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Nils Wierup, Frank Sundler and R Scott Heller

Introduction The pancreatic islets were first described by Langerhans (1869) . He noticed clusters of cells, 100–200 μm in diameter, that were interspersed in the exocrine tissue. He named these clusters Zellhaufen. Langerhans also described that

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D Gill, K J Brocklehurst, H W G Brown and D M Smith

, Coghlan & Leighton 2008 ). Several studies have demonstrated that GKAs increase GSIS from β-cells ( Coghlan & Leighton 2008 ), but the consequences of long-term direct action of GKAs on the islet have only recently begun to be investigated. Of potential

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Daniela Nasteska and David J Hodson

subpopulations ( Gutierrez et al . 2017 ). This ‘heterogeneity’ or ‘diversity’ is driven partly by the organisation of beta cells into islet microorgans ( Benninger & Piston 2014 ) and is unlikely to be properly appreciated by current models of beta cell failure

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Riccarda Granata, Marco Volante, Fabio Settanni, Carlotta Gauna, Corrado Ghé, Marta Annunziata, Barbara Deidda, Iacopo Gesmundo, Thierry Abribat, Aart-Jan van der Lely, Giampiero Muccioli, Ezio Ghigo and Mauro Papotti

has been detected in other central and peripheral tissues ( Kojima et al . 1999 , van der Lely et al . 2004 ). In the endocrine pancreas, it localizes to glucagon-producing α-cells and to the ghrelin-producing ε-cells, suggesting a role in islet

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Talitha van der Meulen and Mark O Huising

Introduction The pancreatic islets consist of several endocrine cell types including insulin-producing β cells, glucagon-producing α cells, somatostatin-producing δ cells, pancreatic polypeptide-producing PP cells, and ghrelin-producing ϵ cells. The

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H Wang, Y Horikawa, L Jin, T Narita, S Yamada, N Shihara, K Tatemoto, M Muramatsu, T Mune and J Takeda

Introduction Pancreatic islets play the critical role in the regulation of blood glucose by secreting hormones from endocrine cells that differentiate from common progenitor cells during fetal development (postnatal origin of β-cell

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Thierry Brun and Benoit R Gauthier

Introduction: diabetes, obesity and pancreatic islet plasticity Plasma glucose levels are regulated by the action of insulin, a hormone that is produced and secreted by the pancreatic islet β-cells in response to nutrients. Diabetes mellitus, which

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Jianling Xie, Norhan M El Sayed, Cheng Qi, Xuechan Zhao, Claire E Moore and Terence P Herbert

investigate how exendin-4 stimulates β-cell proliferation. To these ends, we have demonstrated, in rat islets of Langerhans, that in the presence of glucose, exendin-4 acutely activates mTORC1 via the autocrine/paracrine activation of the IGF1R, whereas EGFR

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NM Morton, V Emilsson, P de Groot, AL Pallett and MA Cawthorne

Leptin is a cytokine secreted from adipose tissue at a rate commensurate with the size of the body's fat stores. In addition to its anorectic and thermogenic central actions, leptin is known to act on peripheral tissues, including the pancreatic beta-cell where it inhibits insulin secretion and reduces insulin transcript levels. However, the role of leptin signalling through its full-length receptor, OB-Rb, in the beta-cell remains unclear. In the present study, we show that leptin activates a signal transducer and activator of transcription (STAT)3 signalling mechanism in pancreatic islets and in a rat model of the pancreatic beta-cell, RINm5F. Leptin induced DNA binding to a STAT consensus oligonucleotide and resulted in transcriptional activation from STAT reporter constructs in a manner consistent with STAT3 activation. Western blot analysis confirmed activation of STAT3 in RINm5F and isolated rat islets. Conditions that mimic increased metabolic activity resulted in attenuation of leptin-mediated STAT DNA binding but had no significant effect on STAT3 tyrosine phosphorylation in RINm5F cells. In addition, leptin activated the mitogen activated protein (MAP) kinase pathway in RINm5F cells. The present study provides a framework for OB-Rb signalling mechanisms in the programming of the beta-cell by leptin and suggests that increased metabolic activity may modulate this function.

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M. Welsh, D. L. Eizirik and E. Strandell

ABSTRACT

To elucidate the role of thermal stress on the function of pancreatic β cells, isolated mouse pancreatic islets were incubated for 30 min at 42°C. This resulted in decreased glucose-stimulated insulin secretion, inhibited total protein and pro-insulin synthesis and the induction of heat-shock proteins with molecular weights of 64 and 88 kDa. Six days later, the islets exposed to heat shock showed a lower DNA content, indicating islet cell death. However, the insulin secretory response and rates of oxygen consumption in the presence of glucose were normal. It is suggested that the induction of heat-shock proteins does not permanently impair β-cell function, but rather protects these cells from lasting damage.