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Relevant bibliographies by topics / Beta cell insulin secretion

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Academic literature on the topic 'Beta cell insulin secretion'

Author: Grafiati

Published: 11 March 2023

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Journal articles on the topic "Beta cell insulin secretion"

1

Sjoholm, A. "Nitric oxide donor SIN-1 inhibits insulin release." American Journal of Physiology-Cell Physiology 271, no. 4 (October 1, 1996): C1098—C1102. http://dx.doi.org/10.1152/ajpcell.1996.271.4.c1098.

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Preceding the onset of insulin-dependent diabetes mellitus, pancreatic islets are infiltrated by macrophages secreting interleukin-1 beta, which exerts cytotoxic and inhibitory actions on islet beta-cell insulin secretion through induction of nitric oxide (NO) synthesis. The influence of the NO donor 3-morpholinosydnonimine (SIN-1) on insulin secretion from isolated pancreatic islets in response to various secretagogues was investigated. Stimulation of insulin release evoked by glucose, phospholipase C activation with carbachol, and protein kinase C activation with phorbol ester were obtained by SIN-1, whereas the response to adenylyl cyclase activation or K(+)-induced depolarization was not affected. It is concluded that enzymes involved in glucose catabolism, phospholipase C or protein kinase C, may be targeted by NO. Reversal of SIN-1 inhibition of glucose-stimulated insulin release by dithiothreitol suggests that NO may inhibit insulin secretion partly by S-nitrosylation of thiol residues in key proteins in the stimulus-secretion coupling. These adverse effects of NO on the beta-cell stimulus-secretion coupling may be of importance for the development of the impaired insulin secretion characterizing diabetes mellitus.

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Fernández-Díaz, Cristina M., Beatriz Merino, José F. López-Acosta, Pilar Cidad, Miguel A. de la Fuente, Carmen D. Lobatón, Alfredo Moreno, Malcolm A. Leissring, Germán Perdomo, and Irene Cózar-Castellano. "Pancreatic β-cell-specific deletion of insulin-degrading enzyme leads to dysregulated insulin secretion and β-cell functional immaturity." American Journal of Physiology-Endocrinology and Metabolism 317, no. 5 (November 1, 2019): E805—E819. http://dx.doi.org/10.1152/ajpendo.00040.2019.

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Inhibition of insulin-degrading enzyme (IDE) has been proposed as a possible therapeutic target for type 2 diabetes treatment. However, many aspects of IDE's role in glucose homeostasis need to be clarified. In light of this, new preclinical models are required to elucidate the specific role of this protease in the main tissues related to insulin handling. To address this, here we generated a novel line of mice with selective deletion of the Ide gene within pancreatic beta-cells, B-IDE-KO mice, which have been characterized in terms of multiple metabolic end points, including blood glucose, plasma C-peptide, and intraperitoneal glucose tolerance tests. In addition, glucose-stimulated insulin secretion was quantified in isolated pancreatic islets and beta-cell differentiation markers and insulin secretion machinery were characterized by RT-PCR. Additionally, IDE was genetically and pharmacologically inhibited in INS-1E cells and rodent and human islets, and insulin secretion was assessed. Our results show that, in vivo, life-long deletion of IDE from beta-cells results in increased plasma C-peptide levels. Corroborating these findings, isolated islets from B-IDE-KO mice showed constitutive insulin secretion, a hallmark of beta-cell functional immaturity. Unexpectedly, we found 60% increase in Glut1 (a high-affinity/low- Km glucose transporter), suggesting increased glucose transport into the beta-cell at low glucose levels, which may be related to constitutive insulin secretion. In parallel, IDE inhibition in INS-1E and islet cells resulted in impaired insulin secretion after glucose challenge. We conclude that IDE is required for glucose-stimulated insulin secretion. When IDE is inhibited, insulin secretion machinery is perturbed, causing either inhibition of insulin release at high glucose concentrations or constitutive secretion.

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Dela, F., K. J. Mikines, B. Tronier, and H. Galbo. "Diminished arginine-stimulated insulin secretion in trained men." Journal of Applied Physiology 69, no. 1 (July 1, 1990): 261–67. http://dx.doi.org/10.1152/jappl.1990.69.1.261.

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Glucose-stimulated insulin secretion is depressed by training. To further elucidate the beta-cell adaptation to training, a nonglucose secretagogue was applied. Arginine was infused for 90 min to seven trained and seven untrained young men. Arginine and glucose concentrations increased identically in the groups. The insulin response was biphasic and waned despite increasing arginine concentrations. Both these phases as well as C-peptide responses were reduced in trained subjects, whereas proinsulin responses were similar in the groups. Identical increases were found in glucagon, growth hormone, catecholamines, and production and disappearance of glucose; identical decreases were found in free fatty acids, glycerol, and beta-hydroxybutyrate. In conclusion, in men training diminishes both arginine- and glucose-stimulated insulin secretion, indicating a profound beta-cell adaptation. Being enhanced, the effects of insulin on both production and disposal of glucose are changed in the opposite direction to beta-cell secretion by training. The responses of glucagon- and growth hormone-secreting cells to arginine do not change with training.

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Karimova, Mariana V., Inessa G. Gvazava, and Ekaterina A. Vorotelyak. "Overcoming the Limitations of Stem Cell-Derived Beta Cells." Biomolecules 12, no. 6 (June 9, 2022): 810. http://dx.doi.org/10.3390/biom12060810.

