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