| First Author | Zhang J | Year | 2012 |
| Journal | Diabetes | Volume | 61 |
| Issue | 12 | Pages | 3189-98 |
| PubMed ID | 22923474 | Mgi Jnum | J:208498 |
| Mgi Id | MGI:5563617 | Doi | 10.2337/db12-0249 |
| Citation | Zhang J, et al. (2012) Disruption of growth factor receptor-binding protein 10 in the pancreas enhances beta-cell proliferation and protects mice from streptozotocin-induced beta-cell apoptosis. Diabetes 61(12):3189-98 |
| abstractText | Defects in insulin secretion and reduction in beta-cell mass are associated with type 2 diabetes in humans, and understanding the basis for these dysfunctions may reveal strategies for diabetes therapy. In this study, we show that pancreas-specific knockout of growth factor receptor-binding protein 10 (Grb10), which is highly expressed in pancreas and islets, leads to elevated insulin/IGF-1 signaling in islets, enhanced beta-cell mass and insulin content, and increased insulin secretion in mice. Pancreas-specific disruption of Grb10 expression also improved glucose tolerance in mice fed with a high-fat diet and protected mice from streptozotocin-induced beta-cell apoptosis and body weight loss. Our study has identified Grb10 as an important regulator of beta-cell proliferation and demonstrated that reducing the expression level of Grb10 could provide a novel means to increase beta-cell mass and reduce beta-cell apoptosis. This is critical for effective therapeutic treatment of both type 1 and 2 diabetes. |
