Relevant bibliographies by topics / Pancreatic beta cell function

Academic literature on the topic 'Pancreatic beta cell function'

Author: Grafiati

Published: 9 March 2023

Last updated: 11 March 2023

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Journal articles
Dissertations / Theses
Books
Book chapters
Conference papers
Reports

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Pancreatic beta cell function.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "Pancreatic beta cell function"

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.

Full text

APA, Harvard, Vancouver, ISO, and other styles

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.

Full text

APA, Harvard, Vancouver, ISO, and other styles

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.

Full text

APA, Harvard, Vancouver, ISO, and other styles

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.

Full text

APA, Harvard, Vancouver, ISO, and other styles

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.

Full text

Abstract:

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.

APA, Harvard, Vancouver, ISO, and other styles

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.

Full text

Abstract:

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.

APA, Harvard, Vancouver, ISO, and other styles

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.

Full text

Abstract:

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.

APA, Harvard, Vancouver, ISO, and other styles

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.

Full text

Abstract:

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.

APA, Harvard, Vancouver, ISO, and other styles

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.

Full text

Abstract:

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.

APA, Harvard, Vancouver, ISO, and other styles

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.

Full text

Abstract:

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.

APA, Harvard, Vancouver, ISO, and other styles

More sources

Dissertations / Theses on the topic "Pancreatic beta cell function"

Pinnick, Katherine Elizabeth. "Pancreatic fat accumulation and effects on beta cell function." Thesis, University of Oxford, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.492051.

Full text

Abstract:

Type 2 Diabetes Mellitus (T2DM) is characterised by impaired pancreatic 13-cell function resulting in inadequate insulin secretion. The mechanisms involved in 13-cell dysfunction are largely unknown. Elevated fasting plasma non-esterified fatty acid (NEFA) concentrations have been identified as a risk factor for the development of T2DM. The work in this thesis investigates functional effects of NEFA on the 13-cell. Prolonged exposure to elevated NEFA has previously been associated with impaired insulin secretion, reduced insulin content and altered gene expression and lipid metabolism in the 13-cell. Determining the reversibility of these defects may lead to a greater understanding of the underlying mechanisms. Increased pancreatic fat content is positively associated with body mass index in humans and this may expose the 13-cell to high NEFA concentrations. However, the in vivo concentration and composition of NEFA in the pancreas is not known. An in vitro model of 13-cell 'recovery' from the deleterious effects of fatty acids is presented. The longterm culture (>48h) of mouse islets and INS-1 cells with NEFA (0.5mM) impaired glucose and tolbutamide-stimulated insulin secretion, but this was partially reversed by culture for 24h in the absence of exogenous fatty acids. Culture with oleic acid led to the accumulation of triacylglycerol (TAG) in cytosolic lipid droplets. The protein ADFP was found in close association with these droplets. In contrast, culture with palmitic acid produced large cytoplasmic 'splits'. The removal of exogenous fatty acids from the culture media led to a visible reduction in these morphological features. Extraction of the cellular lipids confirmed an increase in the TAG content following culture with NEFA and demonstrated the incorporation of the experimental fatty acid into the TAG and phospholipid (PL) fractions. Following removal of the fatty acids for 24h, TAG content was reduced and NEFA-induced changes in TAG and PL fatty acid composition were partially reversed. A reduction in TAG content in 'recovering' cells indicated the presence of active Iipases. Culture with NEFA increased lipolysis as shown by the measurement of glycerol in the culture media, but this was reduced in 'recovering' cells. Lipase inhibitors inhibited glycerol release but failed to inhibit a reduction in TAG content, and did not confirm a role for Iipases in the recovery of stimulated insulin secretion. Exposure of INS-1 cells to NEFA increased their oxidative capacity for fatty acids and this remained elevated in 'recovering' cells. Treatment with the CPT-1 inhibitor, etomoxir (10I-lM), impaired the fatty acid oxidative capacity of the 13-cell but did not affect the recovery of insulin secretion. A number of genes were upregulated following prolonged culture with NEFA, these included insulin I and II, CPT-1 and UCP2. These genes all displayed reduced expression in cells cultured further in the absence of exogenous fatty acids. The content and composition of fat in tissues from mice was investigated. The TAG composition reflected the major fatty acids found in the diet, with elevated proportions of palmitic and palmitoleic acid indicating the contribution of de novo lipogenesis and desaturase activity to this fatty acid pool. Pancreatic PL were highly unsaturated compared to liver PL, with arachidonic acid accounting for -25% of the PL fatty acids. In mice fed a high-fat (40%) diet (HFD) which was compositionally matched to a control (5%) diet, a 20-fold increase in pancreatic fat was found by 15 weeks. Adipocytes, which were positively labeled for perilipin were observed in the exocrine tissue of the pancreas in HFD mice and lipid droplets labeled for ADFP were identified in the cytoplasm of exocrine cells. By 15 weeks, the fatty acid composition of the TAG, PL and NEFA fractions showed significant differences between HFD and control mice. Perilipin-positive adipocytes were also identified in human pancreas samples and the percentage adipocyte area in histological sections positively correlated (r=0.64) to total pancreatic TAG content. In conclusion, the in vitro findings show the deleterious effects of fatty acids are not permanent. However, increased fat accumulation in the pancreas, as seen in obesity, could expose the 13-cell to elevated NEFA concentrations which, over many years, may lead to irreversible 13-cell failure.

