Mitochondrial hormesis in pancreatic β cells: does uncoupling protein 2 play a role?

Article Article scientifique Article Mitochondrial hormesis in pancreatic β cells: does uncoupling protein 2 play a role? eng 2012 author Li Ning 640798 author Stojanovski Suzana 557283 author Maechler Pierre 0000-0002-2005-1433 76515 740849 10.1155/2012/740849 23029600 1942-0994 In pancreatic β cells, mitochondrial metabolism translates glucose sensing into signals regulating insulin secretion. Chronic exposure of β cells to excessive nutrients, namely, glucolipotoxicity, impairs β-cell function. This is associated with elevated ROS production from overstimulated mitochondria. Mitochondria are not only the major source of cellular ROS, they are also the primary target of ROS attacks. The mitochondrial uncoupling protein UCP2, even though its uncoupling properties are debated, has been associated with protective functions against ROS toxicity. Hormesis, an adaptive response to cellular stresses, might contribute to the protection against β-cell death, possibly limiting the development of type 2 diabetes. Mitochondrial hormesis, or mitohormesis, is a defense mechanism observed in ROS-induced stress-responses by mitochondria. In β cells, mitochondrial damages induced by sublethal exogenous H(2)O(2) can induce secondary repair and defense mechanisms. In this context, UCP2 is a marker of mitohormesis, being upregulated following stress conditions. When overexpressed in nonstressed naïve cells, UCP2 confers resistance to oxidative stress. Whether treatment with mitohormetic inducers is sufficient to restore or ameliorate secretory function of β cells remains to be determined. Animals Diabetes Mellitus, Type 2/metabolism/pathology Glucose/metabolism Hormesis Humans Insulin/metabolism/secretion Insulin-Secreting Cells/cytology/metabolism/secretion Ion Channels/metabolism Mitochondria/metabolism Mitochondrial Proteins/metabolism Oxidative Stress Reactive Oxygen Species/metabolism Dewey 612 Swiss National Science Foundation Investigating tissue specificity of glutamate pathway and mitochondrial function in the control of metabolic homeostasis 135704 CH Project funding 134 Département de physiologie cellulaire et métabolisme 21C false 402 Mitochondries et métabolisme énergétique 671 Oxidative medicine and cellular longevity 2012 0e779482-c765-4863-9e14-9f47d6c1ec45 Article (Published version) Public Li-OxMedCellLong-2012.pdf 3089146 application/pdf openAccess Faculté de médecine / Section de médecine fondamentale / Département de physiologie cellulaire et métabolisme

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Mitochondrial hormesis in pancreatic β cells: does uncoupling protein 2 play a role?	Oxidative medicine and cellular longevity			2012	687	531

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Stojanovski, Suzana