Component

Bile acids (assay substrates specified per claim)

Bile acids (assay substrates specified per claim). Species, exposure and limitations are retained in each linked claim.

2 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

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. Fecal bile-acid excretion rose by 35%.

    Pectin, structurally heterogeneous plant polysaccharides → Human fecal bile-acid excretion source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/pectin-research/37887.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ad5427835e84a210b32e8ceea45baeece0bc1e4488d5852a5b4244f51dc32a69", "start_char": 0, "end_char": 1141, "text_sha256": "ad5427835e84a210b32e8ceea45baeece0bc1e4488d5852a5b4244f51dc32a69"}
    experimental_model
    Controlled feeding and balance study in five healthy men
    exposure
    Nine-week protocol; 36 g/day pectin during last six weeks
    limitations
    Small older study. Disappearance from stool supported fermentation but did not assign a particular enzyme or metabolic flux.
    nutrient_topic
    Pectin research collection; topical membership is not evidence of a direct dietary effect. · Pectin, structurally heterogeneous plant polysaccharides
    organism
    Homo sapiens
    plain_language
    More bile acids left the body in stool; this study did not directly test hepatic CYP7A1.
    primary_references
    [pectin-p37887] The digestion of pectin in the human gut and its effect on calcium absorption and large bowel function. (1979). https://pubmed.ncbi.nlm.nih.gov/37887/ DOI: 10.1079/bjn19790062
    tissue_or_cell_type
    Whole-gut balance and stool

    Pectin: metabolism, signaling and nutrient connections (2026-09-17) · lines 737–748

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Controlled feeding and balance study in five healthy men · source_derived_draft · unverified_draft

    ### pectin-bile-excretion Fecal bile-acid excretion rose by 35%. Condition category: normal nutrient_topic: Pectin research collection; topical membership is not evidence of a direct dietary effect. plain_language: More bile acids left the body in stool; this study did not directly test hepatic CYP7A1. organism: Homo sapiens tissue_or_cell_type: Whole-gut balance and stool experimental_model: Controlled feeding and balance study in five healthy men limitations: Small older study. Disappearance from stool supported fermentation but did not assign a particular enzyme or metabolic flux. exposure: Nine-week protocol; 36 g/day pectin during last six weeks evidence_span: {"source_cache": "artifacts/pectin-research/37887.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ad5427835e84a210b32e8ceea45baeece0bc1e4488d5852a5b4244f51dc32a69", "start_char": 0, "end_char": 1141, "text_sha256": "ad5427835e84a210b32e8ceea45baeece0bc1e4488d5852a5b4244f51dc32a69"} [pectin-p37887] The digestion of pectin in the human gut and its effect on calcium absorption and large bowel function. (1979). https://pubmed.ncbi.nlm.nih.gov/37887/ DOI: 10.1079/bjn19790062
    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