Experimental drug raises energy expenditure but fails to activate brown fat in human study
Brown fat burns energy to generate heat and is therefore considered a promising target for new obesity treatments. Researchers at the University of Basel and University Hospital Basel have tested whether a drug can activate brown fat in humans. Their results show that a pharmaceutical approach may be more difficult than expected.
Researchers at the University of Basel and University Hospital Basel have tested a drug that may affect brown fat activation in humans. Brown fat burns energy to generate heat and is seen as a potential target for obesity treatments. Unlike white fat that stores energy, brown adipose tissue consumes energy to produce heat; leaner individuals tend to have more active brown fat.
Cold exposure is a natural trigger for brown fat activation. Researchers explored whether stimulating the beta2-adrenergic receptor with a drug called fenoterol could activate brown fat in humans. A study of 11 healthy volunteers found that both mild cold exposure and fenoterol increased energy expenditure, but only cold exposure clearly activated brown fat.
After cold exposure, brown fat tissue consumed more glucose compared to fenoterol treatment. Dr. Matthias Betz stated that increased energy expenditure with fenoterol does not necessarily mean brown fat activation occurred. The researchers are uncertain about the source of the additional energy consumption with fenoterol, which may involve other tissues like skeletal muscle or white adipose tissue.
The findings suggest a more complex regulation of brown fat in humans, potentially involving multiple receptors or biological signals working together. Understanding brown adipose tissue regulation could be crucial for developing effective obesity treatments, as current weight-loss drugs only reduce appetite but can lower energy expenditure over time.
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