Reduced venous endothelial responsiveness after oral lipid overload in healthy volunteers.

The aim of this study was to investigate endothelial venous function, inflammatory markers, and systemic oxidative stress after an oral lipid overload (OLO). We studied 18 healthy adults (9 men; age, 29.2 +/- 0.9 years; body mass index, 22.3 +/- 0.4 kg/m(2)). Blood samples were collected in the fasting state and 3, 4, and 5 hour after the OLO (1000 kcal, 58% fat) for metabolic variables, oxidative stress, inflammatory markers, adiponectin, and resistin. Changes in vein diameter to phenylephrine, acetylcholine, and sodium nitroprusside (dorsal hand vein technique) were measured before and after the OLO. Oral lipid overload increased triglycerides (61 +/- 6 vs 134 +/- 17 mg/dL, P < .001), insulin (7.2 +/- 0.8 vs 10.7 +/- 1.3 muU/mL, P < .05), and resistin (5.38 +/- 0.5 vs 6.81 +/- 0.7 ng/mL, P < .05) and reduced antioxidant capacity (plasma total antioxidant capacity: 186.7 +/- 56 vs 161.8 +/- 50 U Trolox per microliter plasma, P < .01), vascular reactivity (171.3 +/- 85 vs 894.4 +/- 301 ng/mL, P < .001), and maximum acetylcholine venodilation (105.9% +/- 9% vs 61.0% +/- 7%, P < .05). No changes were observed for sodium nitroprusside. Post-OLO triglycerides were positively correlated with phenylephrine dose (rho = 0.38, P < .05) and resistin (rho = 0.43, P < .01) and negatively correlated with the maximum acetylcholine venodilation (rho = -0.36, P < .05). In conclusion, an OLO impaired venoconstriction responsiveness in healthy subjects, probably because of a reduction in the antioxidant capacity.