Mouse models of β-cell K channel dysfunction
ATP-sensitive K (K) channels in pancreatic β-cells couple glucose metabolism to insulin secretion. Reduced K channel activity produces excessive insulin release and hyperinsulinism whereas increased K channel activity leads to lower insulin secretion and diabetes. Paradoxically, mice with genetic de...
| Main Authors: | , |
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| Format: | Journal article |
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2013
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| _version_ | 1826305080519819264 |
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| author | Brereton, M Ashcroft, F |
| author_facet | Brereton, M Ashcroft, F |
| author_sort | Brereton, M |
| collection | OXFORD |
| description | ATP-sensitive K (K) channels in pancreatic β-cells couple glucose metabolism to insulin secretion. Reduced K channel activity produces excessive insulin release and hyperinsulinism whereas increased K channel activity leads to lower insulin secretion and diabetes. Paradoxically, mice with genetic deletion of K channels, or loss-of-function mutations, are only transiently hypoglycaemic during the neonatal period and often display reduced glucose-stimulated insulin secretion subsequently. Mice with K channel gain-of-function mutations are hyperglycaemic and have impaired glucose-stimulated insulin secretion, a phenotype that accurately mimics human diabetes. This review discusses how mice expressing altered K channels have provided valuable insight into β-cell function. © 2013 Elsevier Ltd. All rights reserved. |
| first_indexed | 2024-03-07T06:27:26Z |
| format | Journal article |
| id | oxford-uuid:f4cbae0c-0102-4904-bee1-beecde520cb5 |
| institution | University of Oxford |
| last_indexed | 2024-03-07T06:27:26Z |
| publishDate | 2013 |
| record_format | dspace |
| spelling | oxford-uuid:f4cbae0c-0102-4904-bee1-beecde520cb52022-03-27T12:22:25ZMouse models of β-cell K channel dysfunctionJournal articlehttp://purl.org/coar/resource_type/c_dcae04bcuuid:f4cbae0c-0102-4904-bee1-beecde520cb5Symplectic Elements at Oxford2013Brereton, MAshcroft, FATP-sensitive K (K) channels in pancreatic β-cells couple glucose metabolism to insulin secretion. Reduced K channel activity produces excessive insulin release and hyperinsulinism whereas increased K channel activity leads to lower insulin secretion and diabetes. Paradoxically, mice with genetic deletion of K channels, or loss-of-function mutations, are only transiently hypoglycaemic during the neonatal period and often display reduced glucose-stimulated insulin secretion subsequently. Mice with K channel gain-of-function mutations are hyperglycaemic and have impaired glucose-stimulated insulin secretion, a phenotype that accurately mimics human diabetes. This review discusses how mice expressing altered K channels have provided valuable insight into β-cell function. © 2013 Elsevier Ltd. All rights reserved. |
| spellingShingle | Brereton, M Ashcroft, F Mouse models of β-cell K channel dysfunction |
| title | Mouse models of β-cell K channel dysfunction |
| title_full | Mouse models of β-cell K channel dysfunction |
| title_fullStr | Mouse models of β-cell K channel dysfunction |
| title_full_unstemmed | Mouse models of β-cell K channel dysfunction |
| title_short | Mouse models of β-cell K channel dysfunction |
| title_sort | mouse models of β cell k channel dysfunction |
| work_keys_str_mv | AT breretonm mousemodelsofbcellkchanneldysfunction AT ashcroftf mousemodelsofbcellkchanneldysfunction |