Journal article
Disruption of beta cell acetyl-CoA carboxylase-1 in mice impairs insulin secretion and beta cell mass
- Abstract:
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Aims/hypothesis Pancreatic beta cells secrete insulin to maintain glucose homeostasis, and beta cell failure is a hallmark of type 2 diabetes. Glucose triggers insulin secretion in beta cells via oxidative mitochondrial pathways. However, it also feeds mitochondrial anaplerotic pathways, driving citrate export and cytosolic malonyl-CoA production by the acetyl-CoA carboxylase 1 (ACC1) enzyme. This pathway has been proposed as an alternative glucose-sensing mechanism, supporte... Expand abstract
- Publication status:
- Published
- Peer review status:
- Peer reviewed
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- Files:
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(Version of record, pdf, 1.2MB)
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- Publisher copy:
- 10.1007/s00125-018-4743-7
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Authors
Funding
+ Diabetes Australia Research Trust Viertel Charitable Foundation Fellowship
More from this funder
Funding agency for:
Cantley, J
Grant:
RD Lawrence Fellowship
+ Wellcome Trust
More from this funder
Funding agency for:
Nemes, N
Grant:
Biomedical Vacation Scholarship
Bibliographic Details
- Publisher:
- Springer Verlag Publisher's website
- Journal:
- Diabetologia Journal website
- Volume:
- 62
- Issue:
- 1
- Pages:
- 99–111
- Publication date:
- 2018-10-17
- Acceptance date:
- 2018-08-22
- DOI:
- EISSN:
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1432-0428
- ISSN:
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0012-186X
- Pmid:
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30334081
- Source identifiers:
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929823
Item Description
- Language:
- English
- Keywords:
- Pubs id:
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pubs:929823
- UUID:
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uuid:15d65a93-d975-43c5-a962-f7b62d10c17b
- Local pid:
- pubs:929823
- Deposit date:
- 2018-11-20
Terms of use
- Copyright holder:
- Cantley et al
- Copyright date:
- 2018
- Notes:
- © The Author(s) 2018. This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.
- Licence:
- CC Attribution (CC BY)
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