| First Author | Shibutani Y | Year | 2013 |
| Journal | Kobe J Med Sci | Volume | 59 |
| Issue | 3 | Pages | E72-80 |
| PubMed ID | 24045216 | Mgi Jnum | J:333580 |
| Mgi Id | MGI:6882453 | Citation | Shibutani Y, et al. (2013) Constitutive activation of Rac1 in pancreatic beta cells facilitates F-actin depolymerization but exerts no influence on the increase of pancreatic beta cell mass and facilitation of insulin secretion. Kobe J Med Sci 59(3):E72-80 |
| abstractText | Insulin secretion from pancreatic beta cells has an important role in the onset of type 2 diabetes. Insulin secretion from pancreatic beta cells is regulated by pancreatic beta cell mass and their insulin secretory function. By using pancreatic beta cell-specific Rac1-knockout mice, we recently showed that Rac1 deletion, even with no reduction in pancreatic beta cell mass, inhibits F-actin depolymerization, which causes insulin secretion to decline. However, the effect of Rac1 deficiency on the growth and apoptosis of pancreatic beta cells was not clarified. Further, the effect of constitutive Rac1 activation on the secretion of insulin from pancreatic beta cells has not been studied. Here, we used pancreatic islets isolated from pancreatic beta cell-specific Rac1-knockout mice to evaluate the growth and apoptosis of pancreatic beta cells. We found that Rac1 deficiency does not influence the growth or apoptosis of pancreatic beta cells. Further, when a constitutively activated form of Rac1 (G12V) is expressed, F-actin depolymerization was increased in the pancreatic beta cell lines, which had no effect on pancreatic beta cell growth or glucose-stimulated insulin secretion. These findings indicate that excessive Rac1 expression or activation in pancreatic beta cells facilitates F-actin depolymerization, but has no effect on insulin secretion. |