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Great advances in type 1 diabetes (T1D) and type 2 diabetes (T2D) treatment have been made to this day. However, modern diabetes therapy based on insulin injections and cadaveric islets transplantation has many disadvantages. That is why researchers are developing new methods to regenerate the pancreatic hormone-producing cells in vitro. The most promising approach is the generation of stem cell-derived beta cells that could provide an unlimited source of insulin-secreting cells. Recent studies provide methods to produce beta-like cell clusters that display glucose-stimulated insulin secretion—one of the key characteristics of the beta cell. However, in comparison with native beta cells, stem cell-derived beta cells do not undergo full functional maturation. In this paper we review the development and current state of various protocols, consider advantages, and propose ways to improve them. We examine molecular pathways, epigenetic modifications, intracellular components, and the microenvironment as a possible leverage to promote beta cell functional maturation. A possibility to create islet organoids from stem cell-derived components, as well as their encapsulation and further transplantation, is also examined. We try to combine modern research on beta cells and their crosstalk to create a holistic overview of developing insulin-secreting systems.

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Karatug Kacar, A., S. Gezginci-Oktayoglu, and S. Bolkent. "4-Methylcatechol stimulates apoptosis and reduces insulin secretion by decreasing betacellulin and inhibin beta-A in INS-1 beta-cells." Human & Experimental Toxicology 37, no. 11 (February 23, 2018): 1123–30. http://dx.doi.org/10.1177/0960327118758365.

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Insulinoma INS-1 cell line is a pancreatic beta cell tumor which is characterized with high insulin content and secretion in response to increasing glucose levels. 4-Methylcatechol (4-MC) is a metabolite of quercetin, which is known as a potential drug for inhibition of tumorigenesis. The aim of this study was to determine the applying doses of 4-methylcatechol (4-MC) for triggening cell death and decreasing the cell function of rat insulinoma INS-1 beta cells. The rate of apoptosis and the amount of insulin in the cell and the secretions were determined by the ELISA method. Betacellulin (BTC) and inhibin beta-A amounts in both the cell and the glucose induced secretion were investigated by Western blotting. Furthermore, BTC, Inhibin beta-A, Ins1, Ins2, and GLUT2 gene expression levels were determined by the by the real-time quantitative reverse transcription polymerase chain reaction (qRT-PCR) method. We noted a significant decrease in cell viability, while an increase in apoptotic cell death by 4-MC treatment. It caused a decrease in the secretion of BTC, expressions of both BTC and inhibin beta-A. We showed a decrease in the expressions of Ins1 and GLUT2, while there is no alteration in the level of insulin protein. Insulin secretion levels increased in INS-1 cells given 4-MC by basal glucose concentration while they did not response to high concentration of glucose, which indicates that 4-MC disrupts the functionality of INS-1 cells. These results revealed that 4-MC induces apoptosis and decreases insulin secretion by reducing BTC and inhibin beta-A in insulinoma INS-1 cells. Thus, 4-MC may be offered as a potential molecule for treatment of insulinoma.

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Corbett, J. A., and M. L. McDaniel. "Intraislet release of interleukin 1 inhibits beta cell function by inducing beta cell expression of inducible nitric oxide synthase." Journal of Experimental Medicine 181, no. 2 (February 1, 1995): 559–68. http://dx.doi.org/10.1084/jem.181.2.559.

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Cytokines, released in and around pancreatic islets during insulitis, have been proposed to participate in beta-cell destruction associated with autoimmune diabetes. In this study we have evaluated the hypothesis that local release of the cytokine interleukin 1 (IL-1) by nonendocrine cells of the islet induce the expression of inducible nitric oxide synthase (iNOS) by beta cells which results in the inhibition of beta cell function. Treatment of rat islets with a combination of tumor necrosis factor (TNF) and lipopolysaccharide (LPS), conditions known to activate macrophages, stimulate the expression of iNOS and the formation of nitrite. Although TNF+LPS induce iNOS expression and inhibit insulin secretion by intact islets, this combination does not induce the expression of iNOS by beta or alpha cells purified by fluorescence activated cell sorting (Facs). In contrast, IL-1 beta induces the expression of iNOS and also inhibits insulin secretion by both intact islets and Facs-purified beta cells, whereas TNF+LPS have no inhibitory effects on insulin secretion by purified beta cells. Evidence suggests that TNF+LPS inhibit insulin secretion from islets by stimulating the release of IL-1 which subsequently induces the expression of iNOS by beta cells. The IL-1 receptor antagonist protein completely prevents TNF+LPS-induced inhibition of insulin secretion and attenuates nitrite formation from islets, and neutralization of IL-1 with antisera specific for IL-1 alpha and IL-1 beta attenuates TNF+LPS-induced nitrite formation by islets. Immunohistochemical localization of iNOS and insulin confirm that TNF+LPS induce the expression of iNOS by islet beta cells, and that a small percentage of noninsulin-containing cells also express iNOS. Local release of IL-1 within islets appears to be required for TNF+LPS-induced inhibition of insulin secretion because TNF+LPS do not stimulate nitrite formation from islets physically separated into individual cells. These findings provide the first evidence that a limited number of nonendocrine cells can release sufficient quantities of IL-1 in islets to induce iNOS expression and inhibit the function of the beta cell, which is selectively destroyed during the development of autoimmune diabetes.

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Brüning, Dennis, Kathrin Hatlapatka, Verena Lier-Glaubitz, Vincent Andermark, Stephan Scherneck, Ingo Ott, and Ingo Rustenbeck. "Pharmacological inhibition of thioredoxin reductase increases insulin secretion and diminishes beta cell viability." Naunyn-Schmiedeberg's Archives of Pharmacology 394, no. 6 (January 19, 2021): 1133–42. http://dx.doi.org/10.1007/s00210-020-02046-2.

