The sensitivity of pancreatic beta-cells to mitochondrial injuries triggered by lipotoxicity and oxidative stress.
Pancreatic beta-cells are essential for the maintenance of glucose homoeostasis, and dysfunction of these insulin-secreting cells results in the development of diabetes. In the course of events leading from obesity to Type 2 diabetes, several mechanisms are currently envisaged. Among them, lipids and oxidative stress are considered as toxic candidates for the beta-cell. The cellular link between fatty acids and ROS (reactive oxygen species) is essentially the mitochondrion, a key organelle for the control of insulin secretion. Mitochondria are the main source of ROS and are also the primary target of oxidative attacks. The present review presents the current knowledge of lipotoxicity related to oxidative stress in the context of mitochondrial function in the beta-cell.
Li
Ning
N
Department of Cell Physiology and Metabolism, Faculty of Medicine, University of Geneva, rue Michel-Servet 1, CH-1211 Geneva 4, Switzerland.
Frigerio
Francesca
F
Maechler
Pierre
P
D000818:Animals; D004272:DNA, Mitochondrial / Q000378:metabolism; D003920:Diabetes Mellitus / Q000378:metabolism / Q000503:physiopathology; D006801:Humans; D050417:Insulin-Secreting Cells / Q000166:cytology / Q000378:metabolism; D008055:Lipids / Q000633:toxicity*; D008928:Mitochondria / Q000235:genetics / Q000378:metabolism / Q000473:pathology*; D018384:Oxidative Stress; D017382:Reactive Oxygen Species / Q000378:metabolism
D004272:DNA, Mitochondrial; D008055:Lipids; D017382:Reactive Oxygen Species