Crispr-Cas9 mediated complete deletion of glucagon receptor in mice display hyperglucagonemia and α-cell hyperplasia
Hang Yuan, Qi Kang, Zhehui Li, Xuanxuan Bai, Jianxin Jia, Daxiong Han, Xijie Wu, Mingyu Li
Journal：BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
IF：3.32
DOI：10.1016/j.bbrc.2022.12.079
PMID：36596263
Published：2022-12-28
research field：分子生物学内分泌学遗传学糖尿病研究
Abstract
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, α-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.
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