Orange juice neutralizes the proinflammatory effect of a high-fat, high-carbohydrate meal and prevents endotoxin increase and Toll-like receptor expression.
Level 2 - randomized trial
Controlled clinical trial with parallel groups
PubMed 20200256 · doi:10.3945/ajcn.2009.28584
What was done
Thirty healthy subjects were divided into three groups of 10 and consumed a 900-kcal high-fat, high-carbohydrate (HFHC) meal accompanied by water, 300 kcal of glucose, or 300 kcal of orange juice. Blood samples were collected before the meal and at 1, 3, and 5 hours post-meal. Mononuclear cell expression of p47(phox), phosphorylated and total p38 MAPK, SOCS-3, TLR2, TLR4, and MMP-9, along with plasma endotoxin, plasma MMP-9, and polymorphonuclear cell reactive oxygen species (ROS) generation, were assessed.
What was found
The abstract does not report numerical values, percentages, or confidence intervals. Consumption of the HFHC meal with water or glucose led to significant increases in mononuclear cell protein expression of p47(phox), p38 MAPK, SOCS-3, TLR2, and TLR4; increased mRNA expression of TLR2, TLR4, and MMP-9; and increased plasma concentrations of endotoxin and MMP-9. These increases did not occur when orange juice was consumed with the meal. ROS generation by polymorphonuclear cells was significantly lower after orange juice compared with water or glucose.
Why it matters
The study indicates that bioactive components in orange juice can acutely block postprandial endotoxemia, Toll-like receptor upregulation, and inflammatory stress induced by a calorie-dense meal.
Limits
Sample size is small (n = 30 total, 10 per group) and limited to healthy subjects. The study evaluated only acute 5-hour surrogate biochemical markers without clinical outcomes, the abstract does not describe randomization or blinding procedures, and no numerical effect sizes or error bounds are reported.
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