SYMPOSIUM REVIEW: The role of the KATP channel in glucose homeostasis in health and disease: more than meets the islet

Authors

  • James S. McTaggart,

    1. Henry Wellcome Centre for Gene Function, Department of Physiology, Anatomy and Genetics, and OXION Centre for Ion Channel Studies, Sherrington Building, Parks Road, Oxford OX1 3PT, UK
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  • Rebecca H. Clark,

    1. Henry Wellcome Centre for Gene Function, Department of Physiology, Anatomy and Genetics, and OXION Centre for Ion Channel Studies, Sherrington Building, Parks Road, Oxford OX1 3PT, UK
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  • Frances M. Ashcroft

    1. Henry Wellcome Centre for Gene Function, Department of Physiology, Anatomy and Genetics, and OXION Centre for Ion Channel Studies, Sherrington Building, Parks Road, Oxford OX1 3PT, UK
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  • This review was presented at The Peter Stanfield Festschrift, which took place at the Warwick Medical School, University of Warwick, Coventry, UK on 12 April 2010.

Corresponding author F. M. Ashcroft: Henry Wellcome Centre for Gene Function, Department of Physiology, Anatomy and Genetics, and OXION Centre for Ion Channel Studies, Sherrington Building, Parks Road, Oxford OX1 3PT, UK.  Email: frances.ashcroft@dpag.ox.ac.uk

Abstract

ATP-sensitive potassium (KATP) channels are critical for the maintenance of glucose homeostasis. They are essential for glucose-stimulated insulin secretion from pancreatic β-cells, contribute to the mechanisms by which hypoglycaemia stimulates glucagon release from pancreatic α-cells, and are involved in glucose uptake into skeletal muscle, glucose production and release from the liver, and feeding behaviour. Not surprisingly, loss- or gain-of-function mutations in KATP channel genes have profound effects, giving rise to congenital hyperinsulinaemia and neonatal diabetes respectively. This symposium review focuses on our current understanding of the role of the KATP channel in glucose homeostasis in health and disease.

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