Component

Bacteroides fragilis

Bacteroides fragilis. Species, exposure and limitations are retained in each linked claim.

3 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

Read recorded mechanisms Open recursive mind map

How nutrients influence it

Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.

How nutrients reach it in more than one step

Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.

Tracing routes…

What it does

Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.

Recorded relationships

What it acts on

  1. Co-culture was used to isolate KLE1738 which required the presence of Bacteroides fragilis to grow, bioassay-driven purification of the supernatant led to isolation of the growth factor which surprisingly is the major inhibitory neurotransmitter GABA, GABA was the only tested nutrient that supported the growth of KLE1738, a variety of GABA-producing bacteria were isolated and Bacteroides species produced large quantities of GABA, transcriptome analysis of human stool from healthy individuals showed that GABA-producing pathways are actively expressed by Bacteroides, Parabacteroides and Escherichia species, and relative abundance levels of faecal Bacteroides are negatively correlated with brain signatures associated with depression.

    Bacteroides fragilis → Gamma-aminobutyric acid source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/gaba-research/30531975.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c5ec17a6d5ab61a71d407f753583383c556fb07e10434eb3a3c7b42e4d0953f9", "start_char": 0, "end_char": 1773, "text_sha256": "c5ec17a6d5ab61a71d407f753583383c556fb07e10434eb3a3c7b42e4d0953f9"}
    experimental_model
    Co-culture isolation with bioassay-driven purification, genome-based metabolic modelling, stool transcriptomics and brain imaging
    exposure
    A gut isolate that grows only in the presence of another species, and the growth factor it requires
    limitations
    The correlation with depression imaging is observational and the causal direction is not established. The bacteriology is direct.
    nutrient_topic
    GABA research collection; topical membership is not evidence of a direct clinical effect, and the sign of a GABA response depends on the chloride gradient of the cell it was measured in. · Gamma-aminobutyric acid
    organism
    Human
    plain_language
    One gut bacterium cannot grow without this molecule and another makes it in quantity, and the human gut expresses both halves.
    primary_references
    [gb-p30531975] GABA-modulating bacteria of the human gut microbiota. (2019). https://pubmed.ncbi.nlm.nih.gov/30531975/ DOI: 10.1038/s41564-018-0307-3
    tissue_or_cell_type
    Gut microbiota and brain

    GABA: a ligand with no sign of its own, the cofactor that limits its synthesis, the barrier that keeps it out of the brain, and the immune settings where the same molecule protects and harms (2026-09-22) · lines 495–506

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Co-culture isolation with bioassay-driven purification, genome-based metabolic modelling, stool transcriptomics and brain imaging · source_derived_draft · unverified_draft

    ### gb-gut-bacteria-make-and-consume-gaba Co-culture was used to isolate KLE1738 which required the presence of Bacteroides fragilis to grow, bioassay-driven purification of the supernatant led to isolation of the growth factor which surprisingly is the major inhibitory neurotransmitter GABA, GABA was the only tested nutrient that supported the growth of KLE1738, a variety of GABA-producing bacteria were isolated and Bacteroides species produced large quantities of GABA, transcriptome analysis of human stool from healthy individuals showed that GABA-producing pathways are actively expressed by Bacteroides, Parabacteroides and Escherichia species, and relative abundance levels of faecal Bacteroides are negatively correlated with brain signatures associated with depression. Condition category: normal nutrient_topic: GABA research collection; topical membership is not evidence of a direct clinical effect, and the sign of a GABA response depends on the chloride gradient of the cell it was measured in. plain_language: One gut bacterium cannot grow without this molecule and another makes it in quantity, and the human gut expresses both halves. organism: Human tissue_or_cell_type: Gut microbiota and brain experimental_model: Co-culture isolation with bioassay-driven purification, genome-based metabolic modelling, stool transcriptomics and brain imaging limitations: The correlation with depression imaging is observational and the causal direction is not established. The bacteriology is direct. exposure: A gut isolate that grows only in the presence of another species, and the growth factor it requires evidence_span: {"source_cache": "artifacts/gaba-research/30531975.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c5ec17a6d5ab61a71d407f753583383c556fb07e10434eb3a3c7b42e4d0953f9", "start_char": 0, "end_char": 1773, "text_sha256": "c5ec17a6d5ab61a71d407f753583383c556fb07e10434eb3a3c7b42e4d0953f9"} [gb-p30531975] GABA-modulating bacteria of the human gut microbiota. (2019). https://pubmed.ncbi.nlm.nih.gov/30531975/ DOI: 10.1038/s41564-018-0307-3
    Complete structured claim and evidence

  2. High-fat-diet mice colonised with B. fragilis were predisposed to more severe glucose intolerance, and the metabolic benefits of metformin were abrogated.

    Bacteroides fragilis → Glucose tolerance source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/metformin-research/30397356.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0dbf1f5a262207595ede745deeb9fc79ba7732dc4d6af6b5c9d654712d79c1cf", "start_char": 0, "end_char": 1433, "text_sha256": "0dbf1f5a262207595ede745deeb9fc79ba7732dc4d6af6b5c9d654712d79c1cf"}
    experimental_model
    Metagenomic and metabolomic analysis in newly diagnosed type 2 diabetes with mouse colonisation experiments
    exposure
    Three days of metformin in treatment-naive people; B. fragilis colonisation in high-fat-diet mice
    limitations
    A three-day human exposure with a mouse causal test. GUDCA is identified as an intestinal FXR antagonist; whole-body FXR biology is not claimed.
    nutrient_topic
    Metformin research collection; topical membership is not evidence of a direct clinical effect, and pharmacological exposure is not dietary intake. · Metformin
    organism
    Human and mouse
    plain_language
    Putting the bacterium back removed the benefit, which is what makes this more than a correlation.
    primary_references
    [metformin-p30397356] Gut microbiota and intestinal FXR mediate the clinical benefits of metformin. (2018). https://pubmed.ncbi.nlm.nih.gov/30397356/ DOI: 10.1038/s41591-018-0222-4
    tissue_or_cell_type
    Gut lumen and intestinal epithelium

