Insights into pancreatic β cell energy metabolism using rodent β cell models
Morten, Karl J.; Potter, Michelle; Badder, Luned; Sivathondan, Pamela; Dragovic, Rebecca; Neumann, Abigale; Gavin, James; Shrestha, Roshan; Reilly, Svetlana; Phadwal, Kanchan; Lodge, Tiffany A.; Borzychowsk, Angela; Cookson, Sharon; Mitchell, Corey; Morova, Alireza; Simon, Anna Katharina; Uusimaa, Johanna; Hynes, James; Poulton, Joanna (2019-09-25)
Morten KJ, Potter M, Badder L et al. Insights into pancreatic β cell energy metabolism using rodent β cell models [version 3; peer review: 2 approved, 1 not approved]. Wellcome Open Res 2019, 2:14 (https://doi.org/10.12688/wellcomeopenres.10535.3)
© 2019 Morten KJ et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
https://creativecommons.org/licenses/by/4.0/
https://urn.fi/URN:NBN:fi-fe202003259266
Tiivistelmä
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.
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