| First Author | Guo L | Year | 2013 |
| Journal | Diabetes | Volume | 62 |
| Issue | 10 | Pages | 3459-68 |
| PubMed ID | 23775765 | Mgi Jnum | J:208954 |
| Mgi Id | MGI:5565429 | Doi | 10.2337/db12-1833 |
| Citation | Guo L, et al. (2013) PDX1 in ducts is not required for postnatal formation of beta-cells but is necessary for their subsequent maturation. Diabetes 62(10):3459-68 |
| abstractText | Pancreatic duodenal homeobox-1 (Pdx1), a transcription factor required for pancreatic development and maintenance of beta-cell function, was assessed for a possible role in postnatal beta-cell formation from progenitors in the pancreatic ducts by selectively deleting Pdx1 from the ducts. Carbonic anhydrase II (CAII)(Cre);Pdx1(Fl) mice were euglycemic for the first 2 postnatal weeks but showed moderate hyperglycemia from 3 to 7 weeks of age. By 10 weeks, they had near-normal morning fed glucose levels but showed severely impaired glucose tolerance and insulin secretion. Yet the loss of Pdx1 did not result in decreased islet and beta-cell mass at 4 and 10 weeks of age. Within the same pancreas, there was a mixed population of islets, with PDX1 and MAFA protein expression normal in some cells and severely diminished in others. Even at 10 weeks, islets expressed immaturity markers. Thus, we conclude that Pdx1 is not necessary for the postnatal formation of beta-cells but is essential for their full maturation to glucose-responsive beta-cells. |
