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Title: Nupr1 deletion protects against glucose intolerance by increasing beta cell mass
Author: Cappelli, Ana P.; Zoppi, Claudio C.; Barbosa-sampaio, Helena C.; Costa, José M.; Protzek, André O.; Morato, Priscila N.; Boschero, Antonio C.; Carneiro, Everardo M.
Year: 2013
Is part of: Liver International (Print), v. 1, p. n/a - n/a
DOI: https://doi.org/10.1111/liv.12291

Citation: Cappelli, Ana P.; Zoppi, Claudio C.; Barbosa-sampaio, Helena C.; Costa, José M.; Protzek, André O.; Morato, Priscila N.; Boschero, Antonio C.; Carneiro, Everardo M.; Nupr1 deletion protects against glucose intolerance by increasing beta cell mass. Liver International (Print), v.1, p. n/a-n/a, 2013

Abstract: The stress-activated nuclear protein transcription regulator 1 (NUPR1) is induced in response to glucose and TNF-alpha, both of which are elevated in type 2 diabetes, and Nupr1 has been implicated in cell proliferation and apoptosis cascades. We used Nupr1 (-/-) mice to study the role of Nupr1 in glucose homeostasis under normal conditions and following maintenance on a high-fat diet (HFD).



Funding: We gratefully acknowledge grant support from Diabetes UK (ref: 06/0003387, 10/0003995 and 08/0003706), the European Foundation for the Study of Diabetes (EFSD)/Merck Sharp & Dohme (MSD) programme and the Society for Endocrinology (Early Career Grant).
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