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GP73 is a glucogenic hormone contributing to SARS-CoV-2-induced hyperglycemia #MMPMID34992299
Wan L; Gao Q; Deng Y; Ke Y; Ma E; Yang H; Lin H; Li H; Yang Y; Gong J; Li J; Xu Y; Liu J; Li J; Liu J; Zhang X; Huang L; Feng J; Zhang Y; Huang H; Wang H; Wang C; Chen Q; Huang X; Ye Q; Li D; Yan Q; Liu M; Wei M; Mo Y; Li D; Tang K; Lin C; Zheng F; Xu L; Cheng G; Wang P; Yang X; Wu F; Sun Z; Qin C; Wei C; Zhong H
Nat Metab 2022[Jan]; 4 (1): 29-43 PMID34992299show ga
Severe cases of infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) are associated with elevated blood glucose levels and metabolic complications. However, the molecular mechanisms for how SARS-CoV-2 infection alters glycometabolic control are incompletely understood. Here, we connect the circulating protein GP73 with enhanced hepatic gluconeogenesis during SARS-CoV-2 infection. We first demonstrate that GP73 secretion is induced in multiple tissues upon fasting and that GP73 stimulates hepatic gluconeogenesis through the cAMP/PKA signaling pathway. We further show that GP73 secretion is increased in cultured cells infected with SARS-CoV-2, after overexpression of SARS-CoV-2 nucleocapsid and spike proteins and in lungs and livers of mice infected with a mouse-adapted SARS-CoV-2 strain. GP73 blockade with an antibody inhibits excessive glucogenesis stimulated by SARS-CoV-2 in vitro and lowers elevated fasting blood glucose levels in infected mice. In patients with COVID-19, plasma GP73 levels are elevated and positively correlate with blood glucose levels. Our data suggest that GP73 is a glucogenic hormone that likely contributes to SARS-CoV-2-induced abnormalities in systemic glucose metabolism.
|*SARS-CoV-2[MESH]
|Animals[MESH]
|Biomarkers[MESH]
|COVID-19/*complications/*virology[MESH]
|Cyclic AMP-Dependent Protein Kinases/metabolism[MESH]