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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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( Sugden et al. 2001 ) as well as other tissues ( Pilegaard et al. 2003 , Wu et al. 1998 ) and plays a crucial role in the switch between glucose and fatty acid oxidation ( Hue & Taegtmeyer 2009 ). The high expression of PDK4 suggests that a limited

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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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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

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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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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

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