What affects hesperidin’s bioavailability?

Hesperidin is a molecule resistant to the stomach and to the enzymes of the small intestine, and it therefore remains intact until it reaches the colon. In the colon, hesperidin is metabolized by the intestinal microbiota into its aglycone form, hesperetin; a portion of this hesperetin is converted into secondary bioavailable metabolites, which then enter the bloodstream. This emphasizes the potential impact of an individual's microbiota on the bioavailability of hesperidin. However, factors beyond the gut microbiota also play a role. Hesperidin’s source (e.g., sweet orange, tangerines, oral supplements), its form (e.g., juice, capsule, soluble compound), and the processing and storage methods to which it has been subjected also affect its absorption in the lower gastrointestinal tract.^[1] The combined effects of these variables likely contributes to the variablility in the outcomes observed in studies of hesperidin.