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AbstractApparently, both a decrease in beta cell function and in beta cell mass contribute to the progressive worsening of type 2 diabetes. So, it is of particular interest to define factors which are relevant for the regulation of insulin secretion and at the same time for the maintenance of beta cell mass. The NADPH-thioredoxin system has a candidate role for such a dual function. Here, we have characterized the effects of a highly specific inhibitor of thioredoxin reductase, AM12, on the viability and function of insulin-secreting MIN6 cells and isolated NMRI mouse islets. Viability was checked by MTT testing and the fluorescent live-dead assay. Apoptosis was assessed by annexin V assay. Insulin secretion of perifused islets was measured by ELISA. The cytosolic Ca2+ concentration was measured by the Fura technique. Acute exposure of perifused pancreatic islets to 5 μM AM12 was without significant effect on insulin secretion. Islets cultured for 24 h in 0.5 or 5 μM AM12 showed unchanged basal secretion during perifusion, but the response to 30 mM glucose was significantly enhanced by 5 μM. Twenty-four-hour exposure to 5 μM AM12 proved to be without effect on the viability of MIN6 cells, whereas longer exposure was clearly toxic. Islets were more susceptible, showing initial signs of apoptosis after 24-h exposure to 5 μM AM12. The activity of the NADPH-thioredoxin system is indispensable for beta cell viability but may have a limiting effect on glucose-induced insulin secretion.

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Sjoholm, A., and C. Hellerstrom. "TGF-beta stimulates insulin secretion and blocks mitogenic response of pancreatic beta-cells to glucose." American Journal of Physiology-Cell Physiology 260, no. 5 (May 1, 1991): C1046—C1051. http://dx.doi.org/10.1152/ajpcell.1991.260.5.c1046.

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The long-term influence of transforming growth factor-beta (TGF-beta) on replication and insulin secretion by insulin-producing pancreatic beta-cells was investigated. For this purpose, fetal rat pancreatic islets containing a high proportion of beta-cells were isolated and maintained in tissue culture for 3 days at different concentrations of TGF-beta. TGF-beta (5-500 pM) at a glucose concentration of 11.1 mM did not affect the replication of the beta-cells or their insulin content but enhanced secretion of insulin from these cells. TGF-beta (500 pM) counter-acted the mitogenic action of 16.7 mM glucose but failed to affect the glucose-induced increase in islet insulin content or secretion. Growth hormone (GH) also stimulated beta-cell DNA synthesis and insulin secretion, but TGF-beta was unable to prevent these effects. It was found, moreover, that TGF-beta did not prevent the increase in islet polyamine content which occurred in response to glucose or GH, indicating that the effects of TGF-beta are not mediated through this pathway. Addition of neutralizing antibodies to TGF-beta did not affect the mitogenic or secretory responses to glucose or GH, suggesting that TGF-beta does not exert any autocrine or paracrine function in islets.

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Dumortier, Olivier, Gaia Fabris, Didier F. Pisani, Virginie Casamento, Nadine Gautier, Charlotte Hinault, Patricia Lebrun, et al. "microRNA-375 regulates glucose metabolism-related signaling for insulin secretion." Journal of Endocrinology 244, no. 1 (January 2020): 189–200. http://dx.doi.org/10.1530/joe-19-0180.

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Enhanced beta cell glycolytic and oxidative metabolism are necessary for glucose-induced insulin secretion. While several microRNAs modulate beta cell homeostasis, miR-375 stands out as it is highly expressed in beta cells where it regulates beta cell function, proliferation and differentiation. As glucose metabolism is central in all aspects of beta cell functioning, we investigated the role of miR-375 in this process using human and rat islets; the latter being an appropriate model for in-depth investigation. We used forced expression and repression of mR-375 in rat and human primary islet cells followed by analysis of insulin secretion and metabolism. Additionally, miR-375 expression and glucose-induced insulin secretion were compared in islets from rats at different developmental ages. We found that overexpressing of miR-375 in rat and human islet cells blunted insulin secretion in response to glucose but not to α-ketoisocaproate or KCl. Further, miR-375 reduced O2 consumption related to glycolysis and pyruvate metabolism, but not in response to α-ketoisocaproate. Concomitantly, lactate production was augmented suggesting that glucose-derived pyruvate is shifted away from mitochondria. Forced miR-375 expression in rat or human islets increased mRNA levels of pyruvate dehydrogenase kinase-4, but decreased those of pyruvate carboxylase and malate dehydrogenase1. Finally, reduced miR-375 expression was associated with maturation of fetal rat beta cells and acquisition of glucose-induced insulin secretion function. Altogether our findings identify miR-375 as an efficacious regulator of beta cell glucose metabolism and of insulin secretion, and could be determinant to functional beta cell developmental maturation.

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Scullion, S. M. J., E. Gurgul-Convey, M. Elsner, S. Lenzen, P. R. Flatt, and N. H. McClenaghan. "Enhancement of homocysteine toxicity to insulin-secreting BRIN-BD11 cells in combination with alloxan." Journal of Endocrinology 214, no. 2 (May 11, 2012): 233–38. http://dx.doi.org/10.1530/joe-11-0461.

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Previous studies have shown that homocysteine (HC) has a detrimental impact on insulin secretion and pancreatic beta cell function. The aim of the present study was to determine the role of reactive oxygen species (ROS) in the in vitro toxic effects of HC on insulin secretion and function of BRIN-BD11 insulin-secreting cells. In this study, insulin secretion from BRIN-BD11 cells was determined radioimmunologically, cell viability by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide assay and glucokinase activity by a glucose phosphorylation assay following culture with HC plus alloxan (Alx). Treatment with HC resulted in concentration-dependent inhibition of insulin secretion induced by glucose and other insulinotropic agents. HC in combination with Alx resulted in a more pronounced decline in insulin secretion, including that induced by 20 mM alanine, by 43% (P<0.001) and 30 mM KCl by 60% (P<0.001), compared with control culture. The glucokinase phosphorylating capacity in cells cultured with HC plus Alx was significantly lower, compared with control cells. The cells also displayed a significant 84% (P<0.001) decline in cell viability. Prolonged, 72-h culture of insulin-secreting cells with HC followed by 18-h culture without HC did not result in full restoration of beta cell responses to insulinotropic agents. In vitro oxygen consumption was enhanced by a combination of Alx with HC. The study arrived at the conclusion that HC generates ROS in a redox-cycling reaction with Alx that explains the decline in viability of insulin-secreting cells, leading to reduced glucokinase phosphorylating ability, diminished insulin secretory responsiveness and cell death.

