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Journal article

The KCNJ11-E23K gene variant hastens diabetes progression by impairing glucose-induced insulin secretion

Abstract:
The ATP-sensitive K+ (KATP) channel controls blood glucose levels by coupling glucose metabolism to insulin secretion in pancreatic β-cells. E23K, a common polymorphism in the pore-forming KATP channel subunit (KCNJ11) gene, has been linked to increased risk of type 2 diabetes. Understanding the risk-allele-specific pathogenesis has the potential to improve personalized diabetes treatment, but the underlying mechanism has remained elusive. Using a genetically engineered mouse model, we now show that the K23 variant impairs glucose-induced insulin secretion and increases diabetes risk when combined with a high-fat diet (HFD) and obesity. KATP-channels in β-cells with two K23 risk alleles (KK) showed decreased ATP inhibition, and the threshold for glucose-stimulated insulin secretion from KK islets was increased. Consequently, the insulin response to glucose and glycemic control was impaired in KK mice fed a standard diet. On an HFD, the effects of the KK genotype were exacerbated, accelerating diet-induced diabetes progression and causing β-cell failure. We conclude that the K23 variant increases diabetes risk by impairing insulin secretion at threshold glucose levels, thus accelerating loss of β-cell function in the early stages of diabetes progression.
Publication status:
Published
Peer review status:
Peer reviewed

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Publisher copy:
10.2337/db20-0691

Authors


More by this author
Institution:
University of Oxford
Division:
MSD
Department:
Physiology Anatomy & Genetics
Role:
Author
ORCID:
0000-0001-5096-4922
More by this author
Institution:
University of Oxford
Division:
MSD
Department:
Physiology Anatomy & Genetics
Role:
Author
ORCID:
0000-0003-3097-9240
More by this author
Institution:
University of Oxford
Division:
MSD
Department:
RDM
Sub department:
OCDEM
Role:
Author
ORCID:
0000-0002-4637-3879
More by this author
Institution:
University of Oxford
Division:
MPLS
Department:
Physics
Sub department:
Condensed Matter Physics
Role:
Author
ORCID:
0000-0001-6097-3646


More from this funder
Funder identifier:
https://ror.org/03x94j517
Grant:
MR/T002107/1
More from this funder
Funder identifier:
https://ror.org/0472cxd90
Grant:
322620
More from this funder
Funder identifier:
https://ror.org/00cwqg982
Grant:
BB/R017220/1
BB/S008608/1


Publisher:
American Diabetes Association
Journal:
Diabetes More from this journal
Volume:
70
Issue:
5
Pages:
1145-1156
Place of publication:
United States
Publication date:
2021-02-10
Acceptance date:
2021-02-05
DOI:
EISSN:
1939-327X
ISSN:
0012-1797
Pmid:
33568422


Language:
English
Pubs id:
1161434
Local pid:
pubs:1161434
Deposit date:
2024-09-05

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