| First Author | Liu R | Year | 2022 |
| Journal | Nat Commun | Volume | 13 |
| Issue | 1 | Pages | 3545 |
| PubMed ID | 35729232 | Mgi Jnum | J:341741 |
| Mgi Id | MGI:7311030 | Doi | 10.1038/s41467-022-31317-0 |
| Citation | Liu R, et al. (2022) MicroRNA-21 promotes pancreatic beta cell function through modulating glucose uptake. Nat Commun 13(1):3545 |
| abstractText | Pancreatic beta cell dysfunction contributes to the pathogenesis of type 2 diabetes. MiR-21 has been shown to be induced in the islets of glucose intolerant patients and type 2 diabetic mice. However, the role of miR-21 in the regulation of pancreatic beta cell function remains largely elusive. In the current study, we identify the pathway by which miR-21 regulates glucose-stimulated insulin secretion utilizing mice lacking miR-21 in their beta cells (miR-21betaKO). We find that miR-21betaKO mice develop glucose intolerance due to impaired glucose-stimulated insulin secretion. Mechanistic studies reveal that miR-21 enhances glucose uptake and subsequently promotes insulin secretion by up-regulating Glut2 expression in a miR-21-Pdcd4-AP-1 dependent pathway. Over-expression of Glut2 in knockout islets results in rescue of the impaired glucose-stimulated insulin secretion. Furthermore, we demonstrate that delivery of miR-21 into the pancreas of type 2 diabetic db/db male mice is able to promote Glut2 expression and reduce blood glucose level. Taking together, our results reveal that miR-21 in islet beta cell promotes insulin secretion and support a role for miR-21 in the regulation of pancreatic beta cell function in type 2 diabetes. |