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Dissertations / Theses on the topic "Beta cell insulin secretion"

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Stokesberry, Susan Anne. "Functional effects of temperature on pancreatic beta-cell insulin secretion and integrity." Thesis, University of Ulster, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.422895.

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Proks, Peter. "Electrophysiological studies of insulin secretion from pancreatic beta cells." Thesis, University of Oxford, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.318522.

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Idevall, Hagren Olof. "Oscillatory Signaling and Insulin Secretion from Single ß-cells." Doctoral thesis, Uppsala universitet, Institutionen för medicinsk cellbiologi, 2010. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-113686.

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cAMP and Ca2+ are key regulators of exocytosis in many cells, including insulin-secreting pancreatic β-cells. Glucose-stimulated insulin secretion from β-cells is pulsatile and driven by oscillations of the cytoplasmic Ca2+ concentration ([Ca2+]i), but little is known about the kinetics of cAMP signaling and the mechanisms of cAMP action. Evanescent wave microscopy and fluorescent translocation biosensors were used to monitor plasma membrane-related signaling events in single MIN6-cells and primary mouse β-cells. Glucose stimulation of insulin secretion resulted in pronounced oscillations of the membrane phospholipid PIP3 caused by autocrine activation of insulin receptors. Glucose also triggered oscillations of the sub-plasma membrane cAMP concentration ([cAMP]pm). These oscillations were preceded and enhanced by elevations of [Ca2+]i, but conditions raising cytoplasmic ATP triggered [cAMP]pm elevations without accompanying changes in [Ca2+]i. The [cAMP]pm oscillations were also synchronized with PIP3 oscillations and both signals were suppressed after inhibition of adenylyl cyclases. Protein kinase A (PKA) was important for promoting concomitant initial elevations of [cAMP]pm and [Ca2+]i, and PKA inhibitors diminished the PIP3 response when applied before glucose stimulation, but did not affect already manifested PIP3 oscillations. The glucose-induced PIP3 oscillations were markedly suppressed in cells treated with siRNA against the cAMP-dependent guanine nucleotide exchange factor Epac2. Pharmacological activation of Epac restored PIP3 responses after adenylyl cyclase or PKA inhibition. Glucose and other cAMP-elevating stimuli induced redistribution of fluorescence-tagged Epac2 from the cytoplasm to the plasma membrane. This translocation was modulated by [Ca2+]i and depended on intact cyclic nucleotide-binding and Ras-association domains. In conclusion, glucose generates cAMP oscillations in β-cells via a concerted action of Ca2+ and metabolically generated ATP. The oscillations are important for the magnitude and kinetics of insulin secretion. While both protein kinase A and Epac is required for initiation of insulin secretion the cAMP-dependence of established pulsatility is mediated by Epac2.

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Castell, Auví Anna. "The effects of grape seed procyanidin extract on insulin synthesis and secretion." Doctoral thesis, Universitat Rovira i Virgili, 2012. http://hdl.handle.net/10803/79133.

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Las procianidinas son compuestos bioactivos presentes en frutas y vegetales. Aunque se conocen los efectos beneficiosos de estos compuestos en la homeostasis de la glucosa, su acción en la funcionalidad de la célula β no es clara. La presente tesis doctoral se ha centrado en describir los efectos de las procianidinas en la síntesis y secreción de insulina. Nuestros resultados muestran la capacidad de las procianidinas de modificar la funcionalidad de la célula β aumentando la relación insulina plasmática/mRNA, aunque la efectividad del tratamiento depende de la situación fisiológica. En situaciones no patológicas, las procianidinas afectan la insulinemia modificando la síntesis, secreción y/o degradación de la insulina. En situaciones de resistencia a la insulina, el tratamiento crónico con procianidinas disminuye la síntesis y secreción de insulina gracias a su acción limitando el acúmulo de lípidos. En cambio, en un modelo más dañado (obesidad genética), las procianidinas ejercen efectos similares pero no son capaces de mejorar la hipersinulinemia. En conclusión, las procianidinas, en las dosis ensayadas, pueden utilizarse únicamente como compuestos bioactivos limitando la disfuncionalidad de la célula β en sus estados iniciales.
Les procianidines són compostos bioactius presents en fruites i vegetals. Tot i que es coneixen els efectes beneficiosos d’aquests compostos en l’homeòstasi de la glucosa, la seva acció en la funcionalitat de la cèl•lulaβ no és clara. La present tesi doctoral s’ha centrat en descriureels efectes de les procianidines en la síntesi i secreció d’insulina. Els nostres resultats mostren la capacitat de les procianidines de modificar la funcionalitat de la cèl•lula β augmentant la relació insulina plasmàtica/mRNA, tot i que l’efectivitat del tractamentdepèn de la situaciófisiològica. En situacions no patològiques, les procianidines afecten la insulinèmia modificant la síntesi, secreciói/o degradació d’insulina. En situacions de resistència a la insulina, el tractamentcrònicamb procianidines disminueix la síntesi i secreció d’insulina gràcies a la seva acció limitant l’acumulació de lípids. En canvi, en un model més danyat (obesitat genètica), les procianidines exerceixen efectes similars però no son capaces de millorar la hiperinsulinèmia. En conclusió, les procianidines, en les dosis assajades, podenutilitzar-seúnicament coma compostos bioactiuslimitant la disfuncionalitat de la cèl•lula β en els seus estats inicials.
Procyanidins are bioactive compounds found in fruits and vegetables widely consumed. It has been reported that procyanidins show some beneficial effects on glucose homeostasis, although their effects on β-cell functionality remain unresolved. This doctoral thesis is focus on describing the effects of procyanidins on insulin synthesis and secretion. Our results showed that procyanidins modify β-cell functionality through increasing the plasma insulin/mRNA ratio, although the effectiveness of the treatment depends on the physiological situation. Under non-pathological situation, procyanidins affected insulinaemia by modifying insulin synthesis, secretion and/or degradation activity. Under insulin-resistance situation, chronic procyanidins administration decreased insulin synthesis and secretion, thanks to its lipid-lowering effect. Otherwise in a more damaged model, Zucker fatty rat, procyanidins treatment is not able to reduce insulin plasma levels although they repress insulin expression. In conclusion, procyanidins could be used as bioactive compound to limit β-cell dysfunctions under high-palatable diets, but at the assayed doses, it is not enough to counteract a strong metabolic disruption.

