↵2 Supported by a grant from the Florida Department of Citrus (to PD), grant R01DK069805-02 (to PD) from the National Institutes of Health, and grant 08-CR-13 (to PD) from the American Diabetes Association.
↵3 Address correspondence to P Dandona, Diabetes-Endocrinology Center of Western NY, State University of New York at Buffalo, 3 Gates Circle, Buffalo, NY 14209. E-mail: firstname.lastname@example.org.
Background: The intake of glucose or a high-fat, high-carbohydrate (HFHC) meal, but not orange juice, induces an increase in inflammation and oxidative stress in circulating mononuclear cells (MNCs) of normal-weight subjects.
Objective: We investigated the effect of orange juice on HFHC meal–induced inflammation and oxidative stress and the expression of plasma endotoxin and Toll-like receptors (TLRs).
Design: Three groups (10 subjects in each group) of normal, healthy subjects were asked to drink water or 300 kcal glucose or orange juice in combination with a 900-kcal HFHC meal. Blood samples were obtained before and 1, 3, and 5 h after the drinks and meal combinations were consumed.
Results: Protein expression of the NADPH oxidase subunit p47phox, phosphorylated and total p38 mitogen-activated protein kinase, and suppressor of cytokine signaling-3; TLR2 and TLR4 messenger RNA (mRNA) and protein expression; mRNA expression of matrix metalloproteinase (MMP)-9 in MNCs; and plasma concentrations of endotoxin and MMP-9 increased significantly after glucose or water were consumed with the meal but not when orange juice was consumed with the meal. The generation of reactive oxygen species by polymorphonuclear cells was significantly lower when orange juice was added to the meal than when water or glucose was added to the meal.
Conclusions: The combination of glucose or water and the HFHC meal induced oxidative and inflammatory stress and an increase in TLR expression and plasma endotoxin concentrations. In contrast, orange juice intake with the HFHC meal prevented meal-induced oxidative and inflammatory stress, including the increase in endotoxin and TLR expression. These observations may help explain the mechanisms underlying postprandial oxidative stress and inflammation, pathogenesis of insulin resistance, and atherosclerosis.
Received August 27, 2009.
Accepted January 19, 2010.
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