1. Insights into pancreatic β cell energy metabolism using rodent β cell models
- Author
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Corey Mitchell, Kanchan Phadwal, Svetlana Reilly, Johanna Uusimaa, R Dragovic, Pamela Sivathondan, Joanna Poulton, Angela M. Borzychowski, Abigale Neumann, James Gavin, Tiffany A. Lodge, Sharon Cookson, Alireza Morovat, Anna Katharina Simon, Michelle Potter, Karl J. Morten, James Hynes, Luned Badder, and Roshan Shrestha
- Subjects
0301 basic medicine ,Cell type ,insulin secretion ,Cell ,oxidative phosphorylation ,Physiology ,Medicine (miscellaneous) ,beta-cell ,Oxidative phosphorylation ,Mitochondrion ,General Biochemistry, Genetics and Molecular Biology ,03 medical and health sciences ,0302 clinical medicine ,medicine ,030212 general & internal medicine ,Pancreas ,030304 developmental biology ,chemistry.chemical_classification ,reactive oxygen species ,Reactive oxygen species ,0303 health sciences ,business.industry ,Autophagy ,Articles ,Cell biology ,mitochondria ,030104 developmental biology ,medicine.anatomical_structure ,chemistry ,Cell culture ,superoxide ,Beta cell ,business ,030217 neurology & neurosurgery ,Research Article - 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.
- Published
- 2019