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Tang, Shiue-Cheng. "Genetic engineering of non-beta-cells for regulated insulin secretion." Diss., Available online, Georgia Institute of Technology, 2004:, 2003. http://etd.gatech.edu/theses/available/etd-04072004-180222/unrestricted/tang%5Fshiue-cheng%5F200312%5Fphd.pdf.

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Gan, Wan Jun. "Potential mechanisms that control targeted insulin secretion in pancreatic beta cells." Thesis, The University of Sydney, 2018. http://hdl.handle.net/2123/20018.

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Loss of insulin secretion is a recognized characteristic of diabetes. It is therefore an important goal to understand how insulin secretion is controlled and what goes wrong in disease. The discovery of the spatial orientation of insulin granule fusion towards the vasculature adds more complexity to the regulation of insulin secretion. The underlying mechanisms however remain unknown. I therefore have investigated interactions of beta cells with the surrounding microenvironment in order to identify possible factors that regulate the vascular-orientated insulin granule fusion. In Chapter 3, I first investigate the beta cell-vascular basement membrane interaction by culturing dispersed beta cells on surfaces coated with 3 different basement membrane proteins: Laminin 511, Collagen IV or Fibronectin. Poly-l-lysine coated surface is used as the control. 3D two photon live cell imaging showed that insulin granule fusion is targeted towards the cell-protein interface in beta cells cultured on surface coated with either one of the proteins but not the control. The targeting of insulin granule fusion can be further segregated by culturing on surfaces micropatterned with Fibronectin and E-cadherin Fc which represent the beta cell-vasculature and beta cell-beta cell interfaces respectively. Using an integrin beta 1 blocking antibody and focal adhesion kinase inhibitor, I show that the basement membrane-induced targeting of insulin granule fusion is integrin beta 1 and focal adhesion complex dependent. I therefore conclude that the vascular basement membrane proteins and subsequent membrane protein-induced focal adhesion complex formation are crucial factors in establishing and maintaining the spatial targeting of insulin granule fusion. In Chapter 4 and 5, I further studied the polar organisation of beta cells in regulating insulin secretion. In Chapter 4, I first characterised the organisation of beta cells using a pancreatic slice preparation that better retains the native structural organisation of the beta cells than the isolated islets. 3D imaging and analysis of polarity-related proteins reveal that beta cells exhibit 3 distinct polarity domains: the apical, lateral and basal polarity domains. Such polarity organisation is present in single beta cell as well as throughout the whole islet. One of the basolateral polarity determinants, Scribble, was further investigated in Chapter 5 using Scrib+/- mice and rodent beta cell line MIN6. Scrib+/- mice exhibit better blood glucose homeostasis and bigger islet as well as an increase in basal insulin secretion. No differences are found in the spatial orientation of insulin granule fusion and overall glucose-stimulated insulin secretion in the Scrib+/- islets. The Scrib KD MIN6 on the other hand reduced glucose-stimulated insulin secretion. Such reduction of glucose-stimulated insulin secretion in Scrib KD MIN6 is possibly betaPIX independent as the betaPIX and Scribble staining exhibit limited overlapping and the betaPIX KD MIN6 had no effect on the glucose-stimulated insulin secretion. I therefore conclude that beta cells are polarised cell type and suggest that Scribble possibly control beta cell mass and regulate insulin secretion in a betaPIX independent manner. In summary, in this thesis, I showed that the vascular basement membrane is one of the factors orientating the insulin granule fusion towards the vasculature. I have also show that beta cells should be viewed as polarised cell type with distinct polarity domains expressing typical polarity proteins. One of the polarity determinants, Scribble possibly regulates beta cell mass and insulin secretion.

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7

Turbitt, Julie Michelle. "The role of taurine in the regulation of insulin secretion and pancreatic beta-cell function." Thesis, University of Ulster, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.422896.

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Gulino, Angela Marie. "Insulin secretion dynamics of recombinant hepatic and intestinal cells." Thesis, Atlanta, Ga. : Georgia Institute of Technology, 2008. http://hdl.handle.net/1853/28220.

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Herrero, Rodríguez Laura. "Implication of Long-Chain Fatty Acids in Glucose-Induced Insulin Secretion in the Pancreatic Beta-Cell." Doctoral thesis, Universitat de Barcelona, 2004. http://hdl.handle.net/10803/2999.

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INTRODUCTION Carnitine palmitoyltransferase I, which is expressed in the pancreas as the liver isoform (LCPTI), catalyzes the rate-limiting step in the transport of fatty acids into the mitochondria for their oxidation. To directly examine whether the availability of long-chain fatty acyl-CoA affects the regulation of insulin secretion in the Beta-cell, we infected INS(832/13) cells and rat islets with an adenovirus encoding a mutant form of LCPTI (Ad-LCPTI M593S) that is insensitive to its inhibitor malonyl-CoA. C75 is described as a potential drug for treatment of obesity and type 2 diabetes. First known as a synthetic inhibitor of fatty acid synthase, it has been also described as an activator of CPTI, increasing peripheral energy utilization and fatty acid oxidation in mice. To further investigate the C75/CPTI interaction, we have characterized the effects of C75 on CPTI in vitro and in vivo.

OBJECTIVES 1) Study of the malonyl-CoA/CPTI interaction in the pancreatic Beta-cell and its involvement in glucose-stimulated insulin secretion (GSIS). 2) Construction of an INS stable cell line overexpressing LCPTI wt and LCPTI M593S. 3) Determine the effect of C75 on the CPTI activity and palmitate oxidation in pancreatic Beta-cells.