APA, Harvard, Vancouver, ISO, and other styles

Duffy, Joan. "Effects of insulin sensitising agents on pancreatic beta cell function." Thesis, University of Ulster, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.399052.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Nishi, Kiyoto. "Nardilysin Is Required for Maintaining Pancreatic β-Cell Function." 京都大学 (Kyoto University), 2017. http://hdl.handle.net/2433/225463.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Tym, Amy. "Effect of protein glycation by methylglyoxal on pancreatic beta cell function." Thesis, University of Warwick, 2014. http://wrap.warwick.ac.uk/61717/.

Full text

Abstract:

Methylglyoxal is a physiological dicarbonyl metabolite and potent argininedirected glycating agent. It often modifies proteins at functional sites producing loss of positive charge, structural distortion and inactivation. Plasma methylglyoxal is increased in hyperglycaemia associated with diabetes and is linked to the development of vascular complications of diabetes – particularly nephropathy, retinopathy and neuropathy. The effects of dicarbonyl glycation on beta cells and involvement in early stage dysfunction and development of type 2 diabetes mellitus are not known. The aim of this project was to investigate the effect of dicarbonyl protein glycation on beta cell function and related involvement in the development of diabetes. Studies were performed in an in vitro model of beta cell dysfunction - MIN6 insulinoma cells incubated under low and high glucose concentrations, and in a pre-clinical in vivo model of decline of glucose tolerance preceding development of type 2 diabetes - high fat diet-induced insulin resistant mice. Dicarbonyl metabolism and protein damage by glycation and oxidation were studied by stable isotopic dilution analysis liquid chromatography-tandem mass spectrometry. Localisation of methylglyoxal glycation adducts within the pancreas were visualised by immunostaining. Interactions between the extracellular matrix protein, collagen IV, and MIN6 cells in vitro were investigated and impairments in adhesion were assessed following glycation with methylglyoxal. Impairments in adhesion of MIN6 cells to methylglyoxal-glycated collagen IV were assessed using atomic force microscopy force spectroscopy. The results show that MIN6 cells were resistant to accumulation of methylglyoxal when incubated in high glucose concentration although the flux of methylglyoxal was increased 41%. Glycation of collagen IV by methylglyoxal impairs binding to MIN6 cells in vitro resulting in a 91% decrease in the energy necessary to detach cells from the extracellular matrix protein. In high fat diet fed mice the concentration of methylglyoxal in the pancreas was increased. Visualisation of MG-H1 adduct residues in the pancreas showed they were predominantly on the extracellular matrix. In conclusion, protein glycation by methylglyoxal occurs in MIN6 cells in vitro and in the mouse pancreas in vivo. Although the methylglyoxal concentration in the pancreas of high fat diet fed, insulin resistant mice was increased, the lack of a concurrent increase in methylglyoxal protein glycation adducts suggests there may be increased turnover of methylglyoxal-modified proteins. Impairment of beta cell attachment to the extracellular matrix protein, collagen IV, by methylglyoxal and increased protein turnover stimulated by an increased rate of methylglyoxal glycation may impair beta cell function in pre-diabetes in vivo. Glycation by methylglyoxal may contribute to beta cell glucotoxicity and dysfunction with progression to type 2 diabetes mellitus.

