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

Abstract

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.