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Sarah L Armour
Sarah L Armour
Section for Cell Biology and Physiology, Department of Biology, University of Copenhagen, Denmark
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Jade E Stanley
Jade E Stanley
Department of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Nashville, Tennessee, USA
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James Cantley
James Cantley
Division of Cellular and Systems Medicine, School of Medicine, University of Dundee, UK
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E Danielle Dean
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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Division of Diabetes, Endocrinology, & Metabolism, Vanderbilt University Medical Center School of Medicine, Nashville, Tennessee, USA
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Jakob G Knudsen
Jakob G Knudsen
Section for Cell Biology and Physiology, Department of Biology, University of Copenhagen, Denmark
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glucagon secretion is stimulated by long-chain fatty acids ( Olofsson et al. 2004 , Kristinsson et al. 2017 , Bollheimer et al. 2004 ) and amino acids ( Rocha et al. 1972 ). This seems logical as these substrates are released from adipose tissue
Jasleen Kaur
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
Elizabeth R Seaquist
Division of Endocrinology and Diabetes, Department of Medicine, University of Minnesota Medical School, Minneapolis, Minnesota, USA
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been shown to antagonize insulin’s effects on lipolysis in white adipose tissue and liver leading to the mobilization of fat stores ( Habegger et al. 2013 ). In addition, glucagon was noted to stimulate beta-oxidation of fatty acids, inhibit
Rui Gao
Rui Gao
Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, Churchill Hospital, Oxford, UK
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Samuel Acreman
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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Department of Physiology, Institute of Neuroscience and Physiology, Metabolic Research Unit, University of Gothenburg, Göteborg, Sweden
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Jinfang Ma
Jinfang Ma
Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, Churchill Hospital, Oxford, UK
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Fernando Abdulkader
Fernando Abdulkader
Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, Brazil
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Anna Wendt
Anna Wendt
Department of Clinical Sciences Malmö, Islet Cell Exocytosis, Lund University Diabetes Centre, Lund University, Malmö, Sweden
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Quan Zhang
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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CNC - Center for Neuroscience and Cell Biology, CIBB - Centre for Innovative Biomedicine and Biotechnology, University of Coimbra, Coimbra, Portugal
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can transfer phosphate to ADP to produce ATP, as it does in β-cells ( Krippeit-Drews et al. 2003 ). Moreover, it was proposed that α-cells can generate ATP via fatty acid oxidation ( Briant et al. 2018 ). In mice with α-cells lacking CPT1, an