APA, Harvard, Vancouver, ISO, and other styles

Ullsten, Sara. "The Impact of Pancreatic Islet Vascular Heterogeneity on Beta Cell Function and Disease." Doctoral thesis, Uppsala universitet, Institutionen för medicinsk cellbiologi, 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-330805.

Full text

Abstract:

Diabetes Mellitus is a group of complex and heterogeneous metabolic disorders characterized by hyperglycemia. Even though the condition has been extensively studied, its causes and complex pathologies are still not fully understood. The occurring damage to the pancreatic islets is strikingly heterogeneous. In type 1 diabetes, the insulin producing beta cells are all destroyed within some islets, and similarly in type 2 diabetes, some islets may be severely affected by amyloid. At the same time other islets, in the near vicinity of the ones that are affected by disease, may appear fully normal in both diseases. Little is known about this heterogeneity in susceptibility to disease between pancreatic islets. This thesis examines the physiological and pathophysiological characteristics of islet subpopulations. Two subpopulations of islets were studied; one constituting highly vascularized islets with superior beta cell functionality, and one of low-oxygenated islets with low metabolic activity. The highly functional islets were found to be more susceptible to cellular stress both in vitro and in vivo, and developed more islet amyloid when metabolically challenged. Highly functional islets preferentially had a direct venous drainage, facilitating the distribution of islet hormones to the peripheral tissues. Further, these islets had an increased capacity for insulin secretion at low glucose levels, a response that was observed abolished in patients with recent onset type 1 diabetes. The second investigated islet subpopulation, low-oxygenated islets, was found to be an over time stable subpopulation of islets with low vascular density and beta cell proliferation. In summary, two subpopulations of islets can be identified in the pancreas based on dissimilarities in vascular support and blood flow. These subpopulations appear to have different physiological functions of importance for the maintenance of glucose homeostasis. However, they also seem to differ in vulnerability, and a preferential death of the highly functional islets may accelerate the progression of both type 1 and type 2 diabetes.

APA, Harvard, Vancouver, ISO, and other styles

Brown, James. "Regulation of uncoupling protein-2 expression, cell function and viability in pancreatic islets and beta-cells." Thesis, University of Wolverhampton, 2005. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.419783.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Mitchell, Ryan. "The effects of type 2 diabetes associated risk loci on pancreatic beta cell function." Thesis, Imperial College London, 2016. http://hdl.handle.net/10044/1/39040.

Full text

Abstract:

The pancreatic islets of Langerhans play a fundamental role in the stabilisation of blood glucose levels. Pancreatic islets are spherical structures composed of multiple cell types, with each individual cell type secreting a peptide hormone, such as insulin and glucagon, which regulates whole body glucose homoeostasis. Defective hormone secretion from islet cells is a hallmark of certain metabolic diseases, including type 2 diabetes mellitus (T2D). The most abundant islet cell type is the pancreatic β-cell, a specialised cell type that secretes the hypoglycaemic hormone insulin in response to raised glucose levels. Alterations in both β-cell mass and function are the causative factor for the development of T2D. Both genetic and environmental factors are known to underlie the decline in β-cell function typical of T2D. Specifically, genome wide association studies (GWAS) have identified over 100 genomic loci that are associated with T2D risk. Among these loci, variants that lie within/near ADCY5, SLC30A8 and PAX6 show associations with both T2D and abnormal glycaemic parameters typical of a diabetic phenotype. Therefore, the aims of this thesis were to understand how variants associated with T2D manifest at the level of the pancreatic islet. The expression of these genes was therefore manipulated through the generation of tissue-specific transgenic and knockout mice and by RNA interference in human tissue. Reducing the expression of ADCY5, encoding adenylate cyclase five, in human islet tissue reduced glucose-stimulated insulin secretion. This was accompanied by impairments in the metabolic and non-metabolic parameters that govern the secretory response of islets to glucose and other secretagogue. Deleting ZnT8, a β-cell zinc transporter and the gene product of the Slc30a8 gene, in the mouse β-cell significantly impaired the ability of these animals to mount effective responses to glucose. Interestingly, the reverse phenotype, i.e. improved glucose tolerance, was seen in animal models that overexpress ZnT8 in the β-cell. Finally, deletion of Pax6 in the adult mouse resulted in a drastic diabetic phenotype accompanied with changes in the cellular architecture of the islet and alterations in β-cell glucose signalling. Therefore, ADCY5, SLC30A8/ZnT8 and PAX6 gene variants likely negatively impact upon β-cell mass and function leading to a diabetic phenotype. Furthermore, these genes highlight distinct pathways, intrinsic to the pancreatic β-cell, which could be therapeutically targeted in the treatment of T2D.

