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dc.contributor.authorNewsholme, Philip
dc.contributor.authorRebelato, E.
dc.contributor.authorAbdulkader, F.
dc.contributor.authorKrause, M.
dc.contributor.authorCarpinelli, A.
dc.contributor.authorCuri, R.
dc.identifier.citationNewsholme, P. and Rebelato, E. and Abdulkader, F. and Krause, M. and Carpinelli, A. and Curi, R. 2012. Reactive oxygen and nitrogen species generation, antioxidant defenses, and β-cell function: a critical role for amino acids. Journal of Endocrinology. 214: pp. 11-20.

Growing evidence indicates that the regulation of intracellular reactive oxygen species (ROS) and reactive nitrogen species (RNS) levels is essential for maintaining normal β-cell glucose responsiveness. While long-term exposure to high glucose induces oxidative stress in β cells, conflicting results have been published regarding the impact of ROS on acute glucose exposure and their role in glucose stimulated insulin secretion (GSIS). Although β cells are considered to be particularly vulnerable to oxidative damage, as they express relatively low levels of some peroxide-metabolizing enzymes such as catalase and glutathione (GSH) peroxidase, other less known GSH-based antioxidant systems are expressed in β cells at higher levels. Herein, we discuss the key mechanisms of ROS/RNS production and their physiological function in pancreatic β cells. We also hypothesize that specific interactions between RNS and ROS may be the cause of the vulnerability of pancreatic β cells to oxidative damage. In addition, using a hypothetical metabolic model based on the data available in the literature, we emphasize the importance of amino acid availability for GSH synthesis and for the maintenance of β-cell function and viability during periods of metabolic disturbance before the clinical onset of diabetes.

dc.publisherBioScientifica Ltd.
dc.subjectamino acids
dc.subjectantioxidant defences
dc.titleReactive oxygen and nitrogen species generation, antioxidant defenses, and β-cell function: a critical role for amino acids
dc.typeJournal Article
dcterms.source.titleJournal of Endocrinology
curtin.accessStatusOpen access via publisher

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