by using transient expression and DNA binding assays. A short portion (-247 to -197 bp) of the rat insulin I gene, the FF minienhancer, contains three interacting transcriptional regulatory elements. The FF minienhancer binds at least two nuclear complexes with limited tissue distribution. Sequences similar to that of the FF minienhancer are present in the 5' flanking DNA of the human IAPP and rat beta GK genes and also the rat insulin II and mouse insulin I and II genes. Similar minienhancer constructs from the insulin and IAPP genes function as cell-specific transcriptional regulatory elements and compete for binding of the same nuclear factors, while the beta GK construct competes for protein binding but functions poorly as a minienhancer. These observations suggest that the patterns of expression of the beta-cell-specific genes result in part from sharing the same transcriptional regulators.

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