GP73 is a glucogenic hormone contributing to SARS-CoV-2-induced hyperglycemia

Wan, Luming; Gao, Qi; Deng, Yong-Qiang; Ke, Yuehua; Ma, Enhao; Yang, Huan; Lin, Hanqing; Li, Huilong; Yang, Yali; Gong, Jing; Xu, Yingbin; Liu, Jing; Li, Jianmin; Liu, Jialong; Zhang, Xuemiao; Huang, Li; Feng, Jiangyue; Zhang, Yanhong; Huang, Hanqing; Wang, Huapeng; Wang, Changjun; Chen, Qi; Huang, Xing‐Yao; Ye, Qing; Li, Dongyu; Yan, Qiulin; Liu, Muyi; Wang, Meng; Mo, Yunhai; Li, Dongrui; Tang, Ke; Cui, Lin; Zheng, Fei; Xu, Lei; Cheng, Gong; Wang, Pei‐Hui; Yang, Xiaopan; Wu, Feixiang; Sun, Zhiwei; Qin, Cheng‐Feng; Wei, Congwen; Zhong, Hui

doi:10.1038/s42255-021-00508-2

Cited by 45 publications

(42 citation statements)

References 43 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Recently, Wan et al reported that GP73, a Golgi protein induced by infections, was increased during recent SARS-CoV-2 infection ( Wan et al, 2022 ). Furthermore, they showed that injection of recombinant GP73 raised blood glucose in mice within 15 min.…”

Section: Metabolic Dysfunction and Acute Sars-cov-2mentioning

confidence: 99%

Post-acute sequelae of COVID-19: A metabolic perspective

Scherer

Kirwan

Rosen

2022

eLife

View full text Add to dashboard Cite

The SARS-CoV-2 pandemic continues to rage around the world. At the same time, despite strong public health measures and high vaccination rates in some countries, a post-COVID-19 syndrome has emerged which lacks a clear definition, prevalence, or etiology. However, fatigue, dyspnea, brain fog, and lack of smell and/or taste are often characteristic of patients with this syndrome. These are evident more than a month after infection, and are labeled as Post-Acute Sequelae of CoV-2 (PASC) or commonly referred to as long-COVID. Metabolic dysfunction (i.e., obesity, insulin resistance, and diabetes mellitus) is a predisposing risk factor for severe acute COVID-19, and there is emerging evidence that this factor plus a chronic inflammatory state may predispose to PASC. In this article, we explore the potential pathogenic metabolic mechanisms that could underly both severe acute COVID-19 and PASC, and then consider how these might be targeted for future therapeutic approaches.

show abstract

Section: Metabolic Dysfunction and Acute Sars-cov-2mentioning

confidence: 99%

Post-acute sequelae of COVID-19: A metabolic perspective

Scherer

Kirwan

Rosen

2022

eLife

View full text Add to dashboard Cite

show abstract

“…Later studies showed that both viral and non-viral liver diseases enhance the production and secretion of GP73, which may serve as a serological marker for these conditions 6 . Here, Wan and colleagues 4 found that GP73 is induced in multiple metabolic tissues in mice upon fasting or upon high-fat diet feeding and is coordinately elevated in the circulation of mice and humans in these contexts. To assess the acute metabolic effect of circulating GP73, Wan et al 4 injected mice with a purified recombinant form of the secreted protein (rmGP73).…”

mentioning

confidence: 92%

“…Here, Wan and colleagues 4 found that GP73 is induced in multiple metabolic tissues in mice upon fasting or upon high-fat diet feeding and is coordinately elevated in the circulation of mice and humans in these contexts. To assess the acute metabolic effect of circulating GP73, Wan et al 4 injected mice with a purified recombinant form of the secreted protein (rmGP73). They observed a rapid (within 15 minutes) and sharp increase in blood glucose and insulin that was abolished by administration of a GP73-specific antibody.…”

mentioning

confidence: 92%

“…Indeed, SARS-CoV-2 infection is often associated with elevations in blood glucose that impact disease severity and clinical outcomes 3 , but the mechanism(s) underlying COVID-associated dysglycaemia in vivo, the target tissue(s) involved and the chronicity of disrupted glycaemic control following resolution of acute illness are poorly understood. In this issue of Nature Metabolism, Wan and colleagues 4 fill an important gap in the field by identifying a new function for Golgi protein 73 (GP73) as a stress-induced secreted factor that elevates blood glucose and is required for SARS-CoV-2 associated dysglycaemia (Fig. 1).…”

mentioning

confidence: 99%

“…An increase in blood glucose may reflect either enhanced HGP or decreased glucose utilization (or both). To determine which of these processes was affected by rmGP73, Wan et al 4 performed nutrient tolerance tests in mice 2 hours after injection with phosphate-buffered saline or rmGP73. They found that rmGP73 provoked significantly greater glycaemic excursions in response to glucose, pyruvate and alanine.…”

mentioning

confidence: 99%

See 2 more Smart Citations

GP73 links SARS-CoV-2 infection with dysglycaemia

Coate

2022

Nat Metab

View full text Add to dashboard Cite

show abstract

Dissecting the Interrelationship between COVID‐19 and Diabetes Mellitus

2023

View full text Add to dashboard Cite

COVID‐19 disease, caused by severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2), has led to enormous morbidity and mortality worldwide. After gaining entry into the human host, the virus initially infects the upper and lower respiratory tract, subsequently invading multiple organs, including the pancreas. While on one hand, diabetes mellitus (DM) is a significant risk factor for severe COVID‐19 infection and associated death, recent reports have shown the onset of DM in COVID‐19‐recovered patients. SARS‐CoV‐2 infiltrates the pancreatic islets and activates stress response and inflammatory signaling pathways, impairs glucose metabolism, and consequently leads to their death. Indeed, the pancreatic autopsy samples of COVID‐19 patients reveal the presence of SARS‐CoV‐2 particles in β‐cells. The current review describes how the virus enters the host cells and activates an immunological response. Further, it takes a closer look into the interrelationship between COVID‐19 and DM with the aim to provide mechanistic insights into the process by which SARS‐CoV‐2 infects the pancreas and mediates dysfunction and death of endocrine islets. The effects of known anti‐diabetic interventions for COVID‐19 management are also discussed. The application of mesenchymal stem cells (MSCs) as a future therapy for pancreatic β‐cells damage to reverse COVID‐19‐induced DM is also emphasized.

show abstract

GP73 is a glucogenic hormone contributing to SARS-CoV-2-induced hyperglycemia

Cited by 45 publications

References 43 publications

Post-acute sequelae of COVID-19: A metabolic perspective

Post-acute sequelae of COVID-19: A metabolic perspective

GP73 links SARS-CoV-2 infection with dysglycaemia

Dissecting the Interrelationship between COVID‐19 and Diabetes Mellitus

Contact Info

Product

Resources

About