| First Author | Rankin MM | Year | 2013 |
| Journal | Diabetes | Volume | 62 |
| Issue | 5 | Pages | 1634-45 |
| PubMed ID | 23349489 | Mgi Jnum | J:208567 |
| Mgi Id | MGI:5563717 | Doi | 10.2337/db12-0848 |
| Citation | Rankin MM, et al. (2013) beta-Cells are not generated in pancreatic duct ligation-induced injury in adult mice. Diabetes 62(5):1634-45 |
| abstractText | The existence of adult beta-cell progenitors remains the most controversial developmental biology topic in diabetes research. It has been reported that beta-cell progenitors can be activated by ductal ligation-induced injury of adult mouse pancreas and apparently act in a cell-autonomous manner to double the functional beta-cell mass within a week by differentiation and proliferation. Here, we demonstrate that pancreatic duct ligation (PDL) does not activate progenitors to contribute to beta-cell mass expansion. Rather, PDL stimulates massive pancreatic injury, which alters pancreatic composition and thus complicates accurate measurement of beta-cell content via traditional morphometry methodologies that superficially sample the pancreas. To overcome this potential bias, we quantified beta-cells from the entire pancreas and observed that beta-cell mass and insulin content are totally unchanged by PDL-induced injury. Lineage-tracing studies using sequential administration of thymidine analogs, rat insulin 2 promoter-driven cre-lox, and low-frequency ubiquitous cre-lox reveal that PDL does not convert progenitors to the beta-cell lineage. Thus, we conclude that beta-cells are not generated in injured adult mouse pancreas. |
