Scientific article

Mitochondrial dysfunction in pancreatic β cells

Published inTrends in endocrinology and metabolism, vol. 23, no. 9, p. 477-487
Publication date2012

In pancreatic β cells, mitochondria play a central role in coupling glucose metabolism to insulin exocytosis, thereby ensuring strict control of glucose-stimulated insulin secretion. Defects in mitochondrial function impair this metabolic coupling, and ultimately promote apoptosis and β cell death. Various factors have been identified that may contribute to mitochondrial dysfunction. In this review we address the emerging concept of complex links between these factors. We also discuss the role of the mitochondrial genome and mutations associated with diabetes, the effect of oxidative stress and reactive oxygen species, the sensitivity of mitochondria to lipotoxicity, and the adaptive dynamics of mitochondrial morphology. Better comprehension of the molecular mechanisms contributing to mitochondrial dysfunction will help drive the development of effective therapeutic approaches.

  • Animals
  • Humans
  • Insulin/metabolism/secretion
  • Insulin-Secreting Cells/metabolism/secretion
  • Mitochondria/metabolism
  • Reactive Oxygen Species/metabolism
Citation (ISO format)
SUPALE, Sachin et al. Mitochondrial dysfunction in pancreatic β cells. In: Trends in endocrinology and metabolism, 2012, vol. 23, n° 9, p. 477–487. doi: 10.1016/j.tem.2012.06.002
Main files (1)
Article (Published version)
ISSN of the journal1043-2760

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