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<ns4:p><ns4:italic><ns4:bold>Background</ns4:bold>: </ns4:italic>Mitochondrial diabetes is primarily caused by β-cell failure, a cell type whose unique properties are important in pathogenesis.</ns4:p><ns4:p> <ns4:italic><ns4:bold>Methods</ns4:bold>: </ns4:italic>By reducing glucose, we induced energetic stress in two rodent β-cell models to assess effects on cellular function.</ns4:p><ns4:p> <ns4:italic><ns4:bold>Results</ns4:bold>: </ns4:italic>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.</ns4:p><ns4:p> <ns4:italic><ns4:bold>Conclusions</ns4:bold>: </ns4:italic>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.</ns4:p>

Original publication

DOI

10.12688/wellcomeopenres.10535.2

Type

Journal article

Journal

Wellcome Open Research

Publisher

F1000 ( Faculty of 1000 Ltd)

Publication Date

11/10/2017

Volume

2

Pages

14 - 14