| First Author | Moritani M | Year | 2005 |
| Journal | Mol Cell Endocrinol | Volume | 229 |
| Issue | 1-2 | Pages | 175-84 |
| PubMed ID | 15607541 | Mgi Jnum | J:104920 |
| Mgi Id | MGI:3613127 | Doi | 10.1016/j.mce.2004.08.007 |
| Citation | Moritani M, et al. (2005) Hypoplasia of endocrine and exocrine pancreas in homozygous transgenic TGF-beta1. Mol Cell Endocrinol 229(1-2):175-84 |
| abstractText | We generated the homozygous transgenic mice with expression of the active form of TGF-beta1 by the glucagon promoter (homozygous NOD-TGF-beta1). The homozygous NOD-TGF-beta1 showed severe diabetes in 84.6%, impaired glucose tolerance, and low serum insulin levels. The final size of endocrine and whole pancreas decreased, respectively, to 6 and 34%, compared to wild-type mice. The homozygous N(2) backcross to C57BL/6 (B6-TGF-beta1) showed no diabetes, but impaired glucose tolerance and low serum insulin levels. In homozygous NOD-TGF-beta1, the expression of p15(INK4b) was induced by 3.4-fold in pancreatic islets than that in wild-type mice. Based on these, we conclude first that excessive paracrine TGF-beta1 signaling in islets results in endocrine and exocrine pancreatic hypoplasia, second that TGF-beta1decrease the final size of endocrine and exocrine pancreas presumably through regulating cell cycle via p15(INK4b) at least in endocrine pancreas, and third that hypoplastic action of TGF-beta1 of pancreatic islets is independent of the genetic background. |
