The influence of mitochondrial-targeted antioxidant supplementation of acute hyperglycemia-induced vascular dysfunction

PURPOSE: To determine if an underlying mechanism by which acute hyperglycemia induces endothelial dysfunction is mediated by mitochondrial-derived reactive oxygen species (mtROS). We hypothesized that mitochondrial-targeted antioxidant, MitoQ, will acutely (single dose, 80 mg) attenuate the decline in endothelial function from acute hyperglycemia. METHODS: Eleven apparently healthy, active adults (n=11, 7M/4F, age: 43.8±6.5 yrs) performed two research trials (placebo and MitoQ) from a double-blind, randomized, crossover control study design. Participants underwent a blood draw and measures of vascular endothelial function, assessed via brachial artery flow-mediated dilation (FMDBA) before (baseline) and 1 hr. after oral consumption of 75g glucose. RESULTS: Acute hyperglycemia did not lower FMDBA (%) in either the placebo (6.85±0.65 to 5.68±0.65 %) or MitoQ (6.53±0.90 to 6.17±1.00%) groups (p=0.447). No difference was detected in blood glucose concentrations from either placebo (94.4±2.1 to 106.6±15.3 mg/dL) or MitoQ (95.7±3.2 to 106.2±13.9 mg/dL) pre- to post- consumption of the oral glucose load (p=0.920). Additionally, no difference was detected in blood insulin concentrations from either placebo (6.8±1.2 to 49.4±14.7 IU/mL) or MitoQ (7.4±1.7 to 44.8±13.7 IU/mL) pre- to post- consumption of the oral glucose load (p=0.776). A main effect for time was detected for insulin from pre- to post- oral glucose load on placebo and MitoQ trials (p<0.001). CONCLUSIONS: An acute dose of mitochondrial-targeted antioxidant, MitoQ, had no effect on vascular endothelial function or glucose and insulin responses in response to acute hyperglycemia. Additional research is needed to examine if fitness or physical activity status play a role in this relationship between MitoQ supplementation and acute hyperglycemia-induced vascular dysfunction.