The role of short-chain fatty acids in microbiota–gut–brain communication
Open accessAbstract
Short-chain fatty acids (SCFAs), the main metabolites produced by bacterial fermentation of dietary fibre in the gastrointestinal tract, are speculated to have a key role in microbiota-gut-brain crosstalk. However, the pathways through which SCFAs might influence psychological functioning, including affective and cognitive processes and their neural basis, have not been fully elucidated. Furthermore, research directly exploring the role of SCFAs as potential mediators of the effects of microbiota-targeted interventions on affective and cognitive functioning is sparse, especially in humans. This Review summarizes existing knowledge on the potential of SCFAs to directly or indirectly mediate microbiota-gut-brain interactions. The effects of SCFAs on cellular systems and their interaction with gut-brain signalling pathways including immune, endocrine, neural and humoral routes are described. The effects of microbiota-targeted interventions such as prebiotics, probiotics and diet on psychological functioning and the putative mediating role of SCFA signalling will also be discussed, as well as the relationship between SCFAs and psychobiological processes. Finally, future directions to facilitate direct investigation of the effect of SCFAs on psychological functioning are outlined.
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The gut microbiota influences the gut barrier and produces neurotransmitters, amino acids and microbial metabolites.
“The gut microbiota influences gut barrier and produce neurotransmitters, amino acids and microbial metabolites61.”
From Association between attention-deficit/hyperactivity disorders and intestinal disorders: A systematic review and Meta-analysis (2025) · cites this paper as [61]
The Introduction identifies short-chain fatty acids as microbial metabolites, and the Immune pathways section reports that they affect intestinal barrier function. The Other direct humoral pathways section says microbial metabolites can promote serotonin synthesis by host cells; it does not establish that the microbiota itself produces neurotransmitters or amino acids. Page numbers are unavailable in our copy. (LLM, conf=0.87)
Experimental — accuracy not yet measuredGut microbiota dysbiosis has been implicated in behavioral and neurologic pathologies, such as depression, Alzheimer's disease, Parkinson's disease, and autism spectrum disorder.
“gut microbiota dysbiosis has been implicated in behavioral and neurologic pathologies, such as depression, Alzheimer's (AD) and Parkinson's (PD) diseases and autism spectrum disorder (ASD) (9, 21, 25–27).”
From The Role of Short-Chain Fatty Acids From Gut Microbiota in Gut-Brain Communication (2020) · cites this paper as [21]
The Introduction (page unavailable) reports altered gut microbial composition in autism spectrum and mood disorders, supporting the autism and depression examples. Section 5 (page unavailable) reports fewer SCFA-producing bacteria in patients with Parkinson’s disease. Its Alzheimer’s discussion concerns effects of SCFAs in a mouse model and in vitro, not an association between gut microbiota dysbiosis and Alzheimer’s disease. (LLM, conf=0.88)
Experimental — accuracy not yet measuredBrain-to-gut signaling can directly affect the microbiota via the immune system or gut functions such as motility, release of neurotransmitters, and intestinal immune tone.
“brain to gut signaling can directly affect the microbiota, either via immune system or gut functions such as motility, release of neurotransmitters and intestinal immune tone (12, 17, 21, 31).”
From The Role of Short-Chain Fatty Acids From Gut Microbiota in Gut-Brain Communication (2020) · cites this paper as [21]
The Introduction (page unavailable) says brain signals can alter gut sensorimotor and secretory functions and identifies the immune system as a possible route of microbiota–gut–brain communication. It does not establish that those brain-to-gut signals directly change the microbiota, nor does it specify neurotransmitter release or intestinal immune tone as routes for such a change. (LLM, conf=0.84)
Experimental — accuracy not yet measuredThe gut microbiota can interact with the central nervous system via gut modulation or directly via metabolites and endotoxin translocation from the lumen to the circulation.
“the gut microbiota can interact with the CNS via gut modulation or directly via metabolites and endotoxin translocation from the lumen to the circulation (9, 17, 21).”
From The Role of Short-Chain Fatty Acids From Gut Microbiota in Gut-Brain Communication (2020) · cites this paper as [21]
The Introduction describes microbiota–gut–brain communication through gut-brain, nervous, endocrine and immune pathways. The Immune pathways section says short-chain fatty acids can reach the bloodstream and that intestinal barrier integrity can prevent translocation of bacteria and bacterial products into the circulation. It does not specifically establish endotoxin translocation as a direct route by which the microbiota interacts with the CNS; it describes a possible indirect route through systemic inflammation. (LLM, conf=0.82)
Experimental — accuracy not yet measuredAltered short-chain fatty acid production has been demonstrated in a variety of neuropathologies.
