title: Mitochondrial dysfunction in pancreatic β cells.
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.
authors: Department of Cell Physiology and Metabolism, University of Geneva Medical Centre, 1211 Geneva 4, Switzerland.
authors: Sachin
authors: S
authors: Supale
authors: Ning
authors: N
authors: Li
authors: Thierry
authors: T
authors: Brun
authors: Pierre
authors: P
authors: Maechler
mesh_terms: D000818:Animals; D006801:Humans; D007328:Insulin / Q000378:metabolism*; D000078790:Insulin Secretion; D050417:Insulin-Secreting Cells / Q000378:metabolism*; D008928:Mitochondria / Q000378:metabolism*; D017382:Reactive Oxygen Species / Q000378:metabolism
chemical_list: D007328:Insulin; D017382:Reactive Oxygen Species