| First Author | Chen Y | Year | 2016 |
| Journal | Mol Cell Endocrinol | Volume | 437 |
| Pages | 213-223 | PubMed ID | 27568466 |
| Mgi Jnum | J:248792 | Mgi Id | MGI:6095521 |
| Doi | 10.1016/j.mce.2016.08.037 | Citation | Chen Y, et al. (2016) MicroRNA-17-92 cluster regulates pancreatic beta-cell proliferation and adaptation. Mol Cell Endocrinol 437:213-223 |
| abstractText | MiR-17-92 cluster contributes to the regulation of mammalian development, aging and tumorigenesis. The functional roles of miR-17-92 in pancreatic beta-cells are largely unknown. In this study, we found that conditional deletion of miR-17-92 in mouse pancreatic beta-cells (miR-17-92betaKO) significantly reduces glucose tolerance and the first phase of insulin secretion, despite normal ad libitum fed and fasting glucose levels. Proliferation is down-regulated in pancreatic beta-cells after deleting miR-17-92. MiR-17-92betaKO mice show higher phosphatase and tensin homologue (PTEN) and lower phosphorylated AKT in islets. Under high fat diet challenge for 16 weeks, miR-17-92betaKO mice lose compensation and exhibit higher glucose levels, and lower insulin secretion. Collectively, these data suggest that miR-17-92 is a critical contributor to molecular mechanisms regulating glucose-stimulated insulin secretion and pancreatic beta-cell adaptation under metabolic stress. |
