Activation of the Wnt/beta-catenin pathway in pancreatic beta cells during the compensatory islet hyperplasia in prediabetic mice

Author(s)

Maschio, D. A. ; Oliveira, R. B. ; Santos, M. R. ; Carvalho, C. P. F. ; Barbosa-Sampaio, H. C. L. ; Collares-Buzato, C. B.

• Document type: Journal article
• Source: Biochemical and Biophysical Research Communications; v. 478, n. 4, p. 1534-1540, SEP 30 2016.
• Web of Science Citations: 5

Abstract

The Wnt/beta-catenin signaling pathway, also known as the canonical Wnt pathway, plays a role in cell proliferation and differentiation in several tissues/organs. It has been recently described in humans a relationship between type 2 diabetes (T2DM) and mutation in the gene encoding the transcription factor TCF7L2 associated to the Wnt/beta-catenin pathway. In the present study, we demonstrated that hyper plastic pancreatic islets from prediabetic mice fed a high-fat diet (HFD) for 60 d displayed nuclear translocation of active p-catenin associated with significant increases in protein content and gene expression of beta-catenin as well as of cyclins Dl, D2 and c-Myc (target genes of the Wnt pathway) but not of Tcf7I2 (the transcription factor). Meanwhile, these alterations were not observed in pancreatic islets from 30 d HFD-fed mice, that do not display significant beta cell hyperplasia. These data suggest that the Wnt/beta-catenin pathway is activated in pancreatic islets during prediabetes and may play a role in the induction of the compensatory beta cell hyperplasia observed at early phase of T2DM. (C) 2016 Published by Elsevier Inc. (AU)

• FAPESP's process: 15/25442-1 - Role of the canonical and non-canonical Wnt signaling pathway in the beta cell function and proliferation during experimental prediabetes
• Grantee: Carla Beatriz Collares Buzato
• Support Opportunities: Regular Research Grants