RESULTS. In Ad-LCPTI M593S infected INS(832/13) cells LCPTI activity increased six-fold. This was associated with enhanced fatty acid oxidation, at any glucose concentration, and a 60% suppression of GSIS. In isolated rat islets in which LCPTI M593S was overexpressed, GSIS decreased 40%. At high glucose concentration, overexpression of LCPTI M593S reduced partitioning of exogenous palmitate into lipid esterification products, and decreased PKC activation. Moreover, LCPTI M593S expression impaired KATP channel-independent GSIS in INS(832/13) cells.
INS-1 stable clones of LCPTIwt and LCPTImut were constructed, however none of them resulted in an increase in LCPTI protein expression compared to endogenous LCPTI nor in CPTI activity. Therefore, slight basal overexpression of LCPTI could probably be toxic for the cells, as a result of which only those cells that do not contain the LCPTI plasmids survived throughout cell passages.
When INS(823/13) cells are incubated with C75, CPTI activity is inhibited, as is fatty acid oxidation. In vivo, a single intraperitoneal injection of C75 to mice produces a short-term inhibition of CPTI activity in mitochondria from liver and pancreas.

DISCUSSION. The results with LCPTImut provide direct support for the hypothesis proposing that the malonyl-CoA/CPTI interaction is a component of a metabolic signalling network that controls insulin secretion. Overall, the findings with C75 provide compelling evidence that the drug is a potent inhibitor of CPTI.

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Ng, Ming Tak. "Effects of prominsulin C-peptide and other islet peptides on beta-cell function and insulin secretion." Thesis, University of Ulster, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.554231.

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Hyperglycaemia is a significant pathophysiological feature of diabetes mellitus. It has been considered to be a cause as well as a consequence of impaired pancreatic p-cell function and insulin action. The detrimental effects of a hyperglycaemic environment encourage the non-enzymatic glycation of regulatory and functional proteins. This thesis investigated the effects of pro insulin C-peptide and other important islet peptides such as insulin, somatostatin, islet amyloid polypeptide (IAPP) as well as the gut hormone gastric inhibitory polypeptide (GIP) in both native and glycated forms on insulin release and beta cell function in vitro using clonal pancreatic p-ce1ls and isolated mouse islets and in vivo, using Swiss TO lean mice. Pancreatic beta-cells not only secrete insulin into the bloodstream, but also release equimolar amounts of C-peptide. During the last decade, studies have provided definite evidence of C-peptide's active role in physiology and pathophysiology. However very little information currently exists on the direct effects of C-peptide on pancreatic beta cells. This study provides evidence that C-peptide is a biologically active endogenous peptide hormone that exerts tonic inhibitory effects on pancreatic beta cell function and these effects may be partially mediated through intracellular signalling pathways. Suppression of insulin secretion by C-peptide was observed at basal and stimulatory glucose concentrations and was shown to be concentration dependent. The ability of alanine and IBMX to potentiate glucose-induced insulin secretion was severely impaired in the pancreatic cell line and isolated islets in the presence of C-peptide. This inhibition of glucose stimulated insulin secretion may be associated with the mechanism by which cAMP and KATP channel potentiates insulin release. In vivo studies with the administration of C-peptide resulted in a decrease in plasma insulin levels and increase in plasma glucose concentrations. As proinsulin C-peptide clearly exhibited an inhibitory effect on insulin secretion, it was of interest to study the autocrine effect of the other important pancreatic p-cell peptide, insulin. Concentration dependent inhibitory effects of insulin on alanine- and IBMX-stimulated insulin secretion were observed in isolated islets. Validation of this result was confirmed in vivo using Swiss TO mice, where plasma C-peptide levels were decreased following insulin administration. In mechanistic studies, insulin not only inhibited cAMP production at stimulatory glucose concentration, but also decreased GLP-1 and forskolin-stimulated cAMP production in clonal pancreatic cells. Moreover, insulin exerted a negative effect on insulin biosynthesis by decreasing the alanine-stimulated insulin mRNA expression at basal and stimulatory glucose concentration. As expected, inhibitory effects on insulin secretion were also observed for the pancreatic peptides, somatostatin-14 and IAPP whilst the gut incretin hormone GIP exerted insulinotropic activity. Following incubation with glucose in vitro, glycated forms of C-peptide, insulin, somatostain-14 and GIP were all readily detectable by reverse-phase HPLC and MALDI- TOF mass spectrometry. The extent of glycation was shown to be time and glucose concentration dependent. G Iycated human C-peptide exerted an inhibitory effect on insulin secretion, but to a lesser extent than non-glycated C-peptide. Glycated human C- peptide in the presence of alanine, GIP and tolbutamide resulted in 22%, 12% and 27% inhibition, respectively compared to 50%, 52% and 42% inhibition with native human C- peptide. A similar trend was obtained when comparing glycated human insulin and non- glycated human insulin. Suppression of alanine- and IBMX-stimulated C-peptide release was observed with glycated insulin. Glycated insulin reduced cAMP production at stimulatory glucose concentration, GLP-l and forskolin-stimulated cAMP production. Both glycated C-peptide and glycated insulin exhibited a less potent inhibitory effect on insulin secretion. Contrastingly, glycation of somatostatin-14 increased its ability to inhibit insulin secretion. Likewise, glycated GIP was more insulinotropic than its native peptide. These studies indicate that C-peptide may be one of several players in the multifactorial regulation of the pancreatic beta cell. Insulin secretion is an important physiological process which is regulated by multiple regulatory mechanisms. C-peptide may have a compensatory regulatory effect through the fine control of insulin release. Collectively, these studies indicate the need for continuing investigation of the circulating levels of glycated peptides and their effects on the ability to modulate insulin secretion. Further investigations are thus necessary to find out the possible role of glycated peptides in the pathophysiology of type 2 diabetes.

