Abstract
ScopeWe investigate the effects of extracellular vesicles (EVs) obtained from in vitro adipocyte cell models and from obese subjects on glucose transport and insulin responsiveness.Methods and resultsEVs are isolated from the culture supernatant of adipocytes cultured under normoxia, hypoxia (1% oxygen), or exposed to macrophage conditioned media (15% v/v). EVs are isolated from the plasma of lean individuals and subjects with obesity. Cultured adipocytes are incubated with EVs and activation of insulin signalling cascades and insulin‐stimulated glucose transport are measured. EVs released from hypoxic adipocytes impair insulin‐stimulated 2‐deoxyglucose uptake and reduce insulin mediated phosphorylation of AKT. Insulin‐mediated phosphorylation of extracellular regulated kinases (ERK1/2) is not affected. EVs from individuals with obesity decrease insulin stimulated 2‐deoxyglucose uptake in adipocytes (p = 0.0159).ConclusionEVs released by stressed adipocytes impair insulin action in neighboring adipocytes.
Highlights
Scope: We investigate the effects of extracellular vesicles (EVs) obtained from and lipid regulation are impaired
To preserve any species compatibility that could affect the entrance of EVs into cells, we examined the effect of these EVs on insulin action in the Simpson–Golabi–Behmel syndrome (SGBS) human adipocyte cell line
We sought to investigate the hypothesis that EVs released by stressed adipocytes and those circulating in obese subjects could affect insulin action
Summary
Scope: We investigate the effects of extracellular vesicles (EVs) obtained from and lipid regulation are impaired. During in vitro adipocyte cell models and from obese subjects on glucose transport. EVs are isolated from the plasma cal hypoxia which contributes to the dysregulation of production and secretion of adipokines.[2] Adipocytes are exposed to pro-inflammatory cytokines following the recruitment, infiltration, and activaof lean individuals and subjects with obesity. EVs released from hypoxic adipocytes impair insulin-stimulated 2-deoxyglucose uptake and reduce insulin mediated phosphorylation of AKT. In recent years the importance of a novel mechanism for intercellular communication has emerged based on the release of extracellular vesicles (EVs).[3] EVs of various sizes, namely individuals with obesity decrease insulin stimulated 2-deoxyglucose uptake in exosomes
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