echemi logo
Product
  • Product
  • Supplier
  • Inquiry
    Home > Active Ingredient News > Infection > Nat Metab Zhong Hui/Wei Congwen/Qin Chengfeng/Sun Zhiwei and others collaborate to reveal the new mechanism and potential therapeutic target of abnormal blood sugar elevation in patients with new coronary pneumonia

    Nat Metab Zhong Hui/Wei Congwen/Qin Chengfeng/Sun Zhiwei and others collaborate to reveal the new mechanism and potential therapeutic target of abnormal blood sugar elevation in patients with new coronary pneumonia

    • Last Update: 2022-01-26
    • Source: Internet
    • Author: User
    Search more information of high quality chemicals, good prices and reliable suppliers, visit www.echemi.com
    The new coronavirus infection leads to pathological changes in the systemic metabolism of patients, and nearly half of the patients have short-term or long-term abnormal blood sugar, which has a significant impact on the prognosis and quality of life of patients [1,2]
    .

    The abnormal blood sugar caused by the new crown infection is mainly divided into the following three categories: the virus directly attacks the islet beta cells causing new type I diabetes, type II diabetes patients with new crown infection, and non-diabetic patients with abnormal blood sugar after infection with the new crown [3]
    .

    Statistics show that when blood sugar is poorly controlled, the mortality rate of patients with new coronary pneumonia increases from 1.
    1% to 11% [4]
    .

    Therefore, it is of great clinical significance to deeply explore and unearth the molecular mechanism by which 2019-nCoV affects the body's glucose metabolism
    .

    On January 7, 2022, researcher Zhong Hui, associate researcher Wei Congwen and Qin Chengfeng of the Academy of Military Medical Sciences, in cooperation with Sun Zhiwei from Beijing Shunjing Biomedical Technology Co.
    , Ltd.
    , and Wu Feixiang from Guangxi Medical University Affiliated Cancer Hospital, published in the journal Nature Metabolism The article GP73 is a glucogenic hormone contributing to SARS-CoV-2-induced hyperglycemia, and found that the abnormal secretion of the Golgi membrane protein GP73 caused by the new coronavirus infection is an important reason for the abnormal increase of blood sugar in the body caused by the new coronavirus
    .

    GP73 enhances the gluconeogenesis of the liver by activating the cAMP-PKA-CREB signaling pathway, which disrupts the balance between the "source" and "going path" of blood glucose, which in turn leads to abnormal glucose metabolism in patients
    .

    In addition, the study also found that the self-developed GP73-specific antibody can inhibit the glucose-raising effect of GP73 and restore the blood sugar level of mice infected with the new coronavirus to normal, which has positive significance for the treatment and prognosis of patients with the new coronavirus
    .

    Under physiological conditions, GP73 is a type II transmembrane protein located on the cis-Golgi apparatus, which plays a role in maintaining the normal structure and function of the Golgi apparatus
    .

    Research progress in recent years has shown that under pathological conditions such as inflammation, tumor and viral infection, GP73 can be secreted into the cytoplasm and extracellular to play a more extensive role
    .

    In previous studies, Zhong Hui's group found that the expression and secretion of GP73 are regulated by the nutritional status of the body.
    Under the conditions of starvation and high-fat diet, GP73 rapidly accumulates in the liver in an endocrine and autocrine manner, and acts as a "glucose hormone".
    " effect
    .

    The phosphorylation proteomic results of GP73-treated mouse primary hepatocytes showed that, like glucagon, GP73 could activate the PKA-centered cAMP-PKA-CREB signaling pathway and significantly improve the gluconeogenesis capacity of the liver
    .

    Studies have shown that a significant increase in GP73 levels was detected in the serum of patients with new coronary infection, and it was positively correlated with the fasting blood glucose of patients
    .

    Unexpectedly, GP73 remained at a high level in the serum of recovered patients with COVID-19, suggesting that liver damage and cytokine activation caused by viral infection are also the reasons for the abnormal secretion of GP73
    .

    Cytological experimental studies have found that the increase in GP73 levels is mediated by the protein-to-protein interaction between the S and N proteins of the new coronavirus and GP73
    .

