Microbiota-derived metabolites as drivers of gut-brain communication.
Gut Microbes. 2022-07-28; 14(1):
DOI: 10.1080/19490976.2022.2102878
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Ahmed H(1), Leyrolle Q(2), Koistinen V(1)(3), Kärkkäinen O(4), Layé S(5), Delzenne N(2), Hanhineva K(1)(3)(6).
Author information:
(1)Food Sciences Unit, Department of Life Technologies, University of Turku,
Turku, Finland.
(2)Metabolism and Nutrition Research Group, Louvain Drug Research Institute,
UCLouvain, Brussels, Belgium.
(3)School of Medicine, Institute of Public Health and Clinical Nutrition,
University of Eastern Finland, Kuopio, Finland.
(4)School of Pharmacy, University of Eastern Finland, Kuopio, Finland.
(5)Laboratoire NutriNeuro, UMR INRAE 1286, Bordeaux INP, Université de Bordeaux,
Bordeaux, France.
(6)Department of Biology and Biological Engineering, Division of Food and
Nutrition Science, Chalmers University of Technology, Gothenburg, Sweden.
Alterations in the gut microbiota composition have been associated with a range
of neurodevelopmental, neurodegenerative, and neuropsychiatric disorders. The
gut microbes transform and metabolize dietary- and host-derived molecules
generating a diverse group of metabolites with local and systemic effects. The
bi-directional communication between brain and the microbes residing in the gut,
the so-called gut-brain axis, consists of a network of immunological, neuronal,
and endocrine signaling pathways. Although the full variety of mechanisms of the
gut-brain crosstalk is yet to be established, the existing data demonstrates
that a single metabolite or its derivatives are likely among the key inductors
within the gut-brain axis communication. However, more research is needed to
understand the molecular mechanisms underlying how gut microbiota associated
metabolites alter brain functions, and to examine if different interventional
approaches targeting the gut microbiota could be used in prevention and
treatment of neurological disorders, as reviewed herein.Abbreviations:4-EPS
4-ethylphenylsulfate; 5-AVA(B) 5-aminovaleric acid (betaine); Aβ Amyloid beta
protein; AhR Aryl hydrocarbon receptor; ASD Autism spectrum disorder; BBB
Blood-brain barrier; BDNF Brain-derived neurotrophic factor; CNS Central nervous
system; GABA ɣ-aminobutyric acid; GF Germ-free; MIA Maternal immune activation;
SCFA Short-chain fatty acid; 3M-4-TMAB 3-methyl-4-(trimethylammonio)butanoate;
4-TMAP 4-(trimethylammonio)pentanoate; TMA(O) Trimethylamine(-N-oxide); TUDCA
Tauroursodeoxycholic acid; ZO Zonula occludens proteins.
Conflict of interest statement: No potential conflict of interest was reported
by the author(s).