Published in
F1000Research, Wellcome Open Research, (2), p. 14, 2017
DOI: 10.12688/wellcomeopenres.10535.2
F1000Research, Wellcome Open Research, (2), p. 14, 2019
DOI: 10.12688/wellcomeopenres.10535.3
F1000Research, Wellcome Open Research, (2), p. 14, 2017
DOI: 10.12688/wellcomeopenres.10535.1
Links
- ORCID
- F1000Research | PDF
- ORCID
- F1000Research | PDF
- F1000Research | PDF
- [dx.doi.org] | PDF
- [dx.doi.org] | PDF
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Insights into pancreatic β cell energy metabolism using rodent β cell models
,
Abigale Neumann,
James Gavin,
Roshan Shrestha,
Svetlana Reilly ,
Tiffany A. Lodge ,
Kanchan Phadwal,
Corey Mitchell,
Angela Borzychowski
and other authors.
Full text: Download
Abstract
Background: Mitochondrial diabetes is primarily caused by β-cell failure, a cell type whose unique properties are important in pathogenesis. Methods: By reducing glucose, we induced energetic stress in two rodent β-cell models to assess effects on cellular function. Results: Culturing rat insulin-secreting INS-1 cells in low glucose conditions caused a rapid reduction in whole cell respiration, associated with elevated mitochondrial reactive oxygen species production, and an altered glucose-stimulated insulin secretion profile. Prolonged exposure to reduced glucose directly impaired mitochondrial function and reduced autophagy. Conclusions: Insulinoma cell lines have a very different bioenergetic profile to many other cell lines and provide a useful model of mechanisms affecting β-cell mitochondrial function.