Component

Gut microbiota composition

Gut microbiota composition. Species, exposure and limitations are retained in each linked claim.

5 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. Transfer of faecal samples from metformin-treated donors to germ-free mice improved glucose tolerance in the recipients.

    Gut microbiota composition → Glucose tolerance source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/metformin-research/28530702.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "885eedb24772fbd218ff6497da6c39f486d0e0b0293ddd97e8fd7b3f23330b11", "start_char": 0, "end_char": 1137, "text_sha256": "885eedb24772fbd218ff6497da6c39f486d0e0b0293ddd97e8fd7b3f23330b11"}
    experimental_model
    Four-month double-blind randomised trial with faecal transfer to germ-free mice and a gut simulator
    exposure
    Metformin or placebo for 4 months in treatment-naive type 2 diabetes
    limitations
    The faecal transfer carries the causal claim. The metalloprotein observation is a genomic annotation, not a measured metal interaction.
    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
    Moving only the bacteria moved part of the benefit with them.
    primary_references
    [metformin-p28530702] Metformin alters the gut microbiome of individuals with treatment-naive type 2 diabetes, contributing to the therapeutic effects of the drug. (2017). https://pubmed.ncbi.nlm.nih.gov/28530702/ DOI: 10.1038/nm.4345
    tissue_or_cell_type
    Gut microbiome

    Metformin: transport, molecular targets, gut mechanisms and nutrient interactions (2026-09-19) · lines 918–929

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Four-month double-blind randomised trial with faecal transfer to germ-free mice and a gut simulator · source_derived_draft · unverified_draft

    ### metformin-microbiome-transfer Transfer of faecal samples from metformin-treated donors to germ-free mice improved glucose tolerance in the recipients. 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: Moving only the bacteria moved part of the benefit with them. organism: Human and mouse tissue_or_cell_type: Gut microbiome experimental_model: Four-month double-blind randomised trial with faecal transfer to germ-free mice and a gut simulator limitations: The faecal transfer carries the causal claim. The metalloprotein observation is a genomic annotation, not a measured metal interaction. exposure: Metformin or placebo for 4 months in treatment-naive type 2 diabetes evidence_span: {"source_cache": "artifacts/metformin-research/28530702.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "885eedb24772fbd218ff6497da6c39f486d0e0b0293ddd97e8fd7b3f23330b11", "start_char": 0, "end_char": 1137, "text_sha256": "885eedb24772fbd218ff6497da6c39f486d0e0b0293ddd97e8fd7b3f23330b11"} [metformin-p28530702] Metformin alters the gut microbiome of individuals with treatment-naive type 2 diabetes, contributing to the therapeutic effects of the drug. (2017). https://pubmed.ncbi.nlm.nih.gov/28530702/ DOI: 10.1038/nm.4345
    Complete structured claim and evidence

What acts on it

  1. In a gut simulator, many of the metformin-regulated genes in species from two different phyla encoded metalloproteins or metal transporters.

    Metformin → Gut microbiota composition source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/metformin-research/28530702.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "885eedb24772fbd218ff6497da6c39f486d0e0b0293ddd97e8fd7b3f23330b11", "start_char": 0, "end_char": 1137, "text_sha256": "885eedb24772fbd218ff6497da6c39f486d0e0b0293ddd97e8fd7b3f23330b11"}
    experimental_model
    Four-month double-blind randomised trial with faecal transfer to germ-free mice and a gut simulator
    exposure
    Metformin or placebo for 4 months in treatment-naive type 2 diabetes
    limitations
    The faecal transfer carries the causal claim. The metalloprotein observation is a genomic annotation, not a measured metal interaction.
    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 genes the drug touched in bacteria were unusually often metal-handling genes.
    primary_references
    [metformin-p28530702] Metformin alters the gut microbiome of individuals with treatment-naive type 2 diabetes, contributing to the therapeutic effects of the drug. (2017). https://pubmed.ncbi.nlm.nih.gov/28530702/ DOI: 10.1038/nm.4345
    tissue_or_cell_type
    Gut microbiome

    Metformin: transport, molecular targets, gut mechanisms and nutrient interactions (2026-09-19) · lines 931–942

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Four-month double-blind randomised trial with faecal transfer to germ-free mice and a gut simulator · source_derived_draft · unverified_draft

