Scope: To further examine the role of the human milk oligosaccharide 2'fucosyllactose (2´FL) and fucose (Fuc) in cognition. Using 13 C-labeled 2'FL,thestudy previously showed in mice that 13 C-enrichment of the brain is not caused by 13 C1 -2´FL itself, but rather by microbial metabolites. Here, the study applies 13 C1 -Fuc in the same mouse model to investigate its uptake into the brain.
Methods and results: Mice received 13 C1 -Fuc via oral gavage (2 mmol 13 C1 -Fuc/kg-1 body weight) or intravenously (0.4 mmol/kg-1 body weight). 13 C-enrichment is measured in organs, including various brain regions, biological fluids and excrements. By EA-IRMS, the study observes an early rise of 13 C-enrichment in plasma, 30 min after oral dosing. However, 13 C-enrichment in the brain does not occur until 3-5 h post-dosing, when the 13 C-Fuc bolus has already reached the lower gut. Therefore, the researcher assume that 13 C-Fuc is absorbed in the upper small intestine but cannot cross the blood-brain barrier which is also observed after intravenous application of 13 C1 -Fuc.
Conclusions: Late 13 C-enrichment in the rodent brain may be derived from 13 C1 -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.
Keywords: 13C-labeled fucose; biological fluids; brain; metabolism; microbiota.
© 2021 The Authors. Molecular Nutrition & Food Research published by Wiley-VCH GmbH.