Component

Systemic manganese accumulation

Systemic manganese accumulation

3 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

What acts on it

  1. Intestine-specific Zip14 knockout increased liver and brain manganese in mice.

    Mouse intestine-specific Slc39a14 knockout genotype → Systemic manganese accumulation source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    false
    experimental_model
    Intestine-specific Slc39a14 knockout mice
    exposure
    Intestine-specific Slc39a14 knockout versus controls.
    limitations
    Liver and brain are specified outcomes; this statement does not imply every tissue or blood measure rose.
    nutrient_topic
    Manganese research collection; topical membership is not evidence of a direct dietary effect. · Manganese
    organism
    Mus musculus
    plain_language
    Intestinal ZIP14 loss increased manganese retained in distant tissues.
    primary_references
    [mn-trans-31028174] The intestinal metal transporter ZIP14 maintains systemic manganese homeostasis. (2019). https://pubmed.ncbi.nlm.nih.gov/31028174/ DOI: 10.1074/jbc.ra119.008762
    tissue_or