Fucose as a Cleavage Product of 2’Fucosyllactose Does Not Cross the Blood‐Brain Barrier in Mice

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Scope To further examine the role of the human milk oligosaccharide 2’fucosyllactose (2´FL) and fucose (Fuc) in cognition. Using 13C‐labeled 2’FL,thestudy previously showed in mice that 13C‐enrichment of the brain is not caused by 13C1‐2´FL itself, but rather by microbial metabolites. Here, the study applies 13C1‐Fuc in the same mouse model to investigate its uptake into the brain. Methods and Results Mice received 13C1‐Fuc via oral gavage (2 mmol 13C1‐Fuc/kg‐1 body weight) or intravenously (0.4 mmol/kg‐1 body weight). 13C‐enrichment is measured in organs, including various brain regions, biological fluids and excrements. By EA‐IRMS, the study observes an early rise of 13C‐enrichment in plasma, 30 min after oral dosing. However, 13C‐enrichment in the brain does not occur until 3‐5 h post‐dosing, when the 13C‐Fuc bolus has already reached the lower gut. Therefore, the researcher assume that 13C‐Fuc is absorbed in the upper small intestine but cannot cross the blood‐brain barrier which is also observed after intravenous application of 13C1‐Fuc. Conclusions Late 13C‐enrichment in the rodent brain may be derived from 13C1‐Fuc metabolites derived from bacterial fermentation. The precise role that Fuc or 2´FL metabolites might play in gut‐brain communication needs to be investigated in further studies.

Ce résumé expose les affirmations des auteurs. BNTIC ne l’interprète pas comme une validation indépendante des résultats.