Obesity-Related Fat Tissue Signals Identified as a Driver of Age-Related Muscle Loss

Key Takeaways: 

• Researchers have identified a biological mechanism linking obesity-related fat tissue to accelerated muscle loss in older adults.
• Tiny particles released by adipose tissue were shown to directly trigger muscle atrophy in ageing human muscle cells.
• Younger muscle appears biologically protected from these effects, highlighting an age-dependent vulnerability that may inform future therapies.
  
  
  

New insight into sarcopenic obesity

Researchers at the University of Birmingham have identified a previously unrecognised biological pathway through which obesity may contribute to muscle loss in older adults. The findings provide important new insight into sarcopenic obesity, a condition in which excess body fat exists alongside reduced muscle mass and strength.

The study, published in the Journal of Cachexia, Sarcopenia and Muscle and conducted through the National Institute for Health and Care Research (NIHR) Birmingham Biomedical Research Centre (BRC), demonstrates for the first time that signals released from adipose tissue can directly induce muscle wasting in human cells.

Sarcopenic obesity is becoming increasingly common as populations age and is associated with frailty, impaired mobility and poorer overall health outcomes. The condition is estimated to affect approximately 11% of the population.

Fat tissue communication with muscle

The research focused on extracellular vesicles – microscopic particles released by fat tissue that act as biological messengers between organs and tissues.

Investigators discovered that extracellular vesicles derived specifically from obese adipose tissue, rather than lean tissue, caused significant thinning of muscle fibres obtained from older adults. This thinning represents a hallmark feature of muscle atrophy.

The harmful effects were traced to molecular cargo carried within these vesicles, particularly miR-150-5p, a microRNA known to regulate gene expression pathways involved in maintaining muscle structure and function.

These findings suggest that obesity does not simply increase fat mass but fundamentally alters how adipose tissue behaves and communicates with other organs, including skeletal muscle.

Age-dependent vulnerability of muscle

A notable finding of the study was that muscle cells derived from younger adults showed resistance to these obesity-related signals.

When exposed to extracellular vesicles from obese adipose tissue, younger muscle cells did not undergo the same degree of thinning observed in older muscle cells. This indicates that ageing muscle becomes biologically more susceptible to inflammatory and metabolic signals associated with obesity.

Speaking about the findings, first author Dr Joshua Price, Postdoctoral Researcher, explained:

“It isn’t just having more fat tissue that matters. Obesity changes how fat tissue behaves and how it communicates with muscle. Ageing muscle is far more vulnerable to these altered signals, which helps explain why muscle loss accelerates with obesity later in life.”

Identifying a potential therapeutic target

The identification of miR-150-5p as a key molecular driver presents a potential opportunity for therapeutic intervention. Researchers found that inhibiting this microRNA could partially reduce the muscle-wasting effects observed in laboratory models.

Overall, the results suggest a dual biological reality – younger muscle demonstrates protective resilience, while ageing muscle becomes increasingly vulnerable to obesity-related signalling pathways.

Senior author Professor Simon Jones, Professor in Musculoskeletal Ageing at the University of Birmingham and lead for the NIHR Birmingham BRC’s Sarcopenia and Multimorbidity research theme, said:

“Through this research, we’ve identified a key molecular pathway by which obesity can accelerate muscle loss in older adults. Importantly, we found that younger muscle appears resilient to these harmful signals, whereas ageing muscle becomes more vulnerable. This reinforces the importance of maintaining a healthy weight and muscle health as we age.”

He added:

“Our findings also open two potential therapeutic avenues: either blocking or modifying the harmful extracellular vesicles released from obese tissue, or developing strategies to make older muscle more resilient, mimicking the protective effects seen in younger muscle.”

Implications for ageing and obesity care

The study strengthens understanding of how ageing and obesity interact at a cellular level to influence physical decline. Rather than viewing muscle loss solely as a consequence of ageing or inactivity, the findings highlight obesity-related biological signalling as an active contributor.

By demonstrating that altered communication between fat and muscle tissue can directly drive muscle atrophy, the research provides a clearer mechanistic explanation for why people living with obesity may experience accelerated functional decline later in life.

The work was delivered through the NIHR Birmingham Biomedical Research Centre, with Dr Joshua Price serving as a BRC-funded postdoctoral research associate within the Sarcopenia and Multimorbidity research theme.

Together, these findings may support future strategies aimed at preserving muscle health in ageing populations, particularly among people living with obesity, where preventing muscle loss is critical for maintaining independence, mobility and long-term health outcomes.