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

Published in Oxidative Medicine and Cellular Longevity. 2012, vol. 2012, 740849
Abstract 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.
Keywords AnimalsDiabetes Mellitus, Type 2/metabolism/pathologyGlucose/metabolismHormesisHumansInsulin/metabolism/secretionInsulin-Secreting Cells/cytology/metabolism/secretionIon Channels/metabolismMitochondria/metabolismMitochondrial Proteins/metabolismOxidative StressReactive Oxygen Species/metabolism
PMID: 23029600
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Article (Published version) (2.9 MB) - public document Free access
Research group Mitochondries et métabolisme énergétique (671)
Swiss National Science Foundation: 310030B_135704
(ISO format)
LI, Ning, STOJANOVSKI, Suzana, MAECHLER, Pierre. Mitochondrial hormesis in pancreatic β cells: does uncoupling protein 2 play a role?. In: Oxidative Medicine and Cellular Longevity, 2012, vol. 2012, p. 740849. doi: 10.1155/2012/740849 https://archive-ouverte.unige.ch/unige:28230

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Deposited on : 2013-05-29

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