| First Author | Chang TJ | Year | 2011 |
| Journal | Mol Cell Endocrinol | Volume | 335 |
| Issue | 2 | Pages | 104-9 |
| PubMed ID | 21187123 | Mgi Jnum | J:179467 |
| Mgi Id | MGI:5302461 | Doi | 10.1016/j.mce.2010.12.026 |
| Citation | Chang TJ, et al. (2011) Targeted expression of islet neogenesis associated protein to beta cells enhances glucose tolerance and confers resistance to streptozotocin-induced hyperglycemia. Mol Cell Endocrinol 335(2):104-9 |
| abstractText | Islet neogenesis associated protein (INGAP) stimulates experimental pancreatic islet growth, as evidenced by elevated markers of beta cell mass, in rodents, dogs and primates. Previous analyses of mice that have a transgenic expression of INGAP targeted to the exocrine pancreas have indicated additional biological activity attributed to INGAP. In this study we report on mice with a targeted expression of INGAP to the islet beta cell. The beta cell transgenic mice (IP-INGAP) showed enhanced normalization of blood glucose during IPGTT. Further, IP-INGAP mice had a significant delay in development of hyperglycemia following a diabetogenic dose of streptozotocin. INGAP conferred beta cell protection and enhanced islet function. Analysis of oxidative stress genes in IP-INGAP mice revealed a decrease in islet expression of the NADPH oxidase, NOX1, in both basal state and in response to pro-inflammatory cytokine stimulation. These data are consistent with a pleiotropic role for INGAP and reveal new pathways to target in the discovery of improved diabetic therapies. |
