Component

Tissue total zinc content

Tissue total zinc content

1 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 acts on it

  1. Enterocyte-specific Slc39a4 deletion rapidly lowered total zinc in mouse small intestine, liver and pancreas.

    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    false
    experimental_model
    Tamoxifen-inducible enterocyte-specific knockout and tissue elemental analysis
    exposure
    Conditional gene deletion compared with intact controls.
    limitations
    A genetic transport defect is not interchangeable with low intake. Total tissue zinc does not resolve labile versus protein-bound zinc.
    nutrient_topic
    Zinc research collection; topical membership is not evidence of a direct dietary effect. · Zinc
    organism
    Mus musculus
    plain_language
    Disabling intestinal ZIP4 depleted zinc beyond the intestine.
    primary_references
    [zinc-trans-22737083] A mouse model of acrodermatitis enteropathica: loss of intestine zinc transporter ZIP4 (Slc39a4) disrupts the stem cell niche and intestine integrity. (2012). https://pubmed.ncbi.nlm.nih.gov/22737083/ DOI: 10.1371/journal.pgen.1002766
    tissue_or_cell_type
    Small intestine, liver, pancreas
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Zinc: transport, enzyme loading, deficiency and nutrient interactions (2026-09-17) · lines 271–282

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Tamoxifen-inducible enterocyte-specific knockout and tissue elemental analysis · source_derived_draft · unverified_draft

    ### zinc-trans-zip4-knockout-tissue-zinc Enterocyte-specific Slc39a4 deletion rapidly lowered total zinc in mouse small intestine, liver and pancreas. Condition category: machinery_impairment nutrient_topic: Zinc research collection; topical membership is not evidence of a direct dietary effect. plain_language: Disabling intestinal ZIP4 depleted zinc beyond the intestine. organism: Mus musculus tissue_or_cell_type: Small intestine, liver, pancreas experimental_model: Tamoxifen-inducible enterocyte-specific knockout and tissue elemental analysis limitations: A genetic transport defect is not interchangeable with low intake. Total tissue zinc does not resolve labile versus protein-bound zinc. exposure: Conditional gene deletion compared with intact controls. cross_nutrient: false [zinc-trans-22737083] A mouse model of acrodermatitis enteropathica: loss of intestine zinc transporter ZIP4 (Slc39a4) disrupts the stem cell niche and intestine integrity. (2012). https://pubmed.ncbi.nlm.nih.gov/22737083/ DOI: 10.1371/journal.pgen.1002766
    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