Reduction in generation of reactive oxygen species and endothelial dysfunction during postprandial state

Abstract

Background and aims To characterise changes in generation of cellular reactive oxygen species (ROS) in healthy males during the postprandial state, and to analyse the influence of the postprandial state on endothelial ROS generation and endothelial dysfunction. Methods and results Seventeen healthy subjects were recruited. Blood samples were collected in the fasting state and 2, 4, 6 and 8 h after liquid-meal intake (composition: 25% fat, 55% dextromaltose and 14% protein), providing 40 g fat m −2 body surface. Plasma lipids, apolipoproteins, glucose and insulin were measured during this period. Peripheral blood mononuclear cells (PBMCs) were isolated by density-gradient centrifugation. The influence of postprandial state on intracellular ROS generation was measured by two different methods in PBMCs and in a human immortalised endothelial cell line (ECV 304). Artery flow-mediated vasodilation (FMD) was used to evaluate the endothelial function, and oxygen consumption by PBMCs was measured. Reduced ROS generation was observed in all methods and cells during the postprandial period. FMD was impaired 8 h after meal intake (23 ± 6 vs. 13 ± 2, P < 0.05 vs. baseline). The consumption of oxygen was reduced in PBMCs (−14% into 2 h, P < 0.05 vs. baseline and −27% after 4 h, P < 0.01 vs. baseline). ROS generation was correlated with plasma lipids, insulin, apolipoproteins and oxygen consumption. Conclusions In contrast to the previously reported elevation of postprandial oxidative stress, this study shows reduced ROS generation in PBMCs and in ECV 304. Data obtained in both cellular models suggest the existence of a protective response against plasma postprandial oxidative stress.