Component

Tryptamine

Context-specific entity; species, compartment and exposure are stated on each 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. Tryptamine increased epithelial ionic flux and colonoid fluid secretion through 5-HT4 receptors in mice.

    Tryptamine → Mouse colonic ionic and fluid secretion after tryptamine source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Germ-free and human-stool-colonized mouse tissue/colonoids.
    limitations
    Humanized microbiota does not make the host tissue human.
    nutrient_topic
    Tryptophan collection; molecular form, preparation, species, exposure and manipulation remain explicit. · L-Tryptophan
    plain_language
    A microbial tryptophan product can change intestinal fluid movement.
    primary_references
    Gut Microbiota-Produced Tryptamine Activates an Epithelial G-Protein-Coupled Receptor to Increase Colonic Secretion. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29902441/ · DOI 10.1016/j.chom.2018.05.004

    Tryptophan: transport, protein synthesis, neuroactive metabolites, NAD and microbial pathways (2026-09-19) · lines 562–568

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Germ-free and human-stool-colonized mouse tissue/colonoids. · source_derived_draft · unverified_draft

    ## tryptophan-tryptamine-secretion A microbial tryptophan product can change intestinal fluid movement. Tryptamine increased epithelial ionic flux and colonoid fluid secretion through 5-HT4 receptors in mice. Model: Germ-free and human-stool-colonized mouse tissue/colonoids. Limitations: Humanized microbiota does not make the host tissue human. Evidence access: Primary abstract Gut Microbiota-Produced Tryptamine Activates an Epithelial G-Protein-Coupled Receptor to Increase Colonic Secretion. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29902441/ · DOI 10.1016/j.chom.2018.05.004
    Complete structured claim and evidence

  2. Colonizing germ-free mice with B. thetaiotaomicron engineered to produce tryptamine accelerated gastrointestinal transit.

    Tryptamine → Mouse gastrointestinal transit after microbial tryptamine source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Engineered bacterium in gnotobiotic mice.
    limitations
    Not evidence that tryptophan supplements have the same effect in humans.
    nutrient_topic
    Tryptophan collection; molecular form, preparation, species, exposure and manipulation remain explicit. · L-Tryptophan
    plain_language
    Changing microbial production changed movement through the gut.
    primary_references
    Gut Microbiota-Produced Tryptamine Activates an Epithelial G-Protein-Coupled Receptor to Increase Colonic Secretion. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29902441/ · DOI 10.1016/j.chom.2018.05.004

    Tryptophan: transport, protein synthesis, neuroactive metabolites, NAD and microbial pathways (2026-09-19) · lines 578–584

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Engineered bacterium in gnotobiotic mice. · source_derived_draft · unverified_draft

    ## tryptophan-tryptamine-transit Changing microbial production changed movement through the gut. Colonizing germ-free mice with B. thetaiotaomicron engineered to produce tryptamine accelerated gastrointestinal transit. Model: Engineered bacterium in gnotobiotic mice. Limitations: Not evidence that tryptophan supplements have the same effect in humans. Evidence access: Primary abstract Gut Microbiota-Produced Tryptamine Activates an Epithelial G-Protein-Coupled Receptor to Increase Colonic Secretion. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29902441/ · DOI 10.1016/j.chom.2018.05.004
    Complete structured claim and evidence

What acts on it

  1. Purified C. sporogenes CLOSPO_02083 catalyzed tryptophan decarboxylation to tryptamine as a PLP-dependent enzyme.

    Clostridium sporogenes CLOSPO_02083 tryptophan decarboxylase → Tryptamine source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary full text, enzyme identification and biochemical assays
    experimental_model
    Recombinant bacterial enzyme biochemistry.
    limitations
    Does not establish that B6 supplementation increases this product in humans.
    nutrient_topic
    Tryptophan collection; molecular form, preparation, species, exposure and manipulation remain explicit. · L-Tryptophan
    plain_language
    A bacterial B6-dependent enzyme sends tryptophan down another branch.
    primary_references
    Discovery and characterization of gut microbiota decarboxylases that can produce the neurotransmitter tryptamine. · 2014 · https://pubmed.ncbi.nlm.nih.gov/25263219/ · DOI 10.1016/j.chom.2014.09.001

