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June 3, 2022Cells13 citationsOpen Access

Extracellular Vesicles from Adipose Tissue Could Promote Metabolic Adaptation through PI3K/Akt/mTOR

JDJaime Delgadillo‐VelazquezHMHerminia Mendivil-AlvaradoCCCarlos D. Coronado-Alvarado

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.

PICO

P
Population
Obesity and Insulin Resistance
E
Exposure / Comparator
Adipose tissue-derived extracellular vesicles (ADEVs)

Limitations

  • Differences in results across studies may be due to different methodological approaches.
  • More studies are needed to analyze the content of EVs and their impact on insulin-dependent tissues.
  • Lack of standardized procedures for the study of ADEVs.

Abstract

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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Cite This Study

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.

synapsesocial.com/papers/6a9840b1e8073bac3ed7dc10https://doi.org/10.3390/cells11111831
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