Component

Mouse enterocyte-specific Slc39a5 knockout genotype

Engineered conditional loss-of-function genotype, not the wild-type gene. Induced intestinal deletion of mouse Slc39a5.

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 it acts on

  1. Enterocyte-specific Zip5 deletion increased pancreatic zinc in mice eating a zinc-adequate diet.

    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    false
    experimental_model
    Conditional intestinal knockout with tissue elemental analysis
    exposure
    Induced enterocyte deletion on zinc-adequate chow.
    limitations
    This measured redistribution supports but does not directly quantify the proposed blood-to-enterocyte-to-lumen excretion route.
    nutrient_topic
    Zinc research collection; topical membership is not evidence of a direct dietary effect. · Zinc
    organism
    Mus musculus
    plain_language
    Removing intestinal ZIP5 changed where zinc accumulated, increasing the pancreatic pool.
    primary_references
    [zinc-trans-24303081] The zinc transporter Zip5 (Slc39a5) regulates intestinal zinc excretion and protects the pancreas against zinc toxicity. (2013). https://pubmed.ncbi.nlm.nih.gov/24303081/ DOI: 10.1371/journal.pone.0082149
    tissue_or_cell_type
    Intestinal enterocytes; pancreatic zinc endpoint
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Zinc: transport, enzyme loading, deficiency and nutrient interactions (2026-09-17) · lines 388–399

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

    ### zinc-trans-intestinal-zip5-pancreas-zinc Enterocyte-specific Zip5 deletion increased pancreatic zinc in mice eating a zinc-adequate diet. Condition category: machinery_impairment nutrient_topic: Zinc research collection; topical membership is not evidence of a direct dietary effect. plain_language: Removing intestinal ZIP5 changed where zinc accumulated, increasing the pancreatic pool. organism: Mus musculus tissue_or_cell_type: Intestinal enterocytes; pancreatic zinc endpoint experimental_model: Conditional intestinal knockout with tissue elemental analysis limitations: This measured redistribution supports but does not directly quantify the proposed blood-to-enterocyte-to-lumen excretion route. exposure: Induced enterocyte deletion on zinc-adequate chow. cross_nutrient: false [zinc-trans-24303081] The zinc transporter Zip5 (Slc39a5) regulates intestinal zinc excretion and protects the pancreas against zinc toxicity. (2013). https://pubmed.ncbi.nlm.nih.gov/24303081/ DOI: 10.1371/journal.pone.0082149
    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