| First Author | Nomura M | Year | 2014 |
| Journal | Biochem Biophys Res Commun | Volume | 450 |
| Issue | 1 | Pages | 440-6 |
| PubMed ID | 24928396 | Mgi Jnum | J:219439 |
| Mgi Id | MGI:5620835 | Doi | 10.1016/j.bbrc.2014.05.141 |
| Citation | Nomura M, et al. (2014) Activation of activin type IB receptor signals in pancreatic beta cells leads to defective insulin secretion through the attenuation of ATP-sensitive K+ channel activity. Biochem Biophys Res Commun 450(1):440-6 |
| abstractText | In studies of gene-ablated mice, activin signaling through activin type IIB receptors (ActRIIB) and Smad2 has been shown to regulate not only pancreatic beta cell mass but also insulin secretion. However, it still remains unclear whether gain of function of activin signaling is involved in the modulation of pancreatic beta cell mass and insulin secretion. To identify distinct roles of activin signaling in pancreatic beta cells, the Cre-loxP system was used to activate signaling through activin type IB receptor (ActRIB) in pancreatic beta cells. The resultant mice (pancreatic beta cell-specific ActRIB transgenic (Tg) mice; ActRIBCAbetaTg) exhibited a defect in glucose-stimulated insulin secretion (GSIS) and a progressive impairment of glucose tolerance. Patch-clamp techniques revealed that the activity of ATP-sensitive K(+) channels (KATP channels) was decreased in mutant beta cells. These results indicate that an appropriate level of activin signaling may be required for GSIS in pancreatic beta cells, and that activin signaling involves modulation of KATP channel activity. |
