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Reduced somatostatin signalling leads to hypersecretion of glucagon in mice fed a high-fat diet

Authors
  • Kellard, Joely A.1
  • Rorsman, Nils J.G.1
  • Hill, Thomas G.1
  • Armour, Sarah L.2
  • van de Bunt, Martijn3
  • Rorsman, Patrik1, 4, 5
  • Knudsen, Jakob G.1, 2
  • Briant, Linford J.B.1, 6
  • 1 Oxford Centre for Diabetes, Endocrinology and Metabolism, Radcliffe Department of Medicine, Churchill Hospital, Oxford OX3 7LE, UK
  • 2 Section for Cell Biology and Physiology, Department of Biology, University of Copenhagen, Denmark
  • 3 Department of Bioinformatics and Data Mining, Novo Nordisk A/S, Maaloev, Denmark
  • 4 Department of Neuroscience and Physiology, University of Göteborg, Box 430, SE40530 Göteborg, Sweden
  • 5 Oxford National Institute for Health Research, Biomedical Research Centre, Churchill Hospital, Oxford OX3 7LE, UK
  • 6 Department of Computer Science, University of Oxford, Oxford OX1 3QD, UK
Type
Published Article
Journal
Molecular Metabolism
Publisher
Elsevier BV
Publication Date
May 21, 2020
Volume
40
Identifiers
DOI: 10.1016/j.molmet.2020.101021
PMID: 32446876
PMCID: PMC7322681
Source
PubMed Central
Keywords
License
Unknown

Abstract

• HFD feeding causes hyperglucagonaemia in vivo . • Glucagon is inadequately suppressed by glucose in HFD-fed mice. • Alpha-cell [Ca2+]i oscillations and glucagon output are elevated ex vivo in response to HFD feeding. • SST secretion from HFD islets is reduced. • Alpha-cells from HFD-fed mice become ‘resistant’ to SST.

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