Gut microbiota of mice putatively modifies amino acid metabolism in the host brain
Open accessAbstract
Recently, it has been found that the gut microbiota influences functions of the host brain by affecting monoamine metabolism. The present study focused on the relationship between the gut microbiota and the brain amino acids. Specific pathogen-free (SPF) and germ-free (GF) mice were used as experimental models. Plasma and brain regions were sampled from mice at 7 and 16 weeks of age, and analysed for free d- and l-amino acids, which are believed to affect many physiological functions. At 7 weeks of age, plasma concentrations of d-aspartic acid (d-Asp),l-alanine (l-Ala),l-glutamine (l-Gln) and taurine were higher in SPF mice than in GF mice, but no differences were found at 16 weeks of age. Similar patterns were observed for the concentrations of l-Asp in striatum, cerebral cortex and hippocampus, and l-arginine (l-Arg),l-Ala and l-valine (l-Val) in striatum. In addition, the concentrations of l-Asp,d-Ala,l-histidine,l-isoleucine (l-Ile),l-leucine (l-Leu),l-phenylalanine and l-Val were significantly higher in plasma of SPF mice when compared with those of GF mice. The concentrations of l-Arg,l-Gln,l-Ile and l-Leu were significantly higher in SPF than in GF mice, but those of d-Asp,d-serine and l-serine were higher in some brain regions of GF mice than in those of SPF mice. In conclusion, the concentration of amino acids in the host brain seems to be dependent on presence of the gut microbiota. Amino acid metabolism in the host brain may be modified by manipulating microbiota communities.
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Due to the lack of commensal microbes, GF animals have impaired immune systems, dysregulated hormone signaling, altered metabolism, and differences in neurotransmission from conventional counterparts.
“Due to the lack of commensal microbes, GF animals have impaired immune systems, dysregulated hormone signaling, altered metabolism, and differences in neurotransmission from conventional counterparts (Kawase et al., 2017;Neufeld et al., 2011;Pan et al., 2018;Sudo et al., 2004;Weger et al., 2019).”
From The Microbiota-Gut-Brain Axis (2019) · cites this paper as Kawase et al., 2017
The Abstract and Discussion (page numbers not provided) report differences between germ-free and specific-pathogen-free mice in amino-acid metabolism and brain neurotransmitter concentrations. They also describe roles for gut microbes in immune development and the HPA stress response, but do not establish that germ-free animals generally have impaired immune systems or dysregulated hormone signaling. (LLM, conf=0.85)
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- Authors
- Kawase, T., Nagasawa, M., Ikeda, H., Yasuo, S., Koga, Y., & Furuse, M.
- Affiliations
- Kyushu University (JP)
- Tokai University (JP)
- Corresponding author
- Furuse, Mitsuhiro
- Venue
- British Journal of Nutrition
- Publisher
- Cambridge University Press (CUP)
- Published
- 2017-03-28
- Volume
- 117
- Issue
- 6
- Pages
- 775-783
- ISSN
- 0007-1145 (ISSN-L)
- 1475-2662
- OpenAlex
- W2607231229
- Cited by
- 119
- References
- 53
- Citations by year
- 2026: 5 · 2025: 15 · 2024: 14 · 2023: 15 · 2022: 24 · 2021: 19 · 2020: 9 · 2019: 13 · 2018: 5
- FWCI
- 3.02
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- British Journal Of Nutrition (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Dongguan University of Technology
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Amino Acid Enzymes and Metabolism
- Keywords
- gut microbiota, brain amino acids, amino acid metabolism, germ-free mice, specific pathogen-free mice, D-aspartic acid, L-alanine, glutamine, taurine, L-arginine, brain regions, plasma amino acids, monoamine metabolism, microbiome manipulation
- MeSH terms
- Gastrointestinal Microbiome, Amino Acids, Animals, Bacteria, Brain, Mice, Inbred BALB C, Neurotransmitter Agents
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