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Rui Gao Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, Churchill Hospital, Oxford, UK

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Samuel Acreman Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, Churchill Hospital, Oxford, UK
Department of Physiology, Institute of Neuroscience and Physiology, Metabolic Research Unit, University of Gothenburg, Göteborg, Sweden

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Jinfang Ma Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, Churchill Hospital, Oxford, UK

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Fernando Abdulkader Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, Brazil

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Anna Wendt Department of Clinical Sciences Malmö, Islet Cell Exocytosis, Lund University Diabetes Centre, Lund University, Malmö, Sweden

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Quan Zhang Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, Churchill Hospital, Oxford, UK
CNC - Center for Neuroscience and Cell Biology, CIBB - Centre for Innovative Biomedicine and Biotechnology, University of Coimbra, Coimbra, Portugal

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removed. This mixed effect on α-cell membrane potential was also observed in the presence of high glucose and hyperpolarisation could be reversed by blocking somatostatin receptors ( Zhang et al. 2013 ). As such, sulphonylureas could inhibit glucagon

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R Paul Robertson Nutrition Department of Internal Medicine, Division of Metabolism Endocrinology, University of Washington, Seattle, Washington, USA

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hormone somatostatin is required ( Greenbaum et al. 1991 ). These investigators compared inhibition of glucagon secretion during a stepped intravenous glucose infusion in dogs that had ventral lobe-specific beta cell deficiency, achieved by alloxan

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Yasminye D Pettway Department of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Nashville, Tennessee, USA

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Diane C Saunders Department of Medicine, Division of Diabetes, Endocrinology and Metabolism, Vanderbilt University Medical Center, Nashville, Tennessee, USA

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Marcela Brissova Department of Medicine, Division of Diabetes, Endocrinology and Metabolism, Vanderbilt University Medical Center, Nashville, Tennessee, USA

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, δ, γ, and ϵ cells (in order of abundance) defined by their production of the hormones insulin, glucagon, somatostatin, pancreatic polypeptide (PP), and ghrelin, respectively. Additionally, multiple non-endocrine cell types are present within the

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Elliott P Brooks Barbara Davis Center for Diabetes, University of Colorado Denver Anschutz Medical Campus, Aurora, Colorado, USA

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Lori Sussel Barbara Davis Center for Diabetes, University of Colorado Denver Anschutz Medical Campus, Aurora, Colorado, USA

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possessed significant overlap in dysregulated genes when compared to the Nkx2.2 -null transcriptome ( Churchill et al. 2017 ). Global knockout of NeuroD1 resulted in the complete loss of cells expressing glucagon, insulin, and somatostatin ( Naya et al

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Sarah L Armour Section for Cell Biology and Physiology, Department of Biology, University of Copenhagen, Denmark

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Jade E Stanley Department of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Nashville, Tennessee, USA

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James Cantley Division of Cellular and Systems Medicine, School of Medicine, University of Dundee, UK

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E Danielle Dean Department of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Nashville, Tennessee, USA
Division of Diabetes, Endocrinology, & Metabolism, Vanderbilt University Medical Center School of Medicine, Nashville, Tennessee, USA

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Jakob G Knudsen Section for Cell Biology and Physiology, Department of Biology, University of Copenhagen, Denmark

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. 2017 ). Finally, fatty acids have been suggested to inhibit somatostatin secretion ( Gromada et al. 2001 ), which would reduce somatostatin-mediated suppression of glucagon secretion from neighbouring alpha cells. However, this paracrine hypothesis

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