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. 2020 Jul 29;7:171. doi: 10.3389/fmolb.2020.00171

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Copyright © 2020 Zhou and Tan.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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The roles of miRNAs and other cargoes mentioned in the text contained in adipocyte-derived EVs in regulating metabolism and development of obesity-associated disease. ^∗The cargoes in adipocyte-derived EVs adjust in physiological and pathological states. Cold stimulation down regulates the circulating miR-92a in EVs of adipose tissue. Adipocytes may receive EVs that contain membrane proteins from endothelial cells, then transport these proteins into adipocyte-derived EVs. Glucagon signaling enhanced endothelial cell uptake and packaging of extracellular cargos into EVs in mice fed a high-fat diet. ^∗Adipose−derived EVs mediate inter−organ cross-talk. The miR-99b in adipocyte-derived EVs regulated gene expression in the liver. Adipocyte-derived EV-associated MALAT1 regulated signaling in hypothalamic POMC neurons. In obesity, miR-141-3p in adipocyte-derived EVs promoted insulin resistance in hepatocytes and miR-27a in adipocyte-derived EVs promoted insulin resistance in skeletal muscle cells. ^∗Adipose−derived EVs mediate inter−organ cross-talk. Adipose−derived EVs regulate intra−organ cross-talk between adipocytes and ATM. The miR-155 in adipocyte-derived EVs modulates of M1 macrophage polarization. The miR-34a in adipocyte-derived EVs inhibits of M2 polarization. The miRNA 23a/b in adipose−derived EVs promotes hepatic cancer cell growth, migration, and development of chemoresistance. ^∗Adipocyte-derived EVs act as an intermediary between hormones and cells. Melatonin administration increases levels of α−ketoglutarate in EVs secreted by adipocytes; these EVs then promote M2 macrophage activation through increased α−ketoglutarate levels in macrophages.