APA, Harvard, Vancouver, ISO, and other styles

Tsang, Siu-wai. "Involvement of Pdzd2 in the regulation of pancreatic beta-cell functions." View the Table of Contents & Abstract, 2007. http://sunzi.lib.hku.hk/hkuto/record/B39716430.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Tsang, Siu-wai, and 曾少慧. "Involvement of Pdzd2 in the regulation of pancreatic beta-cell functions." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B39793746.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Karlsson, Ella. "Studies of neuropeptides in pancreatic beta cell function with special emphasis on islet amyloid polypeptide (IAPP)." Doctoral thesis, Uppsala University, Department of Medical Cell Biology, 2000. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-560.

Full text

Abstract:

The presence of protein amyloid in pancreas and its association to diabetes was first described 100 years ago in 1901, but was not identified as Islet Amyloid Polypeptide (IAPP) until 1986. The aim of the present work was to determine the role of the beta cell hormone, IAPP, in normal pancreatic islet physiology and during early disturbances of islet function.

Intra-islet peptides, i.e. chromogranin peptides and an extra-islet peptide, i.e. leptin, were studied to identify possible endogenous regulators of IAPP and insulin secretion. Chromogranin-B, but not chromogranin-A or pancreastatin, had the ability to inhibit islet IAPP and insulin release, suggesting that chromogranin-B may serve as an autocrine regulator of IAPP and insulin secretion.

Leptin had a more potent effect on IAPP secretion than on insulin secretion, which was dissociated from effects on islet glucose metabolism. Glucose oxidation rates were increased at physiological leptin concentrations, whereas higher leptin concentrations showed an inhibitory effect and chronically high leptin concentrations had no effect.

Female NOD mice were studied to investigate the release of IAPP in the progression to type 1 diabetes. The release of IAPP was lower than that of insulin from immune cell infiltrated islets, indicating preferential insulin release during the early course of the disease.

IAPP is expressed at an early embryonic stage. The effect of IAPP on cell proliferation in neonatal rat islets was studied in the search for a physiological role of IAPP. IAPP concentrations of (1-1000) nM stimulated neonatal islet cell proliferation mostly in beta cells and to a lesser extent in alpha cells. IAPP did not have any marked effect on the islet cell death frequency. These data indicate a role for IAPP as a potential regulator of beta cell proliferation in neonatal pancreatic islet.

It is concluded that IAPP may be involved in regulation of pancreatic beta cell function both in fetal and adult life.

APA, Harvard, Vancouver, ISO, and other styles

More sources

Books on the topic "Pancreatic beta cell function"

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

Find full text

APA, Harvard, Vancouver, ISO, and other styles

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

Find full text

APA, Harvard, Vancouver, ISO, and other styles

Picton, Sally Frances. Acute and long-term effects of nutrients, nutrient esters. drugs and cytotoxins on pancreatic beta cell function and integrity. [S.l: The Author], 2003.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

Swann, Louise Crystelle. Evaluation of the presence, function and possible mechanism of action of the extracellular calcium receptor in pancreatic Beta cells. [S.l: The author], 2004.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

Gallagher, S. Beta cells: Functions, pathology, and research. New York: Nova Science Publishers, 2011.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

Illani, Atwater, Rojas Eduardo 1936-, and Soria Bernat, eds. Biophysics of the pancreatic [beta]-cell. New York: Plenum Press, 1986.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

Illani, Atwater, Rojas Eduardo, and Soria Bernat, eds. Biophysics of the pancreatic (beta)-cell. New York: Plenum Press, 1987.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

Seino, Susumu, and Graeme I. Bell, eds. Pancreatic Beta Cell in Health and Disease. Tokyo: Springer Japan, 2008. http://dx.doi.org/10.1007/978-4-431-75452-7.

