It is different from the usual fat, the ‘sworn enemy’ of many, a torment when it accumulates around the belly and thighs. Brown fat, also known as Bat (brown adipose tissue), is another type of fat present in our body and has a special mission: it helps burn the calories from the foods we consume by transforming them into heat, which can be useful, especially when we are exposed to cold temperatures such as during winter swimming or cryotherapy. For a long time, scientists thought that only newborns and small animals like mice had it. But new research shows that a number of adults retain brown fat throughout their lives. AND Scientists are looking for a way to activate it safely using drugs that increase its capacity to produce heat, and exploiting its effectiveness in burning calories. New work reveals a possible ‘switch’.
In detail, the research groups of Jan-Wilhelm Kornfeld of the University of Southern Denmark/Novo Nordisk Center for Adipocyte Signaling (Adiposign) and of Dagmar Wachten of the University Hospital and the University of Bonn (Germany) have discovered that a mechanism previously unknown supplement that turns off brown fat immediately after being activated. This limits its effectiveness as an obesity treatment, experts point out. According to the study’s first author, Hande Topel, the ‘key’ is a protein responsible for this shutdown process. It’s called ‘AC3-AT’.
“Looking ahead, we believe that finding ways to block AC3-AT could be a promising strategy for safely activate brown fat and address obesity and related health problems“, says the expert. The research team found the switch-off protein using advanced technology: “When we studied mice that genetically lacked AC3-AT, we found that they were protected from becoming obese, partly because their bodies they were simply better at burning calories and were able to increase their metabolic rates by activating brown fat.”
The scientists then fed two groups of mice a high-fat diet for 15 weeks, which made them obese. The group that had the AC3-AT protein removed gained less weight than the control group and was metabolically healthier. “These mice also had increased lean mass compared to control mice,” points out co-author Ronja Kardinal. “Because AC3-AT is found not only in mice, but also in humans and other species, there are direct therapeutic implications for humans.”
Although the prevalence of brown fat decreases with agingand although adults do not have as much as newborns, brown fat can still be activated, for example by exposure to cold, and increases people’s metabolism rate, which can help stabilize weight loss in conditions where calorie intake is (too) high. The researchers also identified other unknown versions of proteins/genes, which respond to cold exposure, similar to AC3-AT. “However – Wachten points out – further research is needed to clarify the therapeutic impact of these alternative genetic products and their regulatory mechanisms” during the activation of brown fat.
“Understanding these types of molecular mechanisms not only sheds light on the regulation of brown fat, but also promises to unveil similar mechanisms in other cellular pathways. This knowledge can be instrumental in improving our understanding of various diseases and in the development of new treatments,” concludes Kornfeld.
