Ngoc-Anh Le

Ngoc-Anh Le

Biomarker Core Laboratory, USA

Title: Meal-induced oxidative stress in metabolic syndrome


Ngoc-Anh Le completed his PhD in 1979 from University of California San Diego and his post-doctoral training with the SCOR-Atherosclerosis at ColumbiarnUniversity, NYC. He has served as laboratory director for several multicenter trials, including the Strong Heart Study, CARDIA, SAMMPRIS, and BIOSIS. He isrncurrently the director of the Biomarker Core Laboratory, Atlanta Research and Education Foundation, Atlanta VAMC. He has published more than 90 papers inrnpeer reviewed journals.


T2DM is associated with increased risk for cardiovascular disease. Oxidatively modified LDL (oxLDL) is the primaryrncontributor. oxLDL have been measured in plasma but association with disease risk has been mixed. Plasma oxLDL arernaffected by pro- and anti-oxidant metabolites as well as circulating autoantibodies against oxLDL. Oxidative susceptibility ofrnLDL to Cu++ induced oxidation as measured by lag time (min) is a functional assay for oxLDL. We hypothesize that with mealrnconsumption, oxidative susceptibility of LDL is increased and reduction of postprandial lipemia may reduce this susceptibility.rnPatients with metS participated in a randomized, double-blind, placebo-controlled study with cross-over with fenofibric acidrn(FA). After each treatment period, fasting (f) and postprandial (pp) plasma after a standardized mixed meal were collected forrnlipoprotein isolation. Both fasting (f) and postprandial (pp) LDL undergoes spontaneous oxidation (no Cu++) with comparablernlag times (169 and 172). With FA, ppLDL is more protected, i.e. longer lag time (212 vs 151). In the presence of Cu++, lagrntimes of fLDL are reduced for both periods (37 and 44). Compared to fLDL, reductions in ppLDL lag times were statisticallyrnsignificant only during placebo (37 vs 30) and not during FA (44 vs 38). Co-incubation with autologous HDL failed to protectrnLDL from oxidative modification. In summary, (1) ppLDL is more susceptible to oxidative modification, (2) treatment with FArnreduced postprandial lipemia and oxidative susceptibility of ppLDL, and (3) HDL from metS appears to be dysfunctional andrnthis was not normalized by FA therapy.