Conclusion
Findings from this study indicate that regular consumption of DHCs-rich diets holds great promise to alleviate the development of ACR-associated chronic diseases.
Results
Three doses of phloretin (25, 100, and 400 mg kg-1 ), a major dietary DHC, are orally administrated to mice and 24 h urine and fecal samples are collected, respectively. High-resolution MS-based targeted metabolomics reveal for the first time that phloretin and its oxidized metabolite are able to trap endogenous ACR via formation of ACR conjugates. Quantification further demonstrate that a) more than 13% of ingested phloretin can dose-dependently trap 0.77-9.92 nmol of ACR within 24 h; b) phloretin ingestion leads to marked reductions in both free ACR and ACR metabolites in mouse urine compared to control; and c) trapping reactions by phloretin can account for up to 20.1% of the total decreases in endogenous ACR, depending on the administration doses.