Postprandial lipemia induces impairment in antioxidative activity of small high-density lipoprotein (HDL) particles
F.L. Sodréab, E.C. Fariab, S. Chantepiea, M.J. Chapmana, A. Kontusha
INSERM U551, Hôpital de la Pitié, Paris, France and bCampinas State University, Brazil
Introduction: The postprandial state is characterised by elevated oxidative stress, a key factor in atherogenesis. Small HDL3 potently protect against oxidative stress; such antioxidative activity (AOX) is inversely related to levels of oxidative stress in metabolic disease. We evaluated the impact of postprandial lipemia on AOX of HDL.
Methods: Blood was collected from ten healthy normolipidemic males before and 4 and 8h after intake of a liquid meal (25% fat, 55% dextromaltose, 14% protein) providing 40 g fat/m2 body surface. AOX of HDL was measured as the protection of reference normolipidemic low density lipoprotein (LDL) from oxidation induced by an aqueous generator of free radicals (AAPH).
Results: Plasma triglyceride (TG) levels increased in the postprandial phase up to +78% (at 4h after the meal, p<0.01), whereas HDL-cholesterol (HDL-C) decreased up to -5% (p<0.05). AOX of both small HDL3c (up to -17%, p<0.01) and total HDL (up to -21%, p<0.03) was impaired 8h after the meal. AOX of HDL3c was positively correlated with its content of cholesteryl ester (CE; p<0.05). AOX of total HDL was positively correlated with plasma HDL-C and negatively correlated with plasma TG levels and HDL TG content (p<0.05).
Conclusions: Diminished CE content in HDL in the hypertriglyceridemic postprandial phase, which reflects enhanced activity of cholesteryl ester transfer protein (CETP), results in altered HDL core lipid composition and impaired AOX. These features may contribute to enhanced oxidative stress and atherogenesis in the postprandial state.
|