Component

Taurocholate

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

6 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. Adding taurocholic acid, but not glycocholic acid, to a low-fat mouse diet promoted Bilophila wadsworthia expansion.

    Taurocholate → Bilophila expansion in the milk-fat/taurocholate mouse experiments source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Mouse dietary experiments with conjugate comparison.
    limitations
    The intervention was taurocholate, not free taurine alone; microbial community and host genotype matter.
    nutrient_topic
    Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
    plain_language
    Taurine-conjugated bile supplies sulfur that certain microbes can exploit.
    primary_references
    Dietary-fat-induced taurocholic acid promotes pathobiont expansion and colitis in Il10-/- mice. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22722865/ · DOI 10.1038/nature11225

    Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 329–335

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse dietary experiments with conjugate comparison. · source_derived_draft · unverified_draft

    ## taurine-microbial-bilophila Taurine-conjugated bile supplies sulfur that certain microbes can exploit. Adding taurocholic acid, but not glycocholic acid, to a low-fat mouse diet promoted Bilophila wadsworthia expansion. Model: Mouse dietary experiments with conjugate comparison. Limitations: The intervention was taurocholate, not free taurine alone; microbial community and host genotype matter. Evidence access: Primary abstract Dietary-fat-induced taurocholic acid promotes pathobiont expansion and colitis in Il10-/- mice. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22722865/ · DOI 10.1038/nature11225
    Complete structured claim and evidence

  2. Taurocholic-acid feeding promoted colitis in Il10-null mice; milk-fat-associated microbial expansion and inflammation depended on host susceptibility.

    Taurocholate → Colitis in Il10-null mice in the taurocholate study source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Il10-deficient and wild-type mouse comparisons.
    limitations
    Not a demonstration that taurine causes human inflammatory bowel disease.
    nutrient_topic
    Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
    plain_language
    A sulfur-using microbial route worsened inflammation in this susceptible model.
    primary_references
    Dietary-fat-induced taurocholic acid promotes pathobiont expansion and colitis in Il10-/- mice. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22722865/ · DOI 10.1038/nature11225

    Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 337–343

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Il10-deficient and wild-type mouse comparisons. · source_derived_draft · unverified_draft

    ## taurine-microbial-colitis A sulfur-using microbial route worsened inflammation in this susceptible model. Taurocholic-acid feeding promoted colitis in Il10-null mice; milk-fat-associated microbial expansion and inflammation depended on host susceptibility. Model: Il10-deficient and wild-type mouse comparisons. Limitations: Not a demonstration that taurine causes human inflammatory bowel disease. Evidence access: Primary abstract Dietary-fat-induced taurocholic acid promotes pathobiont expansion and colitis in Il10-/- mice. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22722865/ · DOI 10.1038/nature11225
    Complete structured claim and evidence

What acts on it

  1. Expression of cloned human BAAT produced bile acid conjugation activity using taurine, establishing that the enzyme can make taurine-conjugated cholic acid from its activated CoA substrate.

    Human bile acid-CoA:amino acid N-acyltransferase / BAAT → Taurocholate source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Human liver cDNA expressed in bacteria; activity compared with purified liver enzyme.
    limitations
    Conjugated bile acid and free taurine are separate molecules.
    nutrient_topic
    Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
    plain_language
    Taurine becomes chemically attached to bile acids.
    primary_references
    Glycine and taurine conjugation of bile acids by a single enzyme. Molecular cloning and expression of human liver bile acid CoA:amino acid N-acyltransferase. · 1994 · https://pubmed.ncbi.nlm.nih.gov/8034703/

    Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 297–303

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human liver cDNA expressed in bacteria; activity compared with purified liver enzyme. · source_derived_draft · unverified_draft

    ## taurine-baat-taurine Taurine becomes chemically attached to bile acids. Expression of cloned human BAAT produced bile acid conjugation activity using taurine, establishing that the enzyme can make taurine-conjugated cholic acid from its activated CoA substrate. Model: Human liver cDNA expressed in bacteria; activity compared with purified liver enzyme. Limitations: Conjugated bile acid and free taurine are separate molecules. Evidence access: Primary abstract Glycine and taurine conjugation of bile acids by a single enzyme. Molecular cloning and expression of human liver bile acid CoA:amino acid N-acyltransferase. · 1994 · https://pubmed.ncbi.nlm.nih.gov/8034703/
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. L243P, T262M and the double mutant abolished taurocholate and other bile-acid transport in transfected cells.

    Human ileal sodium/bile acid transporter ASBT / SLC10A2 → Ileal epithelial bile acid uptake source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/sodium-research/9109432.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "019508b2d05ec7e21a73ff66bdea9a0b09c6c7e7d8e404de3db49b2a0825ebbe", "start_char": 0, "end_char": 1389, "text_sha256": "019508b2d05ec7e21a73ff66bdea9a0b09c6c7e7d8e404de3db49b2a0825ebbe"}
    experimental_model
    Human family genetics and transfected COS-cell transport assays
    exposure
    L243P, T262M and double-mutant constructs
    limitations
    Family-specific genetic disease; loss of bile-acid transport was tested, whereas individual fat-soluble-vitamin deficiencies were not.
    nutrient_topic
    Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
    organism
    Human SLC10A2
    plain_language
    A sodium-coupled transporter helps recycle bile acids; mutations can break that route.
    primary_references
    [sodium-p9109432] Primary bile acid malabsorption caused by mutations in the ileal sodium-dependent bile acid transporter gene (SLC10A2). (1997). https://pubmed.ncbi.nlm.nih.gov/9109432/ DOI: 10.1172/jci119355
    tissue_or_cell_type
    Ileal bile-acid transporter
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 642–653

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human family genetics and transfected COS-cell transport assays · source_derived_draft · unverified_draft

    ### sodium-asbt-loss L243P, T262M and the double mutant abolished taurocholate and other bile-acid transport in transfected cells. Condition category: machinery_impairment nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A sodium-coupled transporter helps recycle bile acids; mutations can break that route. organism: Human SLC10A2 tissue_or_cell_type: Ileal bile-acid transporter experimental_model: Human family genetics and transfected COS-cell transport assays limitations: Family-specific genetic disease; loss of bile-acid transport was tested, whereas individual fat-soluble-vitamin deficiencies were not. exposure: L243P, T262M and double-mutant constructs evidence_span: {"source_cache": "artifacts/sodium-research/9109432.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "019508b2d05ec7e21a73ff66bdea9a0b09c6c7e7d8e404de3db49b2a0825ebbe", "start_char": 0, "end_char": 1389, "text_sha256": "019508b2d05ec7e21a73ff66bdea9a0b09c6c7e7d8e404de3db49b2a0825ebbe"} [sodium-p9109432] Primary bile acid malabsorption caused by mutations in the ileal sodium-dependent bile acid transporter gene (SLC10A2). (1997). https://pubmed.ncbi.nlm.nih.gov/9109432/ DOI: 10.1172/jci119355
    Complete structured claim and evidence

  2. Patients with defective bile acid amidation lacked glycine and taurine conjugates in urine, bile and serum; four homozygous BAAT mutations were identified among eight tested patients.

    Human bile acid-CoA:amino acid N-acyltransferase / BAAT → Human hepatic bile acid amidation source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary abstract
    experimental_model
    Ten pediatric patients; bile chemistry and genetic investigation.
    limitations
    Not evidence that isolated dietary taurine shortage causes the same phenotype.
    nutrient_topic
    Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
    plain_language
    A broken conjugation enzyme affects both amino-acid routes.
    primary_references
    Genetic defects in bile acid conjugation cause fat-soluble vitamin deficiency. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23415802/ · DOI 10.1053/j.gastro.2013.02.004
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 313–319

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Ten pediatric patients; bile chemistry and genetic investigation. · source_derived_draft · unverified_draft

    ## taurine-baat-loss A broken conjugation enzyme affects both amino-acid routes. Patients with defective bile acid amidation lacked glycine and taurine conjugates in urine, bile and serum; four homozygous BAAT mutations were identified among eight tested patients. Model: Ten pediatric patients; bile chemistry and genetic investigation. Limitations: Not evidence that isolated dietary taurine shortage causes the same phenotype. Evidence access: Primary abstract Genetic defects in bile acid conjugation cause fat-soluble vitamin deficiency. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23415802/ · DOI 10.1053/j.gastro.2013.02.004
    Complete structured claim and evidence

  3. The pediatric bile acid amidation disorder was associated with insufficient effective duodenal bile acids, fat-soluble vitamin deficiency and growth failure in affected children.

    Human hepatic bile acid amidation → Fat-soluble vitamin malabsorption in human bile acid amidation deficiency source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary abstract
    experimental_model
    Human genetic disease cohort and biochemical characterization.
    limitations
    The study tests conjugation failure, not taurine supplement efficacy or one universal vitamin deficit.
    nutrient_topic
    Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
    plain_language
    Failed bile chemistry can make fat-soluble nutrient absorption fail downstream.
    primary_references
    Genetic defects in bile acid conjugation cause fat-soluble vitamin deficiency. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23415802/ · DOI 10.1053/j.gastro.2013.02.004
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 321–327

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human genetic disease cohort and biochemical characterization. · source_derived_draft · unverified_draft

    ## taurine-bile-vitamin-absorption Failed bile chemistry can make fat-soluble nutrient absorption fail downstream. The pediatric bile acid amidation disorder was associated with insufficient effective duodenal bile acids, fat-soluble vitamin deficiency and growth failure in affected children. Model: Human genetic disease cohort and biochemical characterization. Limitations: The study tests conjugation failure, not taurine supplement efficacy or one universal vitamin deficit. Evidence access: Primary abstract Genetic defects in bile acid conjugation cause fat-soluble vitamin deficiency. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23415802/ · DOI 10.1053/j.gastro.2013.02.004
    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