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    Home > Active Ingredient News > Immunology News > Losing weight in addition to keeping your mouth open, you also need to mobilize your mitochondrials

    Losing weight in addition to keeping your mouth open, you also need to mobilize your mitochondrials

    • Last Update: 2020-12-27
    • Source: Internet
    • Author: User
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    Today, obesity has become an increasingly common metabolic disease and an independent risk factor for the development of many diseases, such as type 2 diabetes, cardiovascular disease and cancer.
    38 percent of adults and 16 percent of children and adolescents face obesity.
    although the mechanism of obesity is due to more calorie intake than consumption, recent studies have shown that the immune system regulates neuroendocrine pathways, controlling not only food intake but also energy consumption.
    December 4, 2020, cell-Metabolish published online a new study by Steven L. Teitelbaum of the Department of Pathology and Immunology at the University of Washington School of Medicine.
    study found that in fat cells and macrophages, intercellular mitochondrial metastasis can be used as a mechanism for immune metabolic disorders to regulate metabolic stability, and that mitochondrial metastasis between cells is impaired when obese.
    to determine whether mitochondrial metastasis occurs between cells in the body, the researchers transplanted CD45.1 wild type (WT) bone marrow into CD45.2 mitochondrial reporting mice.
    bone marrow transplant showed that macrophages in white adipose tissue (WAT) in the body can obtain mitochondrials from fat cells.
    know that mitochondrial ingestion is affected by cell relaxin.
    , little is known about the genes needed for mitochondrial ingestion.
    ya'an used genome-wide CRISPR-Cas9 gene knockout screening to determine the genes necessary for mitochondrial ingestion.
    genetics, enzymatics, and pharmacological methods suggest that the HS biosynthetic process is necessary for mitochondrial ingestion, both in vitro and in vivo.
    , the researchers found that obesity was associated with a decrease in the transfer of mitochondrials from fat cells to macrophages.
    myelin cell Ext1 gene loss can impair mitochondrial metastasis to macrophages and promote fat build-up, reducing energy consumption throughout the body without affecting food intake or physical activity levels.
    All in all, this study reveals a new pattern of immune metabolism disorders in which cells, such as fat cells, transfer their mitochondrials to macrophages to regulate the metabolic stability of the system.
    transfer of mitochondrials between cells may have become a dynamic balancing process that enables immune cells to respond to and regulate their local tissue micro-environment.
    , the treatment of mitochondrial metastasis between cells could be used as a new strategy to improve metabolic diseases.
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