Mary F Carroll1, David S Schade. 1. University of New Mexico School of Medicine, Albuquerque, NM 87131, USA. mcarroll@salud.unm.edu
Abstract
BACKGROUND: This study was designed to determine the optimal timing of vitamins E and C to prevent oxidative stress induced by a high-fat evening meal in type 2 diabetes. METHODS AND RESULTS:Eleven subjects were admitted on 4 occasions. Euglycemia was maintained for 24 hours by insulin infusion. Participants were fed a high-fat test supper equivalent to a McDonald's Big Mac Meal. Blood was drawn for measurement of C-reactive protein (CRP), interleukin 6 (IL-6), plasminogen activator inhibitor-1 (PAI-1), malonyldialdehyde (MDA), and total radical antioxidant parameter (TRAP) before and during the 4 hours after the test meal. Studies were performed in random sequence with vitamin E 800 IU and vitamin C 1 g given either before breakfast or before supper in a double-blind manner on the day of the test meal. Control studies were performed with no vitamins and no test meal administered. There was a significant rise in CRP and PAI-1 after the test supper (P<0.05 compared with "no meal"). Either presupper or prebreakfast vitamins E and C prevented the meal-induced rise in CRP (P=0.03), although presupper vitamins were more effective (P=0.03 compared with prebreakfast vitamins). Only prebreakfast vitamins prevented the meal-induced rise in PAI-1 (P=0.006). There were no significant meal-related changes in the concentrations of IL-6, MDA, or TRAP. CONCLUSIONS: The timing of administration of antioxidant vitamins has variable effects on markers of meal-induced inflammation and fibrinolysis. This observation may be one reason why cardiovascular disease prevention trials using these vitamins have reported conflicting results.
RCT Entities:
BACKGROUND: This study was designed to determine the optimal timing of vitamins E and C to prevent oxidative stress induced by a high-fat evening meal in type 2 diabetes. METHODS AND RESULTS: Eleven subjects were admitted on 4 occasions. Euglycemia was maintained for 24 hours by insulin infusion. Participants were fed a high-fat test supper equivalent to a McDonald's Big Mac Meal. Blood was drawn for measurement of C-reactive protein (CRP), interleukin 6 (IL-6), plasminogen activator inhibitor-1 (PAI-1), malonyldialdehyde (MDA), and total radical antioxidant parameter (TRAP) before and during the 4 hours after the test meal. Studies were performed in random sequence with vitamin E 800 IU and vitamin C 1 g given either before breakfast or before supper in a double-blind manner on the day of the test meal. Control studies were performed with no vitamins and no test meal administered. There was a significant rise in CRP and PAI-1 after the test supper (P<0.05 compared with "no meal"). Either presupper or prebreakfast vitamins E and C prevented the meal-induced rise in CRP (P=0.03), although presupper vitamins were more effective (P=0.03 compared with prebreakfast vitamins). Only prebreakfast vitamins prevented the meal-induced rise in PAI-1 (P=0.006). There were no significant meal-related changes in the concentrations of IL-6, MDA, or TRAP. CONCLUSIONS: The timing of administration of antioxidant vitamins has variable effects on markers of meal-induced inflammation and fibrinolysis. This observation may be one reason why cardiovascular disease prevention trials using these vitamins have reported conflicting results.
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