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    Home > Biochemistry News > Biotechnology News > The function of p38 alpha in the process of white fat beigeing is clarified.

    The function of p38 alpha in the process of white fat beigeing is clarified.

    • Last Update: 2020-08-09
    • Source: Internet
    • Author: User
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    On May 11th, the international academic journal PLoS Biology published the latest research results of the Yinghao Research Group of the Shanghai Institute of Nutrition and Health of the Chinese Academy of Sciences, the latest research results of the published results of the nutrition of the inhibition of the p38 alphain white adipose tissue in obesity.
    the study found that p38 alpha, a member of the pro-split activated protein kinase (MAPK) family, regulates the beigeization process of white adipose tissue and further affects the state of energy metabolism by affecting the PKA/CREB/UCP-1 signaling pathway.
    the high mitochondria content of brown fat, the high expression of the decouple protein UCP1, is very important for the body's energy metabolism and heat production activities.
    in low-temperature stimulation, beige fat cells (beige adipocytes), or beige colorization of white fat, occur in the white fat under the skin of mice.
    beige fat cells have a similar heat-producing function with brown fat, which promotes energy consumption.
    white fat beige, the energy metabolism increased, the whole body metabolism has an improved effect, and can resist the high-fat diet induced obesity formation.
    p38 is an important stress-activated protein among members of the MAPK family and belongs to the serine/suine kinase.
    p38MAP3K/MKK/MAPK,。
    p38 includes four subtypes of alpha, beta, gamma and gamma, each with tissue-specific distribution.
    , p38 alpha is widely expressed in the whole body and is the main subtype of tissue expression in the liver, fat, etc.
    an earlier study by Yinghao's team found that p38 alpha in the liver regulates the process of sugar isogenicity (Jing Y, Liu W and et al. Journal of Hepatology 2014).
    But in fat, the effect of p38 alpha on energy metabolism has not been systematically studied.
    In the latest study, Ph.D. student Zhang Shengjie and others, under the guidance of researcher Ying Hao, found that the weight loss of mice after the specific removal of p38 alpha in adipose tissue, but the body temperature maintenance capacity and brown fat production function was largely unaffected.
    in the low temperature environment, after the absence of white fat p38 alpha can be observed a significant increase in beige fat cells than control, rice coloration activity increased.
    the mice with loss of adipose tissue p38 alpha increased significantly under the stimulation of the beta epinephrine receptor agonisant CL316,243.
    found that p38 alpha was missing or impaired by impaired activity by gene knockout mice and inhibitors, and that the weight gain of db/db mice was resistant to high-fat diet-induced obesity.
    through a series of in vitro level experiments, it was found that the activity of PKA and CREB in white fat cells increased at the same time after p38 alpha was missing, promoting the transcription almost expression of UCP1, accelerating the process of beige colorization of cells and increasing energy consumption.
    the study for the first time clarified the function of p38 alpha in the process of white fat beige, further revealing the specific mechanism of beigeization of white fat cells.
    provides a theoretical basis for the development of drugs to treat metabolic diseases such as obesity as a target for the development of adipose p38 alpha.
    the research received strong support and help from Huang Ruimin and Peng Chengyuan, a technical platform of the Shanghai Institute of Nutrition and Health, a researcher at the Shanghai Institute of Pharmaceutical Research of the Chinese Academy of Sciences, and Tang Wenjun, a researcher at the Shanghai Institute of Organic Chemistry of the Chinese Academy of Sciences.
    the subject was obtained by the Ministry of Science and Technology (2016YFA0500102, 2016YFC1304905), the National Fund Committee (31525012, 31600954,3 1371189, 81570768, 81471016) and support from the Chinese Academy of Sciences Research Fund (XDA12040324, XDA12020108).
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