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Title: Nupr1 deletion protects against glucose intolerance by increasing beta cell mass Author: Barbosa-sampaio, Helena C.; Persaud, S.; Muller, Dany S.; Liu, Bo; Drynda R; Rodriguez De Ledesma, Am; King Aj; Bowe, J; Malicet C; Iovanna, J.; Jones, Peter M. Year: 2013 Is part of: DIABETOLOGIA, v. 56, p. 2477 - 2486 DOI: https://doi.org/10.1007/s00125-013-3006-x Citation: Barbosa-sampaio, Helena C.; Persaud, S.; Muller, Dany S.; Liu, Bo; Drynda R; Rodriguez De Ledesma, Am; King Aj; Bowe, J; Malicet C; Iovanna, J.; Jones, Peter M.; Nupr1 deletion protects against glucose intolerance by increasing beta cell mass. DIABETOLOGIA, v.56, p. 2477-2486, 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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