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Version 3. Wellcome Open Res. 2019 Sep 25 [revised 2019 Sep 25];2:14. doi: 10.12688/wellcomeopenres.10535.3. eCollection 2017.

Insights into pancreatic β cell energy metabolism using rodent β cell models.

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Nuffield Department of Obstetrics & Gynaecology, The Women's Centre, University of Oxford, John Radcliffe Hospital, Oxford, UK.
Department of Cardiovascular Medicine, John Radcliffe Hospital, Oxford, UK.
BRC Translational Immunology Lab, NIHR, Nuffield Department of Medicine, University of Oxford, John Radcliffe Hospital, Oxford, UK.
Institute of Cellular Medicine, Haematological Sciences, Medical School, Newcastle University, Newcastle upon Tyne, UK.
Clinical Biochemistry, John Radcliffe Hospital, Oxford, UK.
Kennedy Institute of Rheumatology, University of Oxford, Oxford, UK.
Department of Paediatrics, University of Oulu, Oulu, Finland.
Luxcel BioSciences Ltd, BioInnovation Centre, University College Cork, Cork, Ireland.


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.


beta-cell; insulin secretion; mitochondria; oxidative phosphorylation; reactive oxygen species; superoxide

Conflict of interest statement

Competing interests: JH is an employee of Luxcel Biosciences. None of the other authors have competing interests.

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