Component

Biliary manganese concentration

Measured manganese in bile; distinct from a rate of biliary excretion.

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 acts on it

  1. ZIP8-LSKO mice had increased bile manganese; ZIP8 localized to hepatocyte canalicular membranes, supporting biliary manganese reclamation.

    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    false
    experimental_model
    Mouse liver-specific Slc39a8 deletion and liver-directed human ZIP8 overexpression
    exposure
    Liver-specific Slc39a8 knockout versus controls.
    limitations
    Bile concentration and anatomical localization support reclamation; concentration is not itself a secretion-rate measurement.
    nutrient_topic
    Manganese research collection; topical membership is not evidence of a direct dietary effect. · Manganese
    organism
    Mus musculus
    plain_language
    Liver ZIP8 helps recover manganese from bile.
    primary_references
    [mn-trans-28481222] Hepatic metal ion transporter ZIP8 regulates manganese homeostasis and manganese-dependent enzyme activity. (2017). https://pubmed.ncbi.nlm.nih.gov/28481222/ DOI: 10.1172/jci90896
    tissue_or_cell_type
    Liver, bile and measured extrahepatic tissues
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Manganese: enzyme cofactors, glycosylation, transport and nutrient interactions (2026-09-17) · lines 162–173

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mouse liver-specific Slc39a8 deletion and liver-directed human ZIP8 overexpression · source_derived_draft · unverified_draft

    ### mn-trans-hepatic-zip8-loss-bile-mn ZIP8-LSKO mice had increased bile manganese; ZIP8 localized to hepatocyte canalicular membranes, supporting biliary manganese reclamation. Condition category: machinery_impairment nutrient_topic: Manganese research collection; topical membership is not evidence of a direct dietary effect. plain_language: Liver ZIP8 helps recover manganese from bile. organism: Mus musculus tissue_or_cell_type: Liver, bile and measured extrahepatic tissues experimental_model: Mouse liver-specific Slc39a8 deletion and liver-directed human ZIP8 overexpression limitations: Bile concentration and anatomical localization support reclamation; concentration is not itself a secretion-rate measurement. exposure: Liver-specific Slc39a8 knockout versus controls. cross_nutrient: false [mn-trans-28481222] Hepatic metal ion transporter ZIP8 regulates manganese homeostasis and manganese-dependent enzyme activity. (2017). https://pubmed.ncbi.nlm.nih.gov/28481222/ DOI: 10.1172/jci90896
    Complete structured claim and evidence
  2. Liver-directed human ZIP8 overexpression decreased bile manganese in mice.

    Experimental context and source evidence
    cross_nutrient
    false
    experimental_model
    Mouse liver-specific Slc39a8 deletion and liver-directed human ZIP8 overexpression
    exposure
    Liver-specific AAV-human-ZIP8 versus study controls.
    limitations
    Bile concentration is distinct from measured excretion flux.
    nutrient_topic
    Manganese research collection; topical membership is not evidence of a direct dietary effect. · Manganese
    organism
    Mus musculus with human ZIP8 transgene
    plain_language
    More liver ZIP8 left less manganese in bile.
    primary_references
    [mn-trans-28481222] Hepatic metal ion transporter ZIP8 regulates manganese homeostasis and manganese-dependent enzyme activity. (2017). https://pubmed.ncbi.nlm.nih.gov/28481222/ DOI: 10.1172/jci90896
    tissue_or_cell_type
    Liver, bile and measured extrahepatic tissues

    Manganese: enzyme cofactors, glycosylation, transport and nutrient interactions (2026-09-17) · lines 175–186

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mouse liver-specific Slc39a8 deletion and liver-directed human ZIP8 overexpression · source_derived_draft · unverified_draft

    ### mn-trans-hepatic-zip8-overexpression-bile-mn Liver-directed human ZIP8 overexpression decreased bile manganese in mice. Condition category: normal nutrient_topic: Manganese research collection; topical membership is not evidence of a direct dietary effect. plain_language: More liver ZIP8 left less manganese in bile. organism: Mus musculus with human ZIP8 transgene tissue_or_cell_type: Liver, bile and measured extrahepatic tissues experimental_model: Mouse liver-specific Slc39a8 deletion and liver-directed human ZIP8 overexpression limitations: Bile concentration is distinct from measured excretion flux. exposure: Liver-specific AAV-human-ZIP8 versus study controls. cross_nutrient: false [mn-trans-28481222] Hepatic metal ion transporter ZIP8 regulates manganese homeostasis and manganese-dependent enzyme activity. (2017). https://pubmed.ncbi.nlm.nih.gov/28481222/ DOI: 10.1172/jci90896
    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