We hypothesized that fruit ingestion provides measurable amounts of salicylic acid (SA) and produces different metabolic and inflammatory responses compared to mere fruit sugars. In a randomized-crossover study, 26 healthy subjects received a peach shake meal (PSM) (SA: 0,06 ± 0,001 mg/100 g) and a mixed sugar meal (MSM), consisting in an aqueous solution with the same sugars found in the peach shake. In order to control for the SA contribution from meals in the previous day, 16 subjects (Group 1) abstained from fruits and vegetables consumption the evening before trials, and 10 subjects (Group 2) maintained their usual diet. Circulating SA, glucose, insulin, free fatty acids, and interleukin-6 were determined. Basal SA was lower in Group 1 than in Group 2 (0.09 ± 0.02 vs. 0.30 ± 0.03 μmol/l, p < 0.001), peaked at 90 min in both groups (0.18 ± 0.01 vs. 0.38 ± 0.02 μmol/l, p < 0.01) and remained above baseline (p < 0.05) up to 3 h. Glycemia increased less after PSM at 15 min (p < 0.01) with a lower average glucose excursion (p < 0.05). Insulin peaked at 45 min with both meals but decreased less rapidly with PSM. Free fatty acids decreased more (p < 0.01), and interleukin-6 increased less (p < 0.05) with PSM. Dietary fruit intake increases the concentration of SA in vivo, and provides non-nutrients capable to modulate the inflammatory and metabolic responses to carbohydrates.