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Nat Metab ; 6(5): 880-898, 2024 May.
Artigo em Inglês | MEDLINE | ID: mdl-38605183

RESUMO

The obesity epidemic continues to worsen worldwide, driving metabolic and chronic inflammatory diseases. Thiazolidinediones, such as rosiglitazone (Rosi), are PPARγ agonists that promote 'M2-like' adipose tissue macrophage (ATM) polarization and cause insulin sensitization. As ATM-derived small extracellular vesicles (ATM-sEVs) from lean mice are known to increase insulin sensitivity, we assessed the metabolic effects of ATM-sEVs from Rosi-treated obese male mice (Rosi-ATM-sEVs). Here we show that Rosi leads to improved glucose and insulin tolerance, transcriptional repolarization of ATMs and increased sEV secretion. Administration of Rosi-ATM-sEVs rescues obesity-induced glucose intolerance and insulin sensitivity in vivo without the known thiazolidinedione-induced adverse effects of weight gain or haemodilution. Rosi-ATM-sEVs directly increase insulin sensitivity in adipocytes, myotubes and primary mouse and human hepatocytes. Additionally, we demonstrate that the miRNAs within Rosi-ATM-sEVs, primarily miR-690, are responsible for these beneficial metabolic effects. Thus, using ATM-sEVs with specific miRNAs may provide a therapeutic path to induce insulin sensitization.


Assuntos
Tecido Adiposo , Vesículas Extracelulares , Resistência à Insulina , Macrófagos , Rosiglitazona , Animais , Rosiglitazona/farmacologia , Vesículas Extracelulares/metabolismo , Vesículas Extracelulares/efeitos dos fármacos , Camundongos , Macrófagos/metabolismo , Macrófagos/efeitos dos fármacos , Tecido Adiposo/metabolismo , Tecido Adiposo/efeitos dos fármacos , Masculino , Humanos , MicroRNAs/genética , MicroRNAs/metabolismo , Obesidade/metabolismo , Insulina/metabolismo , Adipócitos/metabolismo , Adipócitos/efeitos dos fármacos , Camundongos Endogâmicos C57BL
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