Key result
Extracellular vesicles derived from adipose tissue act as endocrine mediators that can modulate insulin resistance and metabolic adaptation through the PI3K/Akt/mTOR signaling pathway.
Why the study?
Characterizing the molecular fingerprint of obesity-related ADEVs may provide a clearer picture of metabolic adaptation through PI3K/Akt/mTOR.
This review highlights the potential role of adipose tissue-derived extracellular vesicles in mediating obesity-related metabolic diseases and insulin resistance via the PI3K/Akt/mTOR pathway.
May guide research into EV-based interventions for metabolic disorders; leaves open clinical translation pending rigorous trials.
Extracellular vesicles (EVs) are nanoparticles secreted by cells under physiological and pathological conditions, such as metabolic diseases. In this context, EVs are considered potential key mediators in the physiopathology of obesity. It has been reported that EVs derived from adipose tissue (ADEVs) contribute to the development of a local inflammatory response that leads to adipose tissue dysfunction. In addition, it has been proposed that EVs are associated with the onset and progression of several obesity-related metabolic diseases such as insulin resistance. In particular, characterizing the molecular fingerprint of obesity-related ADEVs can provide a bigger picture that better reflects metabolic adaptation though PI3K/Akt/mTOR. Hence, in this review we describe the possible crosstalk communication of ADEVs with metabolically active organs and the intracellular response in the insulin signaling pathway.
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Delgadillo‐Velazquez et al. (2022) conducted a review in Obesity and Insulin Resistance. Adipose tissue-derived extracellular vesicles (ADEVs) was evaluated. Extracellular vesicles derived from adipose tissue act as endocrine mediators that can modulate insulin resistance and metabolic adaptation through the PI3K/Akt/mTOR signaling pathway.
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