    ### metformin-microbial-metalloproteins In a gut simulator, many of the metformin-regulated genes in species from two different phyla encoded metalloproteins or metal transporters. 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 genes the drug touched in bacteria were unusually often metal-handling genes. organism: Human and mouse tissue_or_cell_type: Gut microbiome experimental_model: Four-month double-blind randomised trial with faecal transfer to germ-free mice and a gut simulator limitations: The faecal transfer carries the causal claim. The metalloprotein observation is a genomic annotation, not a measured metal interaction. exposure: Metformin or placebo for 4 months in treatment-naive type 2 diabetes evidence_span: {"source_cache": "artifacts/metformin-research/28530702.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "885eedb24772fbd218ff6497da6c39f486d0e0b0293ddd97e8fd7b3f23330b11", "start_char": 0, "end_char": 1137, "text_sha256": "885eedb24772fbd218ff6497da6c39f486d0e0b0293ddd97e8fd7b3f23330b11"} [metformin-p28530702] Metformin alters the gut microbiome of individuals with treatment-naive type 2 diabetes, contributing to the therapeutic effects of the drug. (2017). https://pubmed.ncbi.nlm.nih.gov/28530702/ DOI: 10.1038/nm.4345
    Complete structured claim and evidence

  2. Metformin had strong effects on the gut microbiome in a four-month double-blind randomised trial, verified in a placebo subgroup that later switched to metformin.

    Metformin → Gut microbiota composition source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/metformin-research/28530702.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "885eedb24772fbd218ff6497da6c39f486d0e0b0293ddd97e8fd7b3f23330b11", "start_char": 0, "end_char": 1137, "text_sha256": "885eedb24772fbd218ff6497da6c39f486d0e0b0293ddd97e8fd7b3f23330b11"}
    experimental_model
    Four-month double-blind randomised trial with faecal transfer to germ-free mice and a gut simulator
    exposure
    Metformin or placebo for 4 months in treatment-naive type 2 diabetes
    limitations
    The faecal transfer carries the causal claim. The metalloprotein observation is a genomic annotation, not a measured metal interaction.
    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 reshapes the gut community within months.
    primary_references
    [metformin-p28530702] Metformin alters the gut microbiome of individuals with treatment-naive type 2 diabetes, contributing to the therapeutic effects of the drug. (2017). https://pubmed.ncbi.nlm.nih.gov/28530702/ DOI: 10.1038/nm.4345
    tissue_or_cell_type
    Gut microbiome

    Metformin: transport, molecular targets, gut mechanisms and nutrient interactions (2026-09-19) · lines 905–916

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Four-month double-blind randomised trial with faecal transfer to germ-free mice and a gut simulator · source_derived_draft · unverified_draft

    ### metformin-microbiome-shift Metformin had strong effects on the gut microbiome in a four-month double-blind randomised trial, verified in a placebo subgroup that later switched to metformin. 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 reshapes the gut community within months. organism: Human and mouse tissue_or_cell_type: Gut microbiome experimental_model: Four-month double-blind randomised trial with faecal transfer to germ-free mice and a gut simulator limitations: The faecal transfer carries the causal claim. The metalloprotein observation is a genomic annotation, not a measured metal interaction. exposure: Metformin or placebo for 4 months in treatment-naive type 2 diabetes evidence_span: {"source_cache": "artifacts/metformin-research/28530702.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "885eedb24772fbd218ff6497da6c39f486d0e0b0293ddd97e8fd7b3f23330b11", "start_char": 0, "end_char": 1137, "text_sha256": "885eedb24772fbd218ff6497da6c39f486d0e0b0293ddd97e8fd7b3f23330b11"} [metformin-p28530702] Metformin alters the gut microbiome of individuals with treatment-naive type 2 diabetes, contributing to the therapeutic effects of the drug. (2017). https://pubmed.ncbi.nlm.nih.gov/28530702/ DOI: 10.1038/nm.4345
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Oat-beta-glucan enhances anti-PD-1 efficacy in murine models by selectively expanding Faecalibacterium prausnitzii, combining anti-PD-1 with either oat-beta-glucan or F. prausnitzii boosts intratumoral dendritic cell and CD8+ T cell infiltration and cytotoxic activation compared with anti-PD-1 monotherapy, metabolomics identifies F. prausnitzii-derived butyrate and indole-3-propionic acid as key mediators with butyrate activating dendritic cells via the HDAC8, H3K27ac and NF-kappa-B p65 pathway, in a colorectal cancer cohort undergoing anti-PD-1 treatment higher baseline F. prausnitzii abundance and elevated plasma butyrate and indole-3-propionic acid correlate with improved responses, and a human intervention study confirms oat-beta-glucan safety, its ability to increase butyrate and indole-3-propionic acid, and its capacity to modulate F. prausnitzii.