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Books on the topic "Beta cell insulin secretion"

1

Susumu, Seino, and Bell Graeme, eds. Pancreatic beta cell in health and disease. [Tokyo]: Springer, 2008.

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Kulkarni, Rohit N. Islet cell growth factors. Austin, Tex: Landes Bioscience, 2011.

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Liu, Hui-Kang. Modification of the function of insulin-secreting cells by beta-cell toxins, differentiation drugs, insulin mimetics, steriods, and incretin hormones and their stable analogues. [S.l: The Author], 2003.

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R, Flatt Peter, and Lenzen Sigurd, eds. Frontiers of insulin secretion and pancreatic B-cell research. London: Smith-Gordon, 1994.

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Duffy, Joan. Effects of insulin sensitising agents on pancreatic beta cell function. [S.l: The Author], 2003.

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Bonnevie-Nielsen, Vagn. The endocrine pancreas aspects of Ý-cell function in relation to morphology, insulin secretion and insulin content. Oxford: Published for Medisinsk fysiologisk forenings forlag, Oslo by Blackwell Scientific Publications, 1986.

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Francesco, Belfiore, ed. Molecular and cell biology of type 2 diabetes and its complications. Basel: Karger, 1998.

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patterson, Steven. Homocysteine and the effects of other amino thiols on pancreatic beta cell function and insulin. [S.l: The Author], 2003.

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Macfarlane, Wendy Margaret. An investigation of the role of the [beta] cell transcription factor IUF1 in the glucose sensitivity of insulin gene transcription, and in islet cell ontogeny. Birmingham: University of Birmingham, 1995.

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Seino, Susumu, and Graeme I. Bell. Pancreatic Beta Cell in Health and Disease. Springer, 2009.

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Book chapters on the topic "Beta cell insulin secretion"

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Willenborg, Michael, Kirstin Schumacher, and Ingo Rustenbeck. "Determination of Beta-Cell Function: Insulin Secretion of Isolated Islets." In Animal Models in Diabetes Research, 189–201. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-62703-068-7_12.

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Pavelka, Margit, and Jürgen Roth. "Endocrine Secretion: Insulin-Producing Beta Cells of Islets of Langerhans." In Functional Ultrastructure, 206–7. Vienna: Springer Vienna, 2010. http://dx.doi.org/10.1007/978-3-211-99390-3_107.

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Boyd, A. E., R. S. Hill, T. Y. Nelson, J. M. Oberwetter, and M. Berg. "The Role of Cytosolic Calcium in Insulin Secretion from a Hamster Beta Cell Line." In Advances in Experimental Medicine and Biology, 305–16. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-5314-0_27.

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Nakagawa, Yuko, and Johan Medina. "The Role of the Glucose-Sensing Receptor in Glucose-Induced Insulin Secretion in Pancreatic β-Cells." In Glucose-sensing Receptor in Pancreatic Beta-cells, 61–71. Singapore: Springer Singapore, 2018. http://dx.doi.org/10.1007/978-981-13-0002-8_5.

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Dou, Haiqiang, and Zhuan Zhou. "Action Potential-Induced Ca2+ Influx for Both Acute and Sustained Insulin Secretion in Pancreatic Beta Cells." In Neurosecretion: Secretory Mechanisms, 161–72. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-22989-4_8.

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Crisóstomo, Joana, Francisca Araújo, Pedro Granja, Cristina Barrias, Bruno Sarmento, and Raquel Seiça. "Co-encapsulation of Beta Cells and Nanoparticles Containing GLP-1 Greatly Improves Insulin Secretion in Alginate-Based Bioartificial Pancreas." In IFMBE Proceedings, 1215–22. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-31635-8_147.

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Seino, Susumu, Tadao Shibasaki, and Kohtaro Minami. "β-Cell biology of insulin secretion." In International Textbook of Diabetes Mellitus, 96–107. Chichester, UK: John Wiley & Sons, Ltd, 2015. http://dx.doi.org/10.1002/9781118387658.ch7.

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Miwa, I., Y. Toyoda, and S. Yoshie. "Glucokinase in β-Cell Insulin-Secretory Granules." In Frontiers in Diabetes, 350–59. Basel: KARGER, 2004. http://dx.doi.org/10.1159/000079029.

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Weir, Gordon C., Susan Bonner-Weir, and Arun Sharma. "Regulation of Insulin Secretion and Islet Cell Function." In Atlas of Diabetes, 1–17. Boston, MA: Springer US, 2011. http://dx.doi.org/10.1007/978-1-4614-1028-7_1.

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Leibiger, B., P. O. Berggren, and I. B. Leibiger. "Regulation of β-Cell GK Gene Transcription by Insulin." In Frontiers in Diabetes, 249–61. Basel: KARGER, 2004. http://dx.doi.org/10.1159/000079021.

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Conference papers on the topic "Beta cell insulin secretion"

1

Tura, Andrea, Manfred Hecking, Michael Wolzt, Marcus D. Saemann, and Giovanni Pacini. "Assessment of beta-cell function and insulin secretion in subjects that underwent renal transplantation." In 2015 37th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2015. http://dx.doi.org/10.1109/embc.2015.7318870.

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Gaus, B., and I. Rustenbeck. "Insulin granule number, mobility and exocytosis as compared with insulin content and secretion after the induction of desensitization or beta-cell rest." In Diabetes Kongress 2021 – 55. Jahrestagung der DDG. Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0041-1727355.

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Tsuda, Y., M. Kato-Negishi, T. Okitsu, and S. Takeuchi. "Size-Controlled Islet-Cell Spheroids for Geometric Analysis of Insulin Secretion." In 2009 IEEE 22nd International Conference on Micro Electro Mechanical Systems (MEMS). IEEE, 2009. http://dx.doi.org/10.1109/memsys.2009.4805409.

