| First Author | Higashi S | Year | 2015 |
| Journal | Biochem Biophys Res Commun | Volume | 461 |
| Issue | 4 | Pages | 612-7 |
| PubMed ID | 25912136 | Mgi Jnum | J:228369 |
| Mgi Id | MGI:5706869 | Doi | 10.1016/j.bbrc.2015.04.074 |
| Citation | Higashi S, et al. (2015) p13 overexpression in pancreatic beta-cells ameliorates type 2 diabetes in high-fat-fed mice. Biochem Biophys Res Commun 461(4):612-7 |
| abstractText | We examined the pancreatic function of p13 encoded by 1110001J03Rik, whose expression is decreased in pancreatic islets in high-fat-fed diabetic mice, by generating transgenic mice overexpressing p13 (p13-Tg) in pancreatic beta-cells. p13-Tg mice showed normal basal glucose metabolism; however, under high-fat feeding, these animals showed augmented glucose-induced first-phase and total insulin secretion, improved glucose disposal, greater islet area and increased mitotic insulin-positive cells. In addition, high-fat diet-induced 4-hydroxynonenal immunoreactivity, a reliable marker and causative agent of lipid peroxidative stress, was significantly decreased in p13-Tg mouse islets. These results indicate that p13 is a novel pancreatic factor exerting multiple beneficial effects against type 2 diabetes. |