    Oat mixed-linkage beta-(1->3)/(1->4)-glucan → Efficacy of anti-PD-1 checkpoint blockade source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/glucan-research/42214334.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1e145fb1c4163d9e0cd10a4055b68fa47de521dcf19d25253d42fc9c971d56ba", "start_char": 0, "end_char": 1310, "text_sha256": "1e145fb1c4163d9e0cd10a4055b68fa47de521dcf19d25253d42fc9c971d56ba"}
    experimental_model
    Murine tumour models with selective bacterial expansion and metabolomics, plus a human cohort and a human intervention study
    exposure
    Oat beta-glucan with anti-PD-1 checkpoint blockade in mice, and oat beta-glucan supplementation in people
    limitations
    The causal efficacy claim is demonstrated in mice. The human components are a correlation in a colorectal cancer cohort and an intervention study reporting safety and metabolite change, so no anticancer benefit in people is established here.
    nutrient_topic
    Beta-glucan research collection; topical membership is not evidence of a direct clinical effect, and each preparation is recorded as its own entity with no family link joining any pair. · Beta-glucan
    organism
    Mouse
    plain_language
    The cereal glucan never touches the tumour; it feeds a gut bacterium whose products wake the cells that do.
    primary_references
    [bg-p42214334] Oat-β-glucan potentiates anti-PD-1 efficacy through Faecalibacterium prausnitzii-derived butyrate and indole-3-propionic acid. (2026). https://pubmed.ncbi.nlm.nih.gov/42214334/ DOI: 10.1016/j.chom.2026.05.002
    tissue_or_cell_type
    Gut microbiota and tumour microenvironment

    Beta-glucan: a structural family rather than an agent, what decides whether a bound glucan actually signals, the complement route that a cereal and a yeast preparation share, and the unequal human evidence behind each (2026-09-22) · lines 658–669

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Murine tumour models with selective bacterial expansion and metabolomics, plus a human cohort and a human intervention study · source_derived_draft · unverified_draft

    ### bg-a-cereal-glucan-reaches-immunity Oat-beta-glucan enhances anti-PD-1 efficacy in murine models by selectively expanding Faecalibacterium prausnitzii, combining anti-PD-1 with either oat-beta-glucan or F. prausnitzii boosts intratumoral dendritic cell and CD8+ T cell infiltration and cytotoxic activation compared with anti-PD-1 monotherapy, metabolomics identifies F. prausnitzii-derived butyrate and indole-3-propionic acid as key mediators with butyrate activating dendritic cells via the HDAC8, H3K27ac and NF-kappa-B p65 pathway, in a colorectal cancer cohort undergoing anti-PD-1 treatment higher baseline F. prausnitzii abundance and elevated plasma butyrate and indole-3-propionic acid correlate with improved responses, and a human intervention study confirms oat-beta-glucan safety, its ability to increase butyrate and indole-3-propionic acid, and its capacity to modulate F. prausnitzii. Condition category: normal nutrient_topic: Beta-glucan research collection; topical membership is not evidence of a direct clinical effect, and each preparation is recorded as its own entity with no family link joining any pair. plain_language: The cereal glucan never touches the tumour; it feeds a gut bacterium whose products wake the cells that do. organism: Mouse tissue_or_cell_type: Gut microbiota and tumour microenvironment experimental_model: Murine tumour models with selective bacterial expansion and metabolomics, plus a human cohort and a human intervention study limitations: The causal efficacy claim is demonstrated in mice. The human components are a correlation in a colorectal cancer cohort and an intervention study reporting safety and metabolite change, so no anticancer benefit in people is established here. exposure: Oat beta-glucan with anti-PD-1 checkpoint blockade in mice, and oat beta-glucan supplementation in people evidence_span: {"source_cache": "artifacts/glucan-research/42214334.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1e145fb1c4163d9e0cd10a4055b68fa47de521dcf19d25253d42fc9c971d56ba", "start_char": 0, "end_char": 1310, "text_sha256": "1e145fb1c4163d9e0cd10a4055b68fa47de521dcf19d25253d42fc9c971d56ba"} [bg-p42214334] Oat-β-glucan potentiates anti-PD-1 efficacy through Faecalibacterium prausnitzii-derived butyrate and indole-3-propionic acid. (2026). https://pubmed.ncbi.nlm.nih.gov/42214334/ DOI: 10.1016/j.chom.2026.05.002
    Complete structured claim and evidence