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Pagkalos, Ilias, Pau Herrero, and Pantelis Georgiou. "An analogue implementation of the beta cell insulin release model." In 2013 IEEE International Symposium on Circuits and Systems (ISCAS). IEEE, 2013. http://dx.doi.org/10.1109/iscas.2013.6572384.

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Nam, David, Judith Mantell, David Bull, Paul Verkade, and Alin Achim. "Insulin Granule Segmentation in 3-D TEM Beta Cell Tomograms." In British Machine Vision Conference 2013. British Machine Vision Association, 2013. http://dx.doi.org/10.5244/c.27.113.

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Gässler, A., C. Quiclet, O. Kluth, J. Spranger, and A. Schürmann. "Overexpression of Gjb4 impairs cell proliferation and insulin secretion in primary islets cells." In Late breaking Abstracts – Diabetes Kongress 2018 – 53. Jahrestagung der DDG. Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1657795.

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Mingen Xu, Yongnian Yan, and Xiaohong Wang. "Modeling insulin secretion dysfunction in a three-dimensional culture system by cell-assembly technique." In 2009 IEEE International Conference on Virtual Environments, Human-Computer Interfaces and Measurements Systems (VECIMS). IEEE, 2009. http://dx.doi.org/10.1109/vecims.2009.5068877.

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Decroli, Eva, Yanne Efendi, Alexander Kam, Asman Manaf, and Syafril Syahbuddin. "Description of Insulin Resistance and Beta-Cell Pancreas Dysfunction in Prediabetic Patients." In Proceedings of the 1st EAI International Conference on Medical And Health Research, ICoMHER November 13-14th 2018, Padang, West Sumatera, Indonesia. EAI, 2019. http://dx.doi.org/10.4108/eai.13-11-2018.2283632.

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Mel Ho, Pantelis Georgiou, Suket Singhal, Nick Oliver, and Chris Toumazou. "A bio-inspired closed-loop insulin delivery based on the silicon pancreatic beta-cell." In 2008 IEEE International Symposium on Circuits and Systems - ISCAS 2008. IEEE, 2008. http://dx.doi.org/10.1109/iscas.2008.4541602.

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Di Nardo, Francesco, Pamela Cerasa, Fabrizio Casagrande, Massimo Boemi, Pierpaolo Morosini, and Roberto Burattini. "Insulin secretion rate and ß-cell sensitivity from oral glucose tolerance test in normotensive and normoglycemic humans." In Conference Proceedings. Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2006. http://dx.doi.org/10.1109/iembs.2006.260216.

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Reports on the topic "Beta cell insulin secretion"

1

Elmann, Anat, Orly Lazarov, Joel Kashman, and Rivka Ofir. therapeutic potential of a desert plant and its active compounds for Alzheimer's Disease. United States Department of Agriculture, March 2015. http://dx.doi.org/10.32747/2015.7597913.bard.

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We chose to focus our investigations on the effect of the active forms, TTF and AcA, rather than the whole (crude) extract. 1. To establish cultivation program designed to develop lead cultivar/s (which will be selected from the different Af accessions) with the highest yield of the active compounds TTF and/or achillolide A (AcA). These cultivar/s will be the source for the purification of large amounts of the active compounds when needed in the future for functional foods/drug development. This task was completed. 2. To determine the effect of the Af extract, TTF and AcA on neuronal vulnerability to oxidative stress in cultured neurons expressing FAD-linked mutants.Compounds were tested in N2a neuroblastoma cell line. In addition, we have tested the effects of TTF and AcA on signaling events promoted by H₂O₂ in astrocytes and by β-amyloid in neuronal N2a cells. 3. To determine the effect of the Af extract, TTF and AcA on neuropathology (amyloidosis and tau phosphorylation) in cultured neurons expressing FAD-linked mutants. 4. To determine the effect of A¦ extract, AcA and TTF on FAD-linked neuropathology (amyloidosis, tau phosphorylation and inflammation) in transgenic mice. 5. To examine whether A¦ extract, TTF and AcA can reverse behavioral deficits in APPswe/PS1DE9 mice, and affect learning and memory and cognitive performance in these FAD-linked transgenic mice. Background to the topic.Neuroinflammation, oxidative stress, glutamate toxicity and amyloid beta (Ab) toxicity are involved in the pathogenesis of Alzheimer's diseases. We have previously purified from Achilleafragrantissimatwo active compounds: a protective flavonoid named 3,5,4’-trihydroxy-6,7,3’-trimethoxyflavone (TTF, Fl-72/2) and an anti-inflammatory sesquiterpenelactone named achillolide A (AcA). Major conclusions, solutions, achievements. In this study we could show that TTF and AcA protected cultured astrocytes from H₂O₂ –induced cell death via interference with cell signaling events. TTF inhibited SAPK/JNK, ERK1/2, MEK1 and CREBphosphorylation, while AcA inhibited only ERK1/2 and MEK1 phosphorylation. In addition to its protective activities, TTF had also anti-inflammatory activities, and inhibited the LPS-elicited secretion of the proinflammatorycytokinesInterleukin 6 (IL-6) and IL-1b from cultured microglial cells. Moreover, TTF and AcA protected neuronal cells from glutamate and Abcytotoxicity by reducing the glutamate and amyloid beta induced levels of intracellular reactive oxygen species (ROS) and via interference with cell signaling events induced by Ab. These compounds also reduced amyloid precursor protein net processing in vitro and in vivo in a mouse model for Alzheimer’s disease and improvedperformance in the novel object recognition learning and memory task. Conclusion: TTF and AcA are potential candidates to be developed as drugs or food additives to prevent, postpone or ameliorate Alzheimer’s disease. Implications, both scientific and agricultural.The synthesis ofAcA and TTF is very complicated. Thus, the plant itself will be the source for the isolation of these compounds or their precursors for synthesis. Therefore, Achilleafragrantissima could be developed into a new crop with industrial potential for the Arava-Negev area in Israel, and will generate more working places in this region.

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