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Background: Mitochondrial diabetes is primarily caused by β-cell failure, but there are gaps in our understanding of 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 provide a useful model of mechanisms affecting β-cell mitochondrial function or studying mitochondrial associated drug toxicity.

Original publication

DOI

10.12688/wellcomeopenres.10535.1

Type

Journal article

Journal

Wellcome open research

Publication Date

01/2017

Volume

2

Addresses

Nuffield Department of Obstetrics & Gynaecology, The Women's Centre, University of Oxford, John Radcliffe Hospital, Oxford, UK.