  2. A three-day intervention with granola containing cereal beta-glucan improved the glycemic response and changed the gut microbiota, with circulating acetate and butyrate increasing while propionate did not, in a study in which participants consumed granolas of differing beta-glucan content in fixed sequence and in which the granolas also differed in other constituents.

    Oat mixed-linkage beta-(1->3)/(1->4)-glucan → Circulating short-chain fatty acid concentrations source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/glucan-research/35578615.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "df79afd1ef3d79ffee2a9da5f5f7e487f296cca7e9ccfcda177266b08efed747", "start_char": 0, "end_char": 2197, "text_sha256": "df79afd1ef3d79ffee2a9da5f5f7e487f296cca7e9ccfcda177266b08efed747"}
    experimental_model
    Fixed-sequence crossover intervention with three granolas over three days each
    exposure
    Granola containing low, medium or high cereal beta-glucan, given in that order
    limitations
    Fourteen completers, a fixed sequence rather than randomised order, and granolas that differed in other constituents including inulin. Short-chain fatty acids were measured in blood while faecal samples were used for the microbiota.
    nutrient_topic
    Beta-glucan research collection; topical membership is not evidence of a direct clinical effect, and each preparation is recorded as its own entity with no family link joining any pair. · Beta-glucan
    organism
    Human
    plain_language
    Three days of a cereal glucan raised two of the three main fermentation acids in the blood.
    primary_references
    [bg-p35578615] A Three-Day Intervention With Granola Containing Cereal Beta-Glucan Improves Glycemic Response and Changes the Gut Microbiota in Healthy Individuals: A Crossover Study. (2022). https://pubmed.ncbi.nlm.nih.gov/35578615/ DOI: 10.3389/fnut.2022.796362
    tissue_or_cell_type
    Blood and faecal microbiota

    Beta-glucan: a structural family rather than an agent, what decides whether a bound glucan actually signals, the complement route that a cereal and a yeast preparation share, and the unequal human evidence behind each (2026-09-22) · lines 645–656

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Fixed-sequence crossover intervention with three granolas over three days each · source_derived_draft · unverified_draft

    ### bg-circulating-scfa-rise-with-granola A three-day intervention with granola containing cereal beta-glucan improved the glycemic response and changed the gut microbiota, with circulating acetate and butyrate increasing while propionate did not, in a study in which participants consumed granolas of differing beta-glucan content in fixed sequence and in which the granolas also differed in other constituents. Condition category: normal nutrient_topic: Beta-glucan research collection; topical membership is not evidence of a direct clinical effect, and each preparation is recorded as its own entity with no family link joining any pair. plain_language: Three days of a cereal glucan raised two of the three main fermentation acids in the blood. organism: Human tissue_or_cell_type: Blood and faecal microbiota experimental_model: Fixed-sequence crossover intervention with three granolas over three days each limitations: Fourteen completers, a fixed sequence rather than randomised order, and granolas that differed in other constituents including inulin. Short-chain fatty acids were measured in blood while faecal samples were used for the microbiota. exposure: Granola containing low, medium or high cereal beta-glucan, given in that order evidence_span: {"source_cache": "artifacts/glucan-research/35578615.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "df79afd1ef3d79ffee2a9da5f5f7e487f296cca7e9ccfcda177266b08efed747", "start_char": 0, "end_char": 2197, "text_sha256": "df79afd1ef3d79ffee2a9da5f5f7e487f296cca7e9ccfcda177266b08efed747"} [bg-p35578615] A Three-Day Intervention With Granola Containing Cereal Beta-Glucan Improves Glycemic Response and Changes the Gut Microbiota in Healthy Individuals: A Crossover Study. (2022). https://pubmed.ncbi.nlm.nih.gov/35578615/ DOI: 10.3389/fnut.2022.796362
    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