    After infecting mice with the mouse SARS-CoV-2-adapted strain MASCp6 [5], the researchers also found that the abnormal increase in blood sugar was accompanied by an increase in serum GP73 levels, confirming the pathological feature of GP73 in the circulation caused by SARS-CoV-2 infection
    .

    Finally, the researchers used the self-developed GP73 monoclonal antibody to successfully inhibit the gluconeogenesis of the new coronavirus-infected mouse liver cells, and were able to restore the fasting blood glucose level of the mice to normal
    .

    In conclusion, this study discovered a novel gluconeogenesis-regulating hormone, GP73, which was induced by 2019-nCoV infection, resulting in excessive gluconeogenesis
    .

    The continuously elevated GP73 may directly cause abnormal glucose metabolism in the host, and the use of antibodies to block GP73 in the circulatory system may reduce the abnormal blood sugar and mortality during the new crown infection and recovery period
    .

    Researcher Zhong Hui, Associate Researcher Wei Congwen and Qin Chengfeng of the Academy of Military Medical Sciences, Sun Zhiwei of Beijing Shunjing Biomedical Technology Co.
    , Ltd.
    , Professor Wu Feixiang of the Cancer Hospital Affiliated to Guangxi Medical University and Yang Xiaopan, a postdoctoral fellow of the Academy of Military Medical Sciences are the co-corresponding authors of this article; Assistant Researcher Wan Luming of the Academy of Military Medical Sciences, Gao Qi of Beijing Shunjing Biomedical Technology Co.
    , Ltd.
    , Researcher Deng Yongqiang of the Academy of Military Medical Sciences, Researcher Ke Yuehua of the PLA Center for Disease Control and Prevention, Ma Enhao, a doctoral student of Tsinghua University School of Medicine, Academy of Military Medical Sciences Graduate students Yang Huan and Lin Haotian are the co-first authors of this paper
    .

    Original link: https:// Publisher: Eleven References 1 Ayres, JS A metabolic handbook for the COVID-19 pandemic.
    Nat Metab 2, 572-585 , doi:10.
    1038/s42255-020-0237-2 (2020).
    2 Montefusco, L.
    et al.
    Acute and long-term disruption of glycometabolic control after SARS-CoV-2 infection.
    Nat Metab 3, 774-785, doi :10.
    1038/s42255-021-00407-6 (2021).
    3 Lim, S.
    , Bae, JH, Kwon, HS & Nauck, MA COVID-19 and diabetes mellitus: from pathophysiology to clinical management.
    Nat Rev Endocrinol 17, 11 -30, doi:10.
    1038/s41574-020-00435-4 (2021).
    4 Zhu, L.
    et al.
    Association of Blood Glucose Control and Outcomes in Patients with COVID-19 and Pre-existing Type 2 Diabetes.
    Cell Metab 31 , 1068-1077 e1063, doi:10.
    1016/j.
    cmet.
    2020.
    04.
    021 (2020).
    5 Gu, H.
    et al.
    Adaptation of SARS-CoV-2 in BALB/c mice for testing vaccine efficacy.
    Science 369,1603-1607, doi:10.
    1126/science.
    abc4730 (2020).
    Reprint Notice [Non-original article] The copyright of this article belongs to the author of the article.
    Personal reposting and sharing are welcome.
    Reprinting is prohibited without permission.
    The author has all legal rights, and offenders must be prosecuted
    .

    This article is an English version of an article which is originally in the Chinese language on echemi.com and is provided for information purposes only. This website makes no representation or warranty of any kind, either expressed or implied, as to the accuracy, completeness ownership or reliability of the article or any translations thereof. If you have any concerns or complaints relating to the article, please send an email, providing a detailed description of the concern or complaint, to service@echemi.com. A staff member will contact you within 5 working days. Once verified, infringing content will be removed immediately.

    Contact Us

    The source of this page with content of products and services is from Internet, which doesn't represent ECHEMI's opinion. If you have any queries, please write to service@echemi.com. It will be replied within 5 days.

    Moreover, if you find any instances of plagiarism from the page, please send email to service@echemi.com with relevant evidence.