University of Oulu

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 (

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

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Author: Morten, Karl J.1; Potter, Michelle1; Badder, Luned1;
Organizations: 1Nuffield Department of Obstetrics & Gynaecology, The Women’s Centre, University of Oxford, John Radcliffe Hospital, Oxford, UK
2Department of Cardiovascular Medicine, John Radcliffe Hospital, Oxford, UK
3BRC Translational Immunology Lab, NIHR, Nuffield Department of Medicine, University of Oxford, John Radcliffe Hospital, Oxford, UK
4Institute of Cellular Medicine, Haematological Sciences, Medical School, Newcastle University, Newcastle upon Tyne, UK
5Clinical Biochemistry, John Radcliffe Hospital, Oxford, UK
6Kennedy Institute of Rheumatology, University of Oxford, Oxford, UK
7Department of Paediatrics, University of Oulu, Oulu, Finland
8Luxcel BioSciences Ltd, BioInnovation Centre, University College Cork, Cork, Ireland
Format: article
Version: published version
Access: open
Online Access: PDF Full Text (PDF, 1.5 MB)
Persistent link:
Language: English
Published: F1000 Research, 2019
Publish Date: 2020-03-25


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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Series: Wellcome open research
ISSN: 2398-502X
ISSN-E: 2398-502X
ISSN-L: 2398-502X
Volume: 2
Article number: 14
DOI: 10.12688/wellcomeopenres.10535.3
Type of Publication: A1 Journal article – refereed
Field of Science: 3121 General medicine, internal medicine and other clinical medicine
Funding: This work was supported by the Wellcome Trust [094868], [078535]; The Medical Research Council [74993]; and the Finnish Paediatric Association. PS, AN, CM, LB and RS were supported by a Luxcel Biosciences studentship. MP was supported by Williams fund. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
Copyright information: © 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.