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

This is the authors' abstract. We don't add key points for this paper.

<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>