echemi logo
Product
  • Product
  • Supplier
  • Inquiry
    Home > Medical News > Medical World News > Disrupt tradition! Scientists have found the right way to turn on the body's "fat-burning" switch.

    Disrupt tradition! Scientists have found the right way to turn on the body's "fat-burning" switch.

    • Last Update: 2020-08-23
    • Source: Internet
    • Author: User
    Search more information of high quality chemicals, good prices and reliable suppliers, visit www.echemi.com
    It is well known that the human body has white fat (WAT) and brown fat (BAT) two types of fat, the former is the cause of obesity, while the latter is the obesity of the "star", in low temperature or chemical stimulation, through fatty acid oxidation and heat to promote the decomposition of white fat, speed up metabolism.
    that if a pharmacologically activated approach to brown fat can be developed, obese people can achieve their weight loss goals even if they don't exercise.
    sad that current pharmacologically activated human BAT experiments often fail.
    recently, researchers from the University of Copenhagen in Denmark and the University of Sherbrooke in Canada have finally found an effective way to turn on the "fat-burning" switch in the human body, which will help develop new treatments for obesity and type 2 diabetes.
    study was published in Cell Metabolism on August 4, local time.
    doi.org/10.1016/j.cmet.2020.07.005 When it comes to the fat-burning effects of brown fat, it is important to mention the beta-epinephrine receptabinoid (beta-AR), which mediats metabolic changes including glycolysis and fat decomposition.
    The receptament is divided into beta 1, beta 2 and beta 3 sub-types, where beta-3-AR has previously been shown to be the key to activating BAT in mice to consume excess energy and improve metabolic health, which is why it is thought that the receptament is likely to play the same role in the human body."
    , however, in recent years the beta-AR agitant Mirabegron, a drug used to treat bladder overactiveness, has underperformed in clinical trials to treat obesity.
    the new study, researchers explored why.
    the wrong BAT target, the researchers looked at Milabegron's role in activating BAT and promoting energy consumption throughout the body.
    After comparing the metabolism of BAT oxidation in slim healthy people at low temperatures (18 degrees C) and those stimulated by Mirabegron, the researchers found that low-temperature environments caused BAT activity that far exceeded the effects of Mirabegron-mediated at the maximum allowable dose (200ug).
    At the same time as human hormone and metabolite concentrations at low temperatures, low doses (50ug) and high doses (200ug) Mirabegron, the researchers found that 86% of the increased energy consumption of mirabegron at the maximum allowable dose (200ug) was actually independent of BAT activation, and that a significant proportion of the total fatty acids released after lipid solution in cells remained in place and eventually re-esterified at the main site of lipid solution.
    that is, beta-3-AR may not be the switch that activates BAT.
    Thus, the researchers obtained RNA sequencing data from BAT cells in the deep neck region from a previous study and compared it with BAT data from mice, which showed that beta-AR (ADRB3) was the main beta-AR subtope in mouse BAT, almost undetectable in humans, while beta-AR (ADRB2) was present in large quantities in human BAT, followed by beta-1-AR ADRB1.
    RNA sequencing analysis to determine the relative gene expression of beta-AR subtypes of the three beta-AR subtypes in deep neck adipose biopsies is the key to activating human BAT. To verify this, the researchers looked at the maximum lipid desolation reaction of permanent biochemical cells cultured by beta-AR agonists formoterol and beta-AR agonists milabegron with and without beta-AR antagonists ICI-118551, and found that mirabegron needed to reach a higher concentration to produce the maximum liposol reaction, and that ICI-118551 inhibited the reaction.
    these results suggest that beta-2-AR may be the key to activating human BAT.
    subsequent experiment, the researchers took BAT cells from four volunteers and knocked out small interfering RNA (siRNAs) in ADRB2, at which point ADRB2 mRNA levels were effectively reduced.
    in this case, the non-contective respiration of BAT cells mediated by the epinephrine and beta-AR agitator formoterol decreased significantly, indicating a decrease in BAT heat production.
    addition, the researchers performed instantaneous knockouts on three beta-AR receptors and found that non-contone breathing stimulated by epinephrine was reduced only in the case of ADRB2 knockout.
    , associate professor of health and medicine at the University of Copenhagen and co-author of the report that brown fat cell beta-2-AR knock-out weakens heat production, said the findings have clear therapeutic applications.
    " brown fat consumes calories, increases insulin sensitivity, and even affects appetite.
    our data reveal previously unknown keys to unlocking these functions in humans, which could be significant for people with obesity or type 2 diabetes."
    , this study shows that beta-2-AR is an essential component of human BAT cells to produce heat and break down white fat.
    , the researchers plan to conduct a second phase of the study this fall, using drugs that target beta-2-AR to activate brown fat to verify its effect on fat burning.
    .
    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.