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Title

Upregulation of UCP2 in beta-cells confers partial protection against both oxidative stress and glucotoxicity

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Published in Redox Biology. 2017, vol. 13, p. 541-549
Abstract Deterioration of pancreatic beta-cells plays a critical role in the development of type 2 diabetes. Among the various stressors contributing to these deleterious effects, glucotoxicity and superoxides have been proposed as major players. In this context, the mitochondrial uncoupling protein UCP2 is regularly associated with the stress response. In the present study, we tested the effects of UCP2 upregulation in mouse islets with beta-cell specific overexpression of UCP2 (RIP-UCP2). Islets were subjected to both chronic glucotoxicity (7 days at 30mM glucose) and acute oxidative stress (200µM H2O2 for 10min). Increased UCP2 expression did not alter mitochondrial potential and ATP generation but protected against glucotoxic effects. Glucose-stimulated insulin secretion was altered by both glucotoxicity and oxidative stress, in particular through higher basal insulin release at non-stimulatory glucose concentrations. The secretory response to glucose stimulation was partially preserved in beta-cells overexpressing UCP2. The higher rate of cell death induced by chronic high glucose exposure was lower in RIP-UCP2 islets. Finally, superoxide production was reduced by high glucose, both under acute and chronic conditions, and not modified by UCP2 overexpression. In conclusion, upregulation of UCP2 conferred protective effects to the stressed beta-cell through mechanisms not directly associated with superoxide production.
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PMID: 28755631
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Article (Published version) (1.2 MB) - public document Free access
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Research group Mitochondries et sécrétion d'insuline (671)
Project FNS: 31003A_146984
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LI, Ning, KARACA EMRE, Melis, MAECHLER, Pierre. Upregulation of UCP2 in beta-cells confers partial protection against both oxidative stress and glucotoxicity. In: Redox Biology, 2017, vol. 13, p. 541-549. https://archive-ouverte.unige.ch/unige:99222

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Deposited on : 2017-11-17

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