Full text

APA, Harvard, Vancouver, ISO, and other styles

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

Find full text

APA, Harvard, Vancouver, ISO, and other styles

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

Find full text

APA, Harvard, Vancouver, ISO, and other styles

More sources

Book chapters on the topic "Pancreatic beta cell function"

Dalle, Stéphane, Safia Costes, Gyslaine Bertrand, and Magalie A. Ravier. "Methods to Study Roles of β-Arrestins in the Regulation of Pancreatic β-Cell Function." In Beta-Arrestins, 345–64. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9158-7_22.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Guest, Paul C. "Pulse-Chase Biosynthetic Radiolabeling of Pancreatic Islets to Measure Beta Cell Function." In Methods in Molecular Biology, 331–41. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7614-0_22.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Galimberti, M., V. De Sanctis, G. Lucarelli, P. Polchi, E. Angelucci, D. Baronciani, C. Giardini, et al. "Pancreatic beta-Cell Function Before and After Bone Marrow Transplantation for Thalassemia." In Endocrine Disorders in Thalassemia, 69–72. Milano: Springer Milan, 1995. http://dx.doi.org/10.1007/978-88-470-2183-9_11.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Holz, George G., and Colin A. Leech. "Glucagon-Like Peptide-1 and the Glucose Competence Concept of Pancreatic Beta-Cell Function." In The Insulinotropic Gut Hormone Glucagon-Like Peptide-1, 171–93. Basel: KARGER, 1997. http://dx.doi.org/10.1159/000194735.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Amiranoff, B., M. Laburthe, and A. M. Lorinet. "The galanin receptor: Functional and molecular characterization in the pancreatic beta cell." In Galanin, 199–211. London: Macmillan Education UK, 1991. http://dx.doi.org/10.1007/978-1-349-12664-4_14.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Newsholme, Philip, Kevin N. Keane, Mina Elahy, and Vinicius Fernandes Cruzat. "l-Arginine, Pancreatic Beta Cell Function, and Diabetes: Mechanisms of Stimulated Insulin Release and Pathways of Metabolism." In L-Arginine in Clinical Nutrition, 85–94. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-26009-9_7.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Ruiz-Santiago, Sergio, José Rafael Godínez-Fernández, and Gerardo Jorge Félix-Martínez. "Simulating the Loss of $$\beta $$-cell Mass in a Human Pancreatic Islet: Structural and Functional Implications." In IFMBE Proceedings, 204–11. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-18256-3_22.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Lacy, Paul E. "Pancreatic Beta Cell." In Ciba Foundation Symposium - Aetiology of Diabetes Mellitus and its Complications (Colloquia on Endocrinology, Vol. 15), 75–88. Chichester, UK: John Wiley & Sons, Ltd., 2008. http://dx.doi.org/10.1002/9780470719350.ch5.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Velasco, Myrian, Carlos Larqué, Carlos Manlio Díaz-García, Carmen Sanchez-Soto, and Marcia Hiriart. "Rat Pancreatic Beta-Cell Culture." In Neurotrophic Factors, 261–73. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7571-6_20.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Hawthorne, Wayne John. "Beta Cell Therapies for Type 1 Diabetes." In Pancreatic Islet Biology, 285–322. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-45307-1_12.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Conference papers on the topic "Pancreatic beta cell function"

Lorza-Gil, E., F. Gerst, M. Beilmann, HU Häring, and S. Ullrich. "Improved beta-cell function of human pancreatic microislets." In Diabetes Kongress 2018 – 53. Jahrestagung der DDG. Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1641824.

