Recent research highlights a potentially groundbreaking antibody treatment that might counteract muscle and bone deterioration in individuals using GLP-1 drugs such as Ozempic and Wegovy.
Aging, combined with limited physical activity and the use of advanced weight loss drugs like Wegovy and Zepbound, often results in the concurrent deterioration of muscle mass and bone density. While medications are available to address bone loss, treatments specifically targeting muscle mass reduction are not yet approved. However, a recent study conducted on mice has revealed that bimagrumab, an antibody treatment, effectively prevents the decline in both bone density and muscle mass.
The research, published in the Journal of Cachexia, Sarcopenia, and Muscle, suggests that bimagrumab not only increases muscle mass but also enhances bone density in mice experiencing muscle and bone loss. This discovery indicates that bimagrumab could become a vital tool for those using GLP-1 drugs and others experiencing muscle and bone loss due to aging.
Frederik Duch Bromer, a researcher from Aarhus University in Denmark, emphasized the significance of these findings, stating, ‘Since the rise of incretin therapies like Wegovy and Mounjaro, scientists have been searching for ways to counteract the loss of muscle and bone mass often accompanying rapid weight loss. Our research shows that bimagrumab can mitigate even more severe muscle and bone loss than what typically occurs with weight loss therapies.’ This reveals potential new uses for bimagrumab in preserving lean mass during weight loss while also protecting bone.
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The mechanism behind bimagrumab involves inhibiting the activin signaling pathway, a process linked with increased muscle mass and bone formation, as well as improved blood cell formation. The antibody binds to activin receptors, thereby blocking their activation. Although the use of GLP-1 receptor agonists often associates with muscle mass loss and bone density decrease, bimagrumab is being closely studied for its ability to counteract these effects without adversely impacting blood cell production.
In the study, bimagrumab injections were administered to mice suffering induced muscle paralysis and subsequent bone density decline. After a 21-day treatment period, results showed that bimagrumab increased both muscle mass and bone mineral density in these mice, suggesting a protective effect on muscle and bone health. Despite the potent action of botulinum toxin causing less pronounced effects in immobilized mice, bimagrumab’s positive impact remained evident.
The treatment was also noted for its potential safety in humans. Initial evaluations indicated that bimagrumab did not notably affect blood cell formation or related factors, an essential consideration given the risk of blood clots associated with such treatments. Nevertheless, further research and extensive clinical trials are necessary to thoroughly determine its safety and efficacy in human subjects.
Bromer also highlighted the need to examine bimagrumab’s interaction with bones impacted by obesity. Since weight loss drugs primarily target individuals with obesity, understanding how bimagrumab can aid in preserving bone affected by obesity is crucial moving forward.
The promising results from this study suggest that bimagrumab may become a key asset in combating muscle and bone loss associated with GLP-1 drugs and aging. However, further research is imperative to confirm its efficacy and safety in humans.