    Tryptophan: transport, protein synthesis, neuroactive metabolites, NAD and microbial pathways (2026-09-19) · lines 546–552

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Recombinant bacterial enzyme biochemistry. · source_derived_draft · unverified_draft

    ## tryptophan-clostridial-tryptamine A bacterial B6-dependent enzyme sends tryptophan down another branch. Purified C. sporogenes CLOSPO_02083 catalyzed tryptophan decarboxylation to tryptamine as a PLP-dependent enzyme. Model: Recombinant bacterial enzyme biochemistry. Limitations: Does not establish that B6 supplementation increases this product in humans. Evidence access: Primary full text, enzyme identification and biochemical assays Discovery and characterization of gut microbiota decarboxylases that can produce the neurotransmitter tryptamine. · 2014 · https://pubmed.ncbi.nlm.nih.gov/25263219/ · DOI 10.1016/j.chom.2014.09.001
    Complete structured claim and evidence

  2. Purified R. gnavus RUMGNA_01526 robustly decarboxylated tryptophan despite only 26% sequence identity to the C. sporogenes enzyme.

    Ruminococcus gnavus RUMGNA_01526 tryptophan decarboxylase → Tryptamine source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary full text, enzyme screening and purification
    experimental_model
    Purified bacterial enzyme assays.
    limitations
    Enzyme presence and activity are not universal across human gut communities.
    nutrient_topic
    Tryptophan collection; molecular form, preparation, species, exposure and manipulation remain explicit. · L-Tryptophan
    plain_language
    Different microbes can reach the same metabolite with distinct proteins.
    primary_references
    Discovery and characterization of gut microbiota decarboxylases that can produce the neurotransmitter tryptamine. · 2014 · https://pubmed.ncbi.nlm.nih.gov/25263219/ · DOI 10.1016/j.chom.2014.09.001

    Tryptophan: transport, protein synthesis, neuroactive metabolites, NAD and microbial pathways (2026-09-19) · lines 554–560

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Purified bacterial enzyme assays. · source_derived_draft · unverified_draft

    ## tryptophan-ruminococcal-tryptamine Different microbes can reach the same metabolite with distinct proteins. Purified R. gnavus RUMGNA_01526 robustly decarboxylated tryptophan despite only 26% sequence identity to the C. sporogenes enzyme. Model: Purified bacterial enzyme assays. Limitations: Enzyme presence and activity are not universal across human gut communities. Evidence access: Primary full text, enzyme screening and purification Discovery and characterization of gut microbiota decarboxylases that can produce the neurotransmitter tryptamine. · 2014 · https://pubmed.ncbi.nlm.nih.gov/25263219/ · DOI 10.1016/j.chom.2014.09.001
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Htr4 knockout or receptor antagonism removed the secretory response to tryptamine.

    Mouse serotonin receptor 4 / Htr4 → Mouse colonic ionic and fluid secretion after tryptamine source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary abstract
    experimental_model
    Mouse knockout and pharmacological blockade.
    limitations
    Not a universal receptor requirement for every action of tryptamine.
    nutrient_topic
    Tryptophan collection; molecular form, preparation, species, exposure and manipulation remain explicit. · L-Tryptophan
    plain_language
    The metabolite could not produce this response without its receptor.
    primary_references
    Gut Microbiota-Produced Tryptamine Activates an Epithelial G-Protein-Coupled Receptor to Increase Colonic Secretion. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29902441/ · DOI 10.1016/j.chom.2018.05.004
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Tryptophan: transport, protein synthesis, neuroactive metabolites, NAD and microbial pathways (2026-09-19) · lines 570–576

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse knockout and pharmacological blockade. · source_derived_draft · unverified_draft

    ## tryptophan-htr4-loss The metabolite could not produce this response without its receptor. Htr4 knockout or receptor antagonism removed the secretory response to tryptamine. Model: Mouse knockout and pharmacological blockade. Limitations: Not a universal receptor requirement for every action of tryptamine. Evidence access: Primary abstract Gut Microbiota-Produced Tryptamine Activates an Epithelial G-Protein-Coupled Receptor to Increase Colonic Secretion. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29902441/ · DOI 10.1016/j.chom.2018.05.004
    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