Full text

APA, Harvard, Vancouver, ISO, and other styles

McVerry, Bryan J., Yoshio Watanabe, J. Crout, Euhan J. Lee, Baobo Zou, K. L. Skalka, Lia C. Romano, Adolfo Garcia-Ocana, Laura C. Alonso, and Christopher P. O'Donnell. "Endotoxemia Impairs Compensatory Pancreatic Beta Cell Secretory Function In Mildly Hyperglycemic Mice." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a4692.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Gu, Chenjuan, Min Li, and Qingyun Li. "Impaired Glucose Tolerance And Pancreatic Beta Cell Function In Patients With Obstructive Sleep Apnea." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a2165.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Müller, N., C. Wessel, K. Grieß, C. Polanski, and BF Belgardt. "The Tp53 network regulates pancreatic beta cell survival." In Diabetes Kongress 2018 – 53. Jahrestagung der DDG. Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1641770.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Kluth, O., H. Aga, P. Gottmann, M. Stadion, S. Scherneck, U. Krus, C. Ling, JG Gerdes, and A. Schürmann. "The role of cilia genes in pancreatic beta-cell proliferation." In Diabetes Kongress 2018 – 53. Jahrestagung der DDG. Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1641775.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Grieß, K., C. Polanski, D. Markgraf, E. Lammert, M. Roden, H. Stark, J. Brüning, and BF Belgardt. "The role of ceramide synthases in pancreatic beta cell demise." In Diabetes Kongress 2018 – 53. Jahrestagung der DDG. Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1641776.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Vinchhi, Bakul, Christophe Boss, Aurelie Hermant, Nicolas Bouche, Umberto de Marchi, and Catherine Dehollain. "Optical pancreatic beta cell based biosensor, applications and glucose monitoring." In 2019 IEEE SENSORS. IEEE, 2019. http://dx.doi.org/10.1109/sensors43011.2019.8956793.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Guevara-Flores, D. K., J. M. Munoz-Pacheco, E. Zambrano-Serrano, O. Felix-Beltran, and C. K. Volos. "PWL function-based model of a beta cell." In 2016 5th International Conference on Modern Circuits and Systems Technologies (MOCAST). IEEE, 2016. http://dx.doi.org/10.1109/mocast.2016.7495122.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Deep, Harkanwal, Pantelis Georgiou, and Christofer Toumazou. "A silicon pancreatic beta cell based on the phantom bursting model." In 2011 IEEE Biomedical Circuits and Systems Conference (BioCAS). IEEE, 2011. http://dx.doi.org/10.1109/biocas.2011.6107780.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Sliker, Bailee, Cassie Liu, Brittany Poelaert, Benjamin Goetz, and Joyce C. Solheim. "Abstract B028: Beta 2-microglobulin promotes human pancreatic cancer cell migration." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics; October 26-30, 2017; Philadelphia, PA. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1535-7163.targ-17-b028.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Reports on the topic "Pancreatic beta cell function"

Pernarowski, M., J. Kevorkian, and R. Miura. The Sherman-Rinzel-Keizer model for bursting electrical activity in the pancreatic. beta. -cell. Office of Scientific and Technical Information (OSTI), March 1990. http://dx.doi.org/10.2172/7165555.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Casey, Therese, Sameer J. Mabjeesh, Avi Shamay, and Karen Plaut. Photoperiod effects on milk production in goats: Are they mediated by the molecular clock in the mammary gland? United States Department of Agriculture, January 2014. http://dx.doi.org/10.32747/2014.7598164.bard.

Full text

Abstract:

US scientists, Dr. Theresa Casey and Dr. Karen Plaut, collaborated with Israeli scientists, Dr. SameerMabjeesh and Dr. AviShamay to conduct studies proposed in the BARD Project No. US-4715-14 Photoperiod effects on milk production in goats: Are they mediated by the molecular clock in the mammary gland over the last 3 years. CLOCK and BMAL1 are core components of the circadian clock and as heterodimers function as a transcription factor to drive circadian-rhythms of gene expression. Studies of CLOCK-mutant mice found impaired mammary development in late pregnancy was related to poor lactation performance post-partum. To gain a better understanding of role of clock in regulation of mammary development studies were conducted with the mammary epithelial cell line HC11. Decreasing CLOCK protein levels using shRNA resulted in increased mammary epithelial cell growth rate and impaired differentiation, with lower expression of differentiation markers including ad herens junction protein and fatty acid synthesis genes. When BMAL1 was knocked out using CRISPR-CAS mammary epithelial cells had greater growth rate, but reached stationary phase at a lower density, with FACS indicating cells were growing and dying at a faster rate. Beta-casein milk protein levels were significantly decreased in BMAL1 knockout cells. ChIP-seq analysis was conducted to identify BMAL1 target genes in mammary epithelial cells. Studies conducted in goats found that photoperiod duration and physiological state affected the dynamics of the mammary clock. Effects were likely independent of the photoperiod effects on prolactin levels. Interestingly, circadian rhythms of core body temperature, which functions as a key synchronizing cue sent out by the central clock in the hypothalamus, were profoundly affected by photoperiod and physiological state. Data support that the clock in the mammary gland regulates genes important to development of the gland and milk synthesis. We also found the clock in the mammary is responsive to changes in physiological state and photoperiod, and thus may serve as a mechanism to establish milk production levels in response to environmental cues.

APA, Harvard, Vancouver, ISO, and other styles

We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!