Overexpression of glucose 6 phosphate dehydrogenase preserves mouse pancreatic beta cells function until late in life
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Otros documentos de la autoría: De la Rosa, Adrián; Gomez-Cabrera , Mari Carmen; Vinue, Angela; Gonzalez-Navarro, Herminia; Sanchez-Andres, Juan V.; Viña, J.
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https://doi.org/10.1016/j.freeradbiomed.2020.12.439 |
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Título
Overexpression of glucose 6 phosphate dehydrogenase preserves mouse pancreatic beta cells function until late in lifeAutoría
Fecha de publicación
2021-01Editor
ElsevierISSN
0891-5849Cita bibliográfica
De la Rosa, A., Gomez-Cabrera, M. C., Vinue, A., Gonzalez-Navarro, H., Sanchez-Andres, J. V., & Vina, J. (2021). Overexpression of Glucose 6 Phosphate Dehydrogenase preserves mouse pancreatic beta cells function until late in life. Free Radical Biology and Medicine.Tipo de documento
info:eu-repo/semantics/articleVersión de la editorial
https://www.sciencedirect.com/science/article/abs/pii/S0891584920321122Versión
info:eu-repo/semantics/publishedVersionPalabras clave / Materias
Resumen
NAD(P)H donates electrons for reductive biosynthesis and antioxidant defense across all forms of life. Glucose-6-
phosphate dehydrogenase (G6PD) is a critical enzyme to provide NADPH. G6PD deficiency is present in ... [+]
NAD(P)H donates electrons for reductive biosynthesis and antioxidant defense across all forms of life. Glucose-6-
phosphate dehydrogenase (G6PD) is a critical enzyme to provide NADPH. G6PD deficiency is present in more
than 400 million people worldwide. This enzymopathy provides protection against malaria but sensitizes cells to
oxidative stressors. Oxidative stress has been involved in the pathogenesis of the diabetic complications and
several studies have provided evidences of a link between G6PD deficiency and type 2 diabetes (T2D).
We hypothesized that a moderate overexpression of G6PD (G6PD-Tg) could protect β-cells from age-associated
oxidative stress thus reducing the risk of developing T2D.
Here we report, that G6PD-Tg mice show an improved glucose tolerance and insulin sensitivity when
compared to old age-matched Wild Type (WT) ones. This is accompanied by a decrease in oxidative damage and
stress markers in the pancreas of the old Tg animals (20-24month-old). Pancreatic β-cells progress physiologically towards a state of reduced responsiveness to glucose. In pancreatic islets isolated from G6PD-Tg and WT
animals at different ages, and using electrophysiological techniques, we demonstrate a wider range of response to
glucose in the G6PD-Tg cells that may explain the improvements in glucose tolerance and insulin sensitivity.
Together, our results show that overexpression of G6PD maintains pancreatic β-cells from old mice in a “juvenilelike” state and points to the G6PD dependent generation of NADPH as an important factor to improve the natural
history of diabetes. [-]
Publicado en
Free Radical Biology and Medicine, v. 164, 2021, p. 149-153Datos relacionados
https://doi. org/10.1016/j.freeradbiomed.2020.12.439Entidad financiadora
Instituto de Salud Carlos III | Ministerio de Ciencia e Innovación | Generalitat Valenciana. Conselleria de Sanitat | European Comission
Código del proyecto o subvención
CB16/10/ 00435 (CIBERFES) | PID2019-110906RB-I00/AEI/10.13039/ 501100011033 | PROMETEO/2019/097 | info:eu-repo/grantAgreement/EC/H2020/825546
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info:eu-repo/semantics/restrictedAccess
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