“altered SCFA production has been demonstrated in a variety of neuropathologies (19, 21, 33–35).”
From The Role of Short-Chain Fatty Acids From Gut Microbiota in Gut-Brain Communication (2020) · cites this paper as [21]
Section 5 reports altered faecal SCFA concentrations in Parkinson’s disease, autism spectrum disorder and, in one study, depression, though findings for autism and depression conflict. Section 5.1 cautions that faecal concentrations do not reflect SCFA production rates, so the paper does not establish the claimed alteration in production. (LLM, conf=0.88)
Experimental — accuracy not yet measured
Short-chain fatty acids regulate the expression levels of tryptophan 5-hydroxylase 1 and tyrosine hydroxylase, producing an effect on brain neurochemistry.
“these SCFAs regulate the expression levels of tryptophan 5-hydroxylase 1, the enzyme involved in synthesis of serotonin, and tyrosine hydroxylase, which is involved in a rate-limiting step in the biosynthesis of dopamine, noradrenaline and adrenaline; therefore, producing an effect on brain neurochemistry (21, 55, 56, 116, 117).”
From The Role of Short-Chain Fatty Acids From Gut Microbiota in Gut-Brain Communication (2020) · cites this paper as [21]
Section 3.2.3 reports that propionic acid induced tryptophan 5-hydroxylase 1 expression and that propionate and butyrate induced tyrosine hydroxylase transcription. Those findings were in a PC12 cell line; the section does not establish that these enzyme changes consequently altered brain neurochemistry, and it cautions that uptake of colonic SCFAs into the brain is unlikely. (LLM, conf=0.88)
Experimental — accuracy not yet measuredMicrobial metabolites such as short chain fatty acids exert beneficial effects on psychiatric disorders via the microbiota-gut-brain axis through humoral, hormonal, and immune pathways.
“Microbial metabolites such as short chain fatty acids (SCFAs) exert beneficial effects on psychiatric disorders via the microbiota–gut–brain axis through humoral, hormonal, and immune pathways [12].”
From Effect of Supplementation with Probiotics in Patients with Schizophrenia: Systematic Review and Meta-Analysis of Randomized Controlled Clinical Trials (2025) · cites this paper as [12]
The Introduction and §3.2 describe SCFAs as potential mediators of microbiota–gut–brain signaling, including endocrine and immune pathways. But §5 says direct evidence for psychological effects is sparse and conflicting, and reports both beneficial and adverse findings. The source does not establish that SCFAs generally exert beneficial effects on psychiatric disorders through those pathways. (LLM, conf=0.88)
Experimental — accuracy not yet measuredGrowing evidence supports that short-chain fatty acids exert crucial physiological effects on several organs, including the brain.
“growing evidence supports the idea that SCFAs also exert crucial physiological effects on several organs, including the brain (17, 20, 21).”
From The Role of Short-Chain Fatty Acids From Gut Microbiota in Gut-Brain Communication (2020) · cites this paper as [21]
Short-chain fatty acids that cross into the central nervous system have neuroactive properties.
“Accumulating evidence suggests that SCFAs that cross into the CNS have neuroactive properties.”
From The Role of Short-Chain Fatty Acids From Gut Microbiota in Gut-Brain Communication (2020) · cites this paper as [21]
Short-chain fatty acids may modulate the levels of neurotransmitters and neurotrophic factors.
“It was described that SCFAs may modulate the levels of neurotransmitters and neurotrophic factors.”
From The Role of Short-Chain Fatty Acids From Gut Microbiota in Gut-Brain Communication (2020) · cites this paper as [21]
SCFAs exert physiological activities by acting as endogenous ligands for GPCRs and modulating gene expression by inhibiting HDACs.
“SCFAs exert their physiological activities by acting as endogenous ligands for G-protein-coupled receptors (GPCRs), and modulating gene expression by inhibiting histone deacetylases (HDACs).282”
From Microbiota–gut–brain axis and its therapeutic applications in neurodegenerative diseases (2024) · cites this paper as [282]
SCFAs are endogenous ligands for GPR43 and GPR41, subsequently renamed FFAR2 and FFAR3, respectively.
“SCFAs are endogenous ligands for a subset of GPCRs, including GPR43 and GPR41, which were subsequently renamed as free fatty acid receptor 2 (FFAR2) and FFAR3, respectively.”
From Microbiota–gut–brain axis and its therapeutic applications in neurodegenerative diseases (2024) · cites this paper as [282]
GPR109A, also known as HCAR2, is activated by butyrate and β-D-hydroxy butyrate.
“Another important GPCR activated by SCFA is GPR109A, also known as hydroxycarboxylic acid receptor 2 (HCAR2), which is activated by butyrate and β-D-hydroxy butyrate.282”
From Microbiota–gut–brain axis and its therapeutic applications in neurodegenerative diseases (2024) · cites this paper as [282]
Intracellular SCFAs can influence gene expression via histone deacetylation (HDAC) inhibition.
“and intracellular SCFAs can influence gene expression via histone deacetylation (HDAC) inhibition (Dalile et al., 2019)”
From The modulatory effects of gut microbes and metabolites on blood-brain barrier integrity and brain function in sepsis-associated encephalopathy (2023) · cites this paper as Dalile et al., 2019
SCFAs are endogenous ligands of orphan G protein-coupled receptors (GPCRs).
“Moreover, SCFAs are endogenous ligands of orphan G protein-coupled receptors (GPCRs)”
From The modulatory effects of gut microbes and metabolites on blood-brain barrier integrity and brain function in sepsis-associated encephalopathy (2023) · cites this paper as Dalile et al., 2019
SCFAs modulate neurotransmitter and neurotrophic factor levels and regulate expression of tryptophan 5-hydroxylase and tyrosine hydroxylase.
“SCFAs can modulate the levels of neurotransmitters and neurotrophic factors and regulate the expression of tryptophan 5-hydroxylase, the enzyme involved in the synthesis of serotonin, and tyrosine hydroxylase, the enzyme involved in the rate-limiting step in dopamine, noradrenaline, and adrenaline synthesis (18, 132, 164, 222).”
From Signalling cognition: The gut microbiota and hypothalamic-pituitary-adrenal axis (2023) · cites this paper as [132]
Altered SCFA production is demonstrated in a variety of neuropathologies.
“Altered SCFA production has also been demonstrated in a variety of neuropathologies (42, 116, 127, 130, 132, 292–295).”
From Signalling cognition: The gut microbiota and hypothalamic-pituitary-adrenal axis (2023) · cites this paper as [132]
Other pathways through which SCFAs can influence gut-brain communication and brain function include immune, endocrine, neuronal, vagal, and other humoral pathways.
“Other pathways through which SCFAs can influence gutbrain communication and brain function include immune, endocrine, neuronal, vagal, and other humoral pathways (360).”
From Diet and the Microbiota–Gut–Brain Axis: Sowing the Seeds of Good Mental Health (2021) · cites this paper as [360]
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- Authors
- Dalile, B., Van Oudenhove, L., Vervliet, B., & Verbeke, K.
- Affiliations
- KU Leuven (BE)
- Corresponding author
- Verbeke, Kristin
- Venue
- Nature Reviews Gastroenterology & Hepatology
- Published
- 2019-05-23
- Volume
- 16
- Issue
- 8
- Pages
- 461-478
- ISSN
- 1759-5045 (ISSN-L)
- 1759-5053
- OpenAlex
- W2946372752
- Cited by
- 3,357
- References
- 296
- Citations by year
- 2026: 631 · 2025: 685 · 2024: 567 · 2023: 511 · 2022: 429 · 2021: 334 · 2020: 174 · 2019: 25 · 2014: 1
- FWCI
- 21.30
- Type
- journal article
- Language
- en
- Open access
- green
- lirias.kuleuven.be
- Licence
- Locations
- Nature Reviews Gastroenterology & Hepatology (publishedVersion)
- PubMed (publishedVersion)
- Lirias (submittedVersion, other-oa)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
- Health Sciences › Medicine › Gastroenterology › Gastrointestinal motility and disorders
- Life Sciences › Agricultural and Biological Sciences › Food Science › Probiotics and Fermented Foods
- Keywords
- short-chain fatty acids, microbiota-gut-brain axis, dietary fiber fermentation, gut microbiota, psychological functioning, emotional processing, cognitive processes, prebiotics, probiotics, microbiota-targeted interventions, immune signaling, hormone signaling, psychobiology
- MeSH terms
- Gastrointestinal Microbiome, Animals, Mental Disorders, Brain, Dietary Fiber, Disease Models, Animal, Fatty Acids, Volatile, Humans, Neural Pathways, Signal Transduction, Gastrointestinal Tract
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