| First Author | Zhang M | Year | 2013 |
| Journal | Biochem Biophys Res Commun | Volume | 435 |
| Issue | 3 | Pages | 345-9 |
| PubMed ID | 23660189 | Mgi Jnum | J:202642 |
| Mgi Id | MGI:5520146 | Doi | 10.1016/j.bbrc.2013.04.079 |
| Citation | Zhang M, et al. (2013) Loss of beta-arrestin2 mediates pancreatic-islet dysfunction in mice. Biochem Biophys Res Commun 435(3):345-9 |
| abstractText | Insulin resistance and defective insulin secretion are two major factors contributing to the pathogenesis of type 2 diabetes. beta-Arrestin2 is known to interact with numerous signaling molecules. Our previous study demonstrated that beta-arrestin2 regulates insulin sensitivity in both skeletal muscle and liver, yet its role in insulin secretion remains elusive. In this study, we found that beta-arrestin2 was abundantly expressed in mouse pancreatic beta cells, while its expression was significantly decreased in obese and diabetic mouse models. Hyperglycemic clamp study showed that the acute and late phase of insulin secretion were impaired in beta-arrestin2 knockout mice. Ex vivo study showed that beta-arrestin2 deficient pancreatic islets exhibited blunted glucose-stimulated insulin secretion. Further analysis demonstrated the number of docked insulin granules in beta-arrestin2 deficient islets was markedly decreased compared to wild-type islets, while insulin content and beta cell mass remained unchanged. Our study establishes a new role for beta-arrestin2 in beta-cell functions, and suggests that the down regulation of beta-arrestin2 may contribute to impaired insulin secretion in type 2 diabetes. |
