Component

Human bile acid-CoA:amino acid N-acyltransferase / BAAT

Context-specific entity; species, compartment and exposure are stated on each claim.

4 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. The same expressed human BAAT also catalyzed glycine conjugation of cholic acid.

    Human bile acid-CoA:amino acid N-acyltransferase / BAAT → Glycocholate source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Recombinant human enzyme.
    limitations
    Shared enzyme use does not establish clinical competition or a need to balance glycine and taurine supplements.
    nutrient_topic
    Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
    plain_language
    Glycine and taurine converge on the same bile-conjugating enzyme.
    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 305–311

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

    ## taurine-baat-glycine Glycine and taurine converge on the same bile-conjugating enzyme. The same expressed human BAAT also catalyzed glycine conjugation of cholic acid. Model: Recombinant human enzyme. Limitations: Shared enzyme use does not establish clinical competition or a need to balance glycine and taurine supplements. 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

  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. 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. 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