Why the study?
In obesity and related metabolic disorders, alterations in extracellular vesicles associate with cardiovascular complications, but how postprandial metabolism and diet reshape EV profiles and function required critical appraisal.
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Design
Narrative review
EV alterations in obesity associate with endothelial dysfunction; leaves open their causal role or utility as CVD biomarkers.
Obesity is a major global health burden closely linked to cardiovascular complications, particularly cardiovascular disease (CVD). Extracellular vesicles (EVs), membrane-bound particles released by most cell types, mediate intercellular communication by transporting bioactive lipids, proteins, and nucleic acids. In obesity and related metabolic disorders, shifts in EV abundance, cellular origin, and cargoes have been associated with endothelial dysfunction, insulin resistance, and thrombo-inflammation. This narrative review critically appraises how postprandial metabolism reshapes the EV profile and functionality, integrating recent omics-based and mechanistic studies while distinguishing association from causality. We also examine diet-EV interactions, including how the quantity and quality of dietary fat may reprogramme EV lipids and miRNA cargoes. Evidence for food-derived EVs is emerging, but currently supports only partial gastrointestinal resistance and context-dependent bioactivity. Throughout, we highlight key methodological constraints and emphasize pre-analytical adherence to MISEV guidelines to improve reproducibility and translational relevance. Collectively, clarifying EV dynamics in the postprandial state may advance their use as clinically meaningful biomarkers and potential targets for mitigating obesity-related metabolic dysfunction through informed dietary and lifestyle interventions.
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Marquez‐Paradas et al. (2025) studied this question.
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