UNIGE document Scientific Article - Review
previous document  unige:28014  next document
add to browser collection

Mitochondrial dysfunction in pancreatic β cells

Published in Trends in endocrinology and metabolism. 2012, vol. 23, no. 9, p. 477-87
Abstract 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.
Keywords AnimalsHumansInsulin/metabolism/secretionInsulin-Secreting Cells/metabolism/secretionMitochondria/metabolismReactive Oxygen Species/metabolism
PMID: 22766318
Full text
Article (Published version) (845 Kb) - document accessible for UNIGE members only Limited access to UNIGE
Research group Mitochondries et métabolisme énergétique (671)
Swiss National Science Foundation: 310030B_135704
(ISO format)
SUPALE, Sachin et al. Mitochondrial dysfunction in pancreatic β cells. In: Trends in endocrinology and metabolism, 2012, vol. 23, n° 9, p. 477-87. doi: 10.1016/j.tem.2012.06.002 https://archive-ouverte.unige.ch/unige:28014

482 hits



Deposited on : 2013-05-28

Export document
Format :
Citation style :