This review summarizes advances in our understanding of the structure and function of the ATP-sensitive potassium (KATP) channel of the pancreatic β-cell that have been made over the last 5 years. It discusses recent structural studies of the octameric KATP channel complex and studies of the regulation of KATP channel activity by nucleotides. It then considers the molecular mechanism by which gain-of-function mutations in the Kir6.2 subunit of the KATP channel reduce channel inhibition by ATP and thereby lead to neonatal diabetes, and how identification of these mutations has led to changes in therapy. Finally, it illustrates how mouse models of glucose intolerance or diabetes can provide fresh insight into β-cell function, using the C57BL/6J mouse, whose glucose intolerance arises from mutations in nicotinamide nucleotide transhydrogenase, as an example.
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Conference Article|
March 20 2006
KATP channels and insulin secretion: a key role in health and disease
F.M. Ashcroft
F.M. Ashcroft
1
1University Laboratory of Physiology, University of Oxford, Parks Road, Oxford OX1 3PT, U.K.
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Publisher: Portland Press Ltd
Received:
December 02 2005
Online ISSN: 1470-8752
Print ISSN: 0300-5127
© 2006 The Biochemical Society
2006
Biochem Soc Trans (2006) 34 (2): 243–246.
Article history
Received:
December 02 2005
Citation
F.M. Ashcroft; KATP channels and insulin secretion: a key role in health and disease. Biochem Soc Trans 1 April 2006; 34 (2): 243–246. doi: https://doi.org/10.1042/BST0340243
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