| First Author | Maschio DA | Year | 2016 |
| Journal | Biochem Biophys Res Commun | Volume | 478 |
| Issue | 4 | Pages | 1534-40 |
| PubMed ID | 27576200 | Mgi Jnum | J:239010 |
| Mgi Id | MGI:5824772 | Doi | 10.1016/j.bbrc.2016.08.146 |
| Citation | Maschio DA, et al. (2016) Activation of the Wnt/beta-catenin pathway in pancreatic beta cells during the compensatory islet hyperplasia in prediabetic mice. Biochem Biophys Res Commun 478(4):1534-40 |
| abstractText | 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 hyperplastic pancreatic islets from prediabetic mice fed a high-fat diet (HFD) for 60 d displayed nuclear translocation of active beta-catenin associated with significant increases in protein content and gene expression of beta-catenin as well as of cyclins D1, D2 and c-Myc (target genes of the Wnt pathway) but not of Tcf7l2 (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. |
