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. 2021 Dec 14;12:727371. doi: 10.3389/fendo.2021.727371

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Copyright © 2021 Cao, Chen, Zhang, Wu, Zeng, Zhang and Cai

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

PMC Copyright notice

Illustrative model of the mechanism focusing on hepatic PGRMC1 signaling underlying chronic CLZ-induced hepatic glucose disturbances. The add-on PGRMC1-OE can reverse CLZ-induced hepatic glucose disturbances by upregulating the expression of PGRMC1-EGFR/GLP1R-PI3K-Akt-GSK3β accompanied with the downregulation of nuclear FOXO1. CLZ, CLZ; AG205, the specific inhibitor of PGRMC1; PGRMC1-KD, the knockdown of PGRMC1; PGRMC1-OE, the overexpression of PGRMC1; H&E, hematoxylin and eosin staining; PAS, Periodic acid–Schiff staining; PGRMC1, PROG receptor membrane component 1; EGFR, epidermal growth factor receptor; GLP1R, glucagon-like peptide-1 receptor; PI3K, 3-phosphoinositide-dependent kinase-1; Akt, protein kinase B; GSK3β, glycogen synthase kinase-3β; FOXO1, the fork head box protein 1.