Morten KJ., Potter M., Badder L., Sivathondan P., Dragovic R., Neumann A., Gavin J., Shrestha R., Reilly S., Phadwal K., Lodge TA., Borzychowski A., Cookson S., Mitchell C., Morovat A., Simon AK., Uusimaa J., Hynes J., Poulton J.

<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>

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

Morten KJ., Potter M., Badder L., Sivathondan P., Dragovic R., Neumann A., Gavin J., Shrestha R., Reilly S., Phadwal K., Lodge TA., Borzychowski A., Cookson S., Mitchell C., Morovat A., Simon AK., Uusimaa J., Hynes J., Poulton J.

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