| First Author | Yuan H | Year | 2023 |
| Journal | Biochem Biophys Res Commun | Volume | 643 |
| Pages | 121-128 | PubMed ID | 36596263 |
| Mgi Jnum | J:332550 | Mgi Id | MGI:7427151 |
| Doi | 10.1016/j.bbrc.2022.12.079 | Citation | Yuan H, et al. (2022) Crispr-Cas9 mediated complete deletion of glucagon receptor in mice display hyperglucagonemia and alpha-cell hyperplasia. Biochem Biophys Res Commun 643:121-128 |
| abstractText | Glucagon receptor plays an important role in the regulation of glucose metabolism. Studies have revealed that glucagon receptor antagonism is a potential effective treatment for diabetes. However, the functions of GCGR have not been fully illustrated. Although two Gcgr truncation knockout mice models have been widely used for GCGR function studies, truncated gene may remain neomorphic and/or dominant-negative function. In this study, we took the advantages of Crispr-Cas9 technique and generated a novel allele of GCGR in the mouse that yields complete loss of GCGR protein. Our studies reveal that complete deletion of Gcgr results in hyperglucagonemia, alpha-cell hyperplasia, improvement of glucose tolerance. These results are similar to the Gcgr-truncated mutation in mice. Hence, we provide a novel strain of GCGR knockout mice for the GCGR function studies. |
