Mechanical overload-induced muscle-derived extracellular vesicles promote adipose tissue lipolysis

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The Department of Physiology and Center for Muscle Biology study published in the FASEB Journal found that resistance-like exercise regulates fat cell metabolism at a molecular level.

The study results in mice and humans show that in response to mechanical loading, muscle cells release particles called extracellular vesicles that give fat cells instructions to enter fat-burning mode.

Extracellular vesicles were initially understood as a way for cells to selectively eliminate proteins, lipids and RNA. Recently, scientists discovered that they also play a role in intercellular communication.


How regular physical activity is able to improve health remains poorly understood. The release of factors from skeletal muscle following exercise has been proposed as a possible mechanism mediating such systemic benefits. We describe a mechanism wherein skeletal muscle, in response to a hypertrophic stimulus induced by mechanical overload (MOV), released extracellular vesicles (EVs) containing muscle-specific miR-1 that were preferentially taken up by epidydimal white adipose tissue (eWAT). In eWAT, miR-1 promoted adrenergic signaling and lipolysis by targeting Tfap2α, a known repressor of Adrβ3 expression. Inhibiting EV release prevented the MOV-induced increase in eWAT miR-1 abundance and expression of lipolytic genes. Resistance exercise decreased skeletal muscle miR-1 expression with a concomitant increase in plasma EV miR-1 abundance, suggesting a similar mechanism may be operative in humans. Altogether, these findings demonstrate that skeletal muscle promotes metabolic adaptations in adipose tissue in response to MOV via EV-mediated delivery of miR-1.

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Nelson Vergel

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Scientists think that when we exercise, our muscles release tiny particles called extracellular vesicles (EVs) that can travel through our body and do good things. In this study, researchers found that when mice did a certain type of exercise that made their muscles bigger (called mechanical overload), their muscles released EVs that contained a special molecule called miR-1. These EVs traveled to fat cells in their body and gave them a signal to start burning fat. This happened because miR-1 turned off a gene that normally stops fat cells from burning fat. When the researchers stopped the muscle cells from releasing EVs, the fat cells didn't burn as much fat. They also found that when people did resistance exercise, their muscles released miR-1 in a similar way. This means that when we exercise, our muscles can talk to our fat cells and help them stay healthy.
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