Recipient organisationNIHR Birmingham Biomedical Research Centre
NIHR supportRecorded as supported by this research centre
PeriodMar 2025 — Jun 2025
In plain English
AI plain-English summary
Fat tissue from older adults with obesity releases tiny particles called extracellular vesicles that damage muscle cells, while fat from lean older adults does not. This matters because muscle loss accelerates with age, and obesity makes it worse—yet the biological reason for this difference has been unclear. The research points to a specific culprit: obesity reduces the number of protective stem cells in fat tissue, and the vesicles released by the remaining cells carry harmful protein and genetic cargo into muscle. If the team can show that vesicles from stem cells counteract this damage, it would open a path toward therapies that preserve muscle strength in older people with obesity. The immediate goal is fundamental science—understanding how these vesicles work and what their cargo contains. But similar discoveries about cell-to-cell communication via vesicles have already led to experimental treatments for tissue repair. A deeper grasp of this mechanism could eventually help people stay mobile and independent longer, reducing falls, hospitalisations, and the need for care.
View original technical description
One undesirable characteristic of ageing is loss of muscle strength and mass, which is more pronounced in people with obesity than in lean people. A possible mechanism for a difference in muscle loss between lean and obese older adults is via extracellular vesicles (EVs), tiny particles which are released by the cells in your body and can enter other cells to cause effects. These effects can be positive or negative in different circumstances. Our research suggests that EVs from fat tissue of older adults with obesity contain and transport small pieces of protein and genetic information, known as cargo, that can actually be harmful to the muscle cells that they enter. In contrast, the EVs from fat tissue of lean, healthy older adults does not appear to be harmful to muscle. One reason for this could be that fat tissue is made up of lots of different types of cells, but obesity can cause shifts in the amount of each cell type. One cell type that is less prominent in obese fat tissue is ‘stem cells’. Stem cells within fat tissue are important because they have been shown to have protective effects, so the decrease in stem cells with obesity might explain the difference in the effect of the EVs released. The proposed study will begin to examine whether the negative effect of EVs in obesity can be counteracted by EVs specifically from stem cells. By understanding how these EVs work, and by investigating their cargo, we aim to find ways to improve muscle health, particularly in ageing and obesity. This research could eventually lead to therapies that help people stay strong and independent as they age.
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