Researchers have identified a protein that can deactivate brown fat. This new finding may offer a potential approach to safely activating brown fat to address obesity and its related health issues. Brown fat, also known as brown adipose tissue (BAT), is a type of fat in our bodies that is different from the white fat around our midsection and thighs. Brown fat plays a unique role in burning calories from the foods we consume into heat, which can be beneficial, particularly in cold conditions such as during winter swimming or cryotherapy.For a long time, researchers believed that only small animals like mice and newborns had brown fat. However, recent studies show that a certain number of adults maintain their brown fat throughout life. Because brown fat is highly effective at burning calories, scientists are trying to discover safe ways to activate it using drugs that enhance its heat-producing abilities.
A new study from the research groups of Prof. Jan-Wilhelm Kornfeld from the University of Southern Denmark/the Novo Nordisk Center for Adipocyte Signaling (Adiposign) and Dagmar Wachten from the University Hospital Bonn and the University of Bonn (Germany) has found that brown fat has a built-in mechanism that turns it off shortly after it is activated, limiting its effectiveness as a treatment for obesity. Senior Postdoc Hande Topel, from the University of Southern Denmark and the Novo Nordisk Center for Adipocyte Signaling (Adiposign), identified a protein called ‘AC3-AT’ responsible for this switching-off process.
The discovery of this protein opens up a new strategy for obesity treatment. The team believes that finding ways to block AC3-AT could be a promising approach for safely activating brown fat.
“We have discovered a potential key player in regulating brown fat and addressing obesity and its associated health issues,” Hande Topel said. The team of researchers utilized cutting-edge technology to identify a previously unknown protein responsible for turning off certain functions. Hande Topel elaborated on the findings, stating, “After studying mice that were genetically lacking in AC3-AT, we observed that they were less prone to obesity. This was due in part to their bodies’ enhanced ability to burn calories and their increased metabolic rates resulting from the activation of brown fat.”
Throughout a 15-week period, two sets of mice were subjected to a high-fat diet, causing them to become obese. The group of mice without the AC3-AT protein gained less weight compared to the control group
The study found that mice without the AC3-AT protein were able to accumulate less body fat and increase their lean mass compared to the control group. Ronja Kardinal, a PhD student at the University of Bonn, explained that the findings have direct therapeutic implications for humans since the AC3-AT protein is also found in humans and other species. The research brings hope for strategies that can support weight loss, despite the decrease in brown fat as humans age and the difference in brown fat levels between newborns and adults.The activation of AC3-AT can still occur through cold exposure. This activation can increase the metabolism rate of individuals, which may help stabilize weight loss even in situations where calorie intake is high. Additionally, the study revealed the existence of AC3-AT, a shorter version of the AC3 protein, along with other unknown protein/gene versions that respond to cold exposure like AC3-AT.
However, further research is required to understand the therapeutic effects of these alternative gene products and their regulatory mechanisms.co-author Prof. Dagmar Wachten, who is also the Co-Director of the Institute of Innate Immunity at the UKB and a member of the Cluster of Excellence ImmunoSensation2 and the Transdisciplinary Research Areas (TRA) “Modelling” and “Life & Health” at the University of Bonn. Wachten emphasizes the importance of understanding the molecular mechanisms involved in BAT activation, as it not only provides insight into the regulation of brown fat, but also has potential implications for understanding similar mechanisms in other cellular pathways. This knowledge could be crucial in advancing our understanding of various diseases and in the development of new treatments.author Prof. Jan-Wilhelm Kornfeld from the University of Southern Denmark conducted this study within the DFG Collaborative Research Center Transregio-SFB 333 “Brown and Beige Fat — Organ Interactions, Signaling Pathways and Energy Balance (BATenergy).” The center is focused on gaining a deeper insight into the various adipose tissues and their involvement in metabolic diseases. Additionally, the study was conducted in collaboration with the Novo Nordisk Foundation Center for Adipocyte Signaling (Adiposign) at the University of Southern Denmark, which is dedicated to comprehending fat cell dysfunction in model organisms and obese patients.
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