An oral glucose load decreases postprandial extracellular vesicles in obese adults with and without prediabetes

Although extracellular vesicles (EVs) are a novel biomediator of type 2 diabetes (T2D) and cardiovascular disease (CVD), the effects of hyperglycemia on EVs in humans is unknown. We tested the hypothesis that a 75-g oral glucose tolerance test (OGTT) would promote changes in EVs in relation to CVD risk. Twenty-five obese adults (Age: 52.4 ± 3.2 year, BMI: 32.5 ± 1.2 kg/m²) were screened for normal glucose tolerance (NGT, n = 8) and prediabetes (PD, n = 17) using American Diabetes Association criteria (75 g OGTT and/or HbA1c). Body composition (bioelectrical impedance) and fitness (VO₂peak) were measured. Arterial stiffness (augmentation index; AIx) was measured at 0, 60- and 120-min while insulin, glucose, and free fatty acids were evaluated every 30 min during the OGTT to assess CVD risk. Annexin V positive (AV+) and Annexin V negative (AV−) total EVs, platelet EVs (CD31⁺/CD41⁺; CD41⁺), leukocyte EVs (CD45⁺; CD45⁺/CD41−), platelet endothelial cell adhesion molecule (PECAM) (CD31⁺) and endothelial EVs (CD 31⁺/CD41⁻; CD105⁺) were collected at 0 and 120 min. There were no differences in age, BMI, or body fat between NGT and PD (all P > 0.63). Total EVs, AV+ CD31⁺ (PECAM), and AV⁺ CD31⁺/CD41⁻ (endothelial) EVs decreased after the OGTT (P ≤ 0.04). Circulating insulin at 2-h correlated with elevated post-prandial AV− CD45⁺ (r = 0.48, P = 0.04) while arterial stiffness related to reduced total EVs (r = −0.49, P = 0.03) and AV+ CD41⁺ (platelet) (r = −0.52, P = 0.02). An oral glucose load lowers post-prandial total, platelet, and endothelial EVs in obese adults with NGT and prediabetes in relation to CVD risk.