    Metformin: transport, molecular targets, gut mechanisms and nutrient interactions (2026-09-19) · lines 892–903

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Metagenomic and metabolomic analysis in newly diagnosed type 2 diabetes with mouse colonisation experiments · source_derived_draft · unverified_draft

    ### metformin-bfragilis-colonisation High-fat-diet mice colonised with B. fragilis were predisposed to more severe glucose intolerance, and the metabolic benefits of metformin were abrogated. Condition category: normal nutrient_topic: Metformin research collection; topical membership is not evidence of a direct clinical effect, and pharmacological exposure is not dietary intake. plain_language: Putting the bacterium back removed the benefit, which is what makes this more than a correlation. organism: Human and mouse tissue_or_cell_type: Gut lumen and intestinal epithelium experimental_model: Metagenomic and metabolomic analysis in newly diagnosed type 2 diabetes with mouse colonisation experiments limitations: A three-day human exposure with a mouse causal test. GUDCA is identified as an intestinal FXR antagonist; whole-body FXR biology is not claimed. exposure: Three days of metformin in treatment-naive people; B. fragilis colonisation in high-fat-diet mice evidence_span: {"source_cache": "artifacts/metformin-research/30397356.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0dbf1f5a262207595ede745deeb9fc79ba7732dc4d6af6b5c9d654712d79c1cf", "start_char": 0, "end_char": 1433, "text_sha256": "0dbf1f5a262207595ede745deeb9fc79ba7732dc4d6af6b5c9d654712d79c1cf"} [metformin-p30397356] Gut microbiota and intestinal FXR mediate the clinical benefits of metformin. (2018). https://pubmed.ncbi.nlm.nih.gov/30397356/ DOI: 10.1038/s41591-018-0222-4
    Complete structured claim and evidence

What acts on it

  1. Three days of metformin in newly diagnosed type 2 diabetes decreased Bacteroides fragilis and increased the bile acid glycoursodeoxycholic acid in the gut.

    Metformin → Bacteroides fragilis source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/metformin-research/30397356.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0dbf1f5a262207595ede745deeb9fc79ba7732dc4d6af6b5c9d654712d79c1cf", "start_char": 0, "end_char": 1433, "text_sha256": "0dbf1f5a262207595ede745deeb9fc79ba7732dc4d6af6b5c9d654712d79c1cf"}
    experimental_model
    Metagenomic and metabolomic analysis in newly diagnosed type 2 diabetes with mouse colonisation experiments
    exposure
    Three days of metformin in treatment-naive people; B. fragilis colonisation in high-fat-diet mice
    limitations
    A three-day human exposure with a mouse causal test. GUDCA is identified as an intestinal FXR antagonist; whole-body FXR biology is not claimed.
    nutrient_topic
    Metformin research collection; topical membership is not evidence of a direct clinical effect, and pharmacological exposure is not dietary intake. · Metformin
    organism
    Human and mouse
    plain_language
    The drug changed which bacteria were present and which bile acid built up.
    primary_references
    [metformin-p30397356] Gut microbiota and intestinal FXR mediate the clinical benefits of metformin. (2018). https://pubmed.ncbi.nlm.nih.gov/30397356/ DOI: 10.1038/s41591-018-0222-4
    tissue_or_cell_type
    Gut lumen and intestinal epithelium

    Metformin: transport, molecular targets, gut mechanisms and nutrient interactions (2026-09-19) · lines 866–877

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Metagenomic and metabolomic analysis in newly diagnosed type 2 diabetes with mouse colonisation experiments · source_derived_draft · unverified_draft

    ### metformin-bfragilis-decrease Three days of metformin in newly diagnosed type 2 diabetes decreased Bacteroides fragilis and increased the bile acid glycoursodeoxycholic acid in the gut. Condition category: normal nutrient_topic: Metformin research collection; topical membership is not evidence of a direct clinical effect, and pharmacological exposure is not dietary intake. plain_language: The drug changed which bacteria were present and which bile acid built up. organism: Human and mouse tissue_or_cell_type: Gut lumen and intestinal epithelium experimental_model: Metagenomic and metabolomic analysis in newly diagnosed type 2 diabetes with mouse colonisation experiments limitations: A three-day human exposure with a mouse causal test. GUDCA is identified as an intestinal FXR antagonist; whole-body FXR biology is not claimed. exposure: Three days of metformin in treatment-naive people; B. fragilis colonisation in high-fat-diet mice evidence_span: {"source_cache": "artifacts/metformin-research/30397356.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0dbf1f5a262207595ede745deeb9fc79ba7732dc4d6af6b5c9d654712d79c1cf", "start_char": 0, "end_char": 1433, "text_sha256": "0dbf1f5a262207595ede745deeb9fc79ba7732dc4d6af6b5c9d654712d79c1cf"} [metformin-p30397356] Gut microbiota and intestinal FXR mediate the clinical benefits of metformin. (2018). https://pubmed.ncbi.nlm.nih.gov/30397356/ DOI: 10.1038/s41591-018-0222-4
    Complete structured claim and evidence

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

    Evidence, AI assistance and curation standards