Component
Hepatic iron, manganese and copper accumulation
Jointly measured tissue-metal accumulation in the specified mouse disease model.
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.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
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.
What acts on it
After enterocyte Zip4 deletion in mice, liver iron, manganese and copper gradually accumulated as the zinc-depletion disease progressed.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- cross_nutrient
- false
- evidence_span
- {"source_cache": "artifacts/zinc-transport-sources/22737083-abstract.txt", "locator": "Primary indexed abstract; tissue elemental analysis", "file_sha256": "4643d3986c556a001c45365febbb07095bcdc8bc604e30488d3fb98a23511a4b"}
- 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. Tissue accumulation is not proof of systemic nutritional adequacy of the other metals.
- nutrient_topic
- Zinc research collection; topical membership is not evidence of a direct dietary effect. · Zinc
- organism
- Mus musculus
- plain_language
- Loss of zinc uptake disrupted the distribution of several other metals.
- 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 585–597
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-other-metals After enterocyte Zip4 deletion in mice, liver iron, manganese and copper gradually accumulated as the zinc-depletion disease progressed. Condition category: machinery_impairment nutrient_topic: Zinc research collection; topical membership is not evidence of a direct dietary effect. plain_language: Loss of zinc uptake disrupted the distribution of several other metals. 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. Tissue accumulation is not proof of systemic nutritional adequacy of the other metals. exposure: Conditional gene deletion compared with intact controls. cross_nutrient: false evidence_span: {"source_cache": "artifacts/zinc-transport-sources/22737083-abstract.txt", "locator": "Primary indexed abstract; tissue elemental analysis", "file_sha256": "4643d3986c556a001c45365febbb07095bcdc8bc604e30488d3fb98a23511a4b"} [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
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.