| First Author | Yamaoka T | Year | 2000 |
| Journal | Biochem Biophys Res Commun | Volume | 278 |
| Issue | 2 | Pages | 368-76 |
| PubMed ID | 11097844 | Mgi Jnum | J:65746 |
| Mgi Id | MGI:1927255 | Doi | 10.1006/bbrc.2000.3813 |
| Citation | Yamaoka T, et al. (2000) Diabetes and tumor formation in transgenic mice expressing reg I. Biochem Biophys Res Commun 278(2):368-76 |
| abstractText | To examine the effect of overexpressed regenerating gene (Reg) I on pancreatic beta-cells, we generated transgenic mice expressing Reg I in islets (Reg-Tg mice). Three lines of Reg-Tg mice were established. In line-1 Reg-Tg mice, the expression level of Reg I mRNA in islets was 7 times higher than those in lines 2 and 3 of Reg-Tg mice, and line 1 mice developed diabetes by apoptosis of beta-cells, as well as various malignant tumors. In addition to the decrease in beta-cells, compensatory islet regeneration and proliferation of ductal epithelial cells were observed in line-1 Reg-Tg mice. Because Reg I protein was secreted primarily into pancreatic ducts from acinar cells, it may primarily stimulate the proliferation of ductal epithelial cells, and not beta-cells, and their differentiation into islets. Moreover, the tumor-promoting activity of Reg I protein should be considered for its possible clinical applications. Copyright 2000 Academic Press. |
