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    Home > Active Ingredient News > Endocrine System > Diabetologia: Hong Tianpei's team found that the pancreatic α cell glucagon-liver FGF21 axis regulates cell regeneration β in a mouse model of type 2 diabetes

    Diabetologia: Hong Tianpei's team found that the pancreatic α cell glucagon-liver FGF21 axis regulates cell regeneration β in a mouse model of type 2 diabetes

    • Last Update: 2022-11-14
    • Source: Internet
    • Author: User
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    On November 4, 2022, the research team of Wei Rui, researcher of the Department of Endocrinology, Peking University Third Hospital/Professor Hong Tianpei, published online in Diabetologia, a β top journal specializing in endocrinology and metabolism, "Pancreatic alpha cell glucagon–liver FGF21 axis regulates beta cell" as α"Pancreatic alpha cell glucagon–liver FGF21 axis regulates beta cell" Regeneration in a mouse model of type 2 diabetes

    Diabetes is a major disease
    that endangers human health and life.
    Restoring the total number of functional islets β cells is a potential hope for improving the long-term efficacy of diabetes (or even curing diabetes), so the research on β cell regeneration and its mechanism has always been a hot spot and difficulty in the field of diabetes

    Researcher Wei Rui/Professor Hong Tianpei's research team first reported in iScience in 2019 that glucagon receptor (GCGR) monoclonal antibody (mAb) blocking glucagon signaling can induce islet α cells to β cells in mice with absolute β cell deficiency, thereby promoting β cell regeneration
    The findings of this study were validated
    by the findings of a 2021 study published in PNAS by Professor Holland's team at the University of Texas.

    In 2022, the research team of researcher Wei Rui / Professor Hong Tianpei reported in iScience that GCGR mAbs promote the regeneration of β cells in β cell-deficient type 2 diabetic mice by promoting the transdifferentiation of α cells to β cells and inducing β cell regeneration
    derived from pancreatic stem cells.
    However, the mechanism by which glucagon-GCGR signaling is blocked leads to β cell regeneration is unclear

    This article is one of a series of studies on β cell regeneration and its mechanism by the research team of Prof.
    Wei Rui / Professor Hong Tianpi, aiming to elucidate the mechanism
    of β cell regeneration caused by GCGR block.

    Figure | Pattern diagram of α cellular glucagon–liver FGF21 axis in regulating cell regeneration in β cells

    First, GCGR mAb was shown to promote islet cell regeneration
    in a type 2 diabetes model (db/db mice and high-fat feeding + low-dose streptoxin diabetic mice).

    Secondly, plasma condition culture or co-culture with primary mouse pancreatic islets using mouse β cell lines and primary mouse islets found that there were regulators of ex vivo β cell phenotype in the plasma or primary hepatocytes extracted from GCGR
    mAb-treated mice.

    Subsequently, plasma cytokine profiles were analyzed by solid-phase antibody chip technology and compared with liver mRNA sequencing data to determine fibroblast growth factor 21 (FGF21) as a potential mediating factor

    Furthermore, FGF21 neutralizing antibody, systemic Fgf21 knockout, hepatocyte-specific Fgf21 knockout and other blockades proved that liver-derived FGF21 not only participates in the regulation of GCGR mAb on the phenotype of ex vivo β cells, but also mediates β cell regeneration
    in diabetic mice caused by GCGR mAb.

    This study revealed a new mechanism of GCGR block to improve diabetes control and promote β cell regeneration, and found that the α-cell glucagon-liver FGF21 axis plays an important role in cell regeneration in diabetic mic β e, providing a new perspective
    for further development of therapeutic strategies to promote β cell regeneration.

    Diabetologia, the official journal of the European Diabetes Society (EASD), is one of
    the oldest and most influential professional journals on diabetes.
    The Wei Rui/Hong Tianbei research team has been committed to islet regeneration and β cell function regulation for a long time, and has published more than 10 related papers in SCI journals such as Diabetologia, Metabolism, EBioMedicine, and iScience
    in the past 3 years.

    Cui Xiaona, a postdoctoral fellow in the Department of Endocrinology, and Feng Jin, a master student, are the co-first authors of this paper, and researcher Wei Rui and Professor Hong Tianbei are the co-corresponding authors
    This paper is supported
    by the National Natural Science Foundation of China and the Beijing Municipal Natural Science Foundation.

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