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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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possible that α-cells develop insulin resistance, including blunted insulin-stimulated Akt phosphorylation, during chronic exposure to high glucose and insulin ( Tsuchiyama et al. 2007 ). Defective glucagon regulation can be caused by impaired paracrine

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Jasleen Kaur Division of Endocrinology and Diabetes, Department of Medicine, University of Minnesota Medical School, Minneapolis, Minnesota, USA

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Elizabeth R Seaquist Division of Endocrinology and Diabetes, Department of Medicine, University of Minnesota Medical School, Minneapolis, Minnesota, USA

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Torekov SS 2018 Evidence of a liver-alpha cell axis in humans: hepatic insulin resistance attenuates relationship between fasting plasma glucagon and glucagonotropic amino acids . Diabetologia 61 671 – 680 . ( https://doi.org/10.1007/s00125

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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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Pregnancy represents a scenario of increased metabolic demand, where placenta-derived hormones promote peripheral insulin resistance to meet the increased energy needs of the developing fetus ( Catalano et al. 1993 ). Pregnancy in humans is associated with

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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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Introduction Glucagon is secreted from alpha cells located in pancreatic islets of Langerhans and is an important counter-regulatory hormone to insulin, acting to increase blood glucose. Indeed, it was this physiological hyperglycaemic effect

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