Lying thin is going to come true! Scientists have found the right way to turn on the body's "fat-burning" switch.

Read: If a pharmacological method of activating brown fat can be developed, obese people can achieve weight loss goals even if they don't exercise.
is known to have two types of fats, white fat (WAT) and brown fat (BAT), which are the "causes" of obesity, and the latter are the "stars" of obesity, which, at low temperatures or chemical stimulation, can promote the breakdown of white fat through fatty acid oxidation and heat, and speed up metabolism.
, if a drug can be developed to activate brown fat, obese people can achieve their weight loss goals even if they don't exercise.
sad, however, current pharmacological lysons that activate human BAT 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 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 effect of brown fat, it is necessary to mention the beta epinephrine receptor (beta-AR), which mediates metabolic changes including glycoenzyme and fat breakdown.
the receptor is divided into beta 1, beta 2 and beta 3 subtypes, where beta 3-AR has previously been shown to activate the bat in mice to consume excess energy, improve metabolic health, which is why it is thought that the receptor is also likely to play the same role in the human body.
However, in recent years, the beta 3-AR agonisant Mirabegron, a drug used to treat bladder hyperactivity, has underperformed in clinical trials to treat obesity. in the new study,
, researchers explore the causes.
wrong BAT targets first, the researchers studied the role of Mirabegron in activating BAT and promoting energy consumption throughout the body.
after comparing the oxidation metabolism of BAT in low-temperature environments (18 degrees C) and Mirabegron-induced by healthy people, the researchers found that low-temperature environments caused bat activity far greater than the results mediated by Mirabegron at the maximum permissible dose (200 ug).
in low-temperature environments, low doses (50ug) and high-dose (200ug) Mirabegron, the human hormone and metabolite concentrations were found to be associated with an 86% increase in the energy consumption of mirabegron at the highest allowable dose (200ug) independent of BAT activation, and a large proportion of the total fatty acids released after intracellular lactation remained in place and eventually re-esterationated at the main site of the lipid solution.
, beta 3-AR may not be a bat-activated switch.
, the researchers then obtained RNA sequencing data from BAT cells in the deep neck region and compared it with BAT data from mice, which showed that beta 3-AR (ADRB3) was the main beta-AR subtype in the bat in mice, almost undetectable in the human body, while beta 2-RB2 was present in human BAT, followed by 1-AR (ADRB1).
RNA sequencing analysis determined that the relative gene expression of beta-AR subtypes in the deep neck adipose biopsy is the key to activating human BAT, and that the bat "unlocking" of mice and humans is different? To test this, the researchers looked at the largest lipid dissolution reaction strain of human immortal cells cultured by beta 2-AR agonists formoterol, beta-3-AR agonium mirabegron, and found that mirabegron needed a higher concentration to produce the largest fat-soluble reaction in the case of the beta 2-AR antagonic ICI-118551, and found that the maximum lipid-dissolved reaction was inhibited by the beta-2-AR agonis, the beta-3-AR agonium mirabegron cultured with the largest lipid response.
these results suggest that beta 2-AR may be the key to activating the body's BAT.
in subsequent experiments, the researchers took BAT cells from four volunteers and knocked out small interfering RNA (siRNA) in ADRB2, where ADRB2 mRNA levels were effectively reduced.
in this case, the non-conjugated breathing of BAT cells mediated by norepinephrine and beta 2-AR agonists formoterol decreased significantly, indicating a decrease in BAT heat production.
, the researchers simultaneously performed instantaneous knockout of three beta-AR receptors and found that norepinephrine-stimulated non-conjugated breathing decreased only in the case of ADRB2 knockout.
brown fat cell beta-2-AR knockout weakens the effects of heat production, said the findings have clear therapeutic applications, according to the paper's author, Camilla Sch?el, an associate professor at the University of Copenhagen's School of Health and Medicine.
" the activation of brown fat can burn calories, increase insulin sensitivity, and even affect appetite.
our data reveal seduing the previously unknown key to unlocking human functions, which could be significant for people with obesity or type 2 diabetes."
in all, this study shows that beta 2-AR is an essential ingredient in the heat production and decomposition of white fat in human BAT cells.
next, the researchers plan to launch a second phase of research this fall to test its effectiveness in fat burning by activating brown fat by using a drug that targets beta 2-AR.
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