Component

Human hepatic bile acid amidation

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

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

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

    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

What acts on it

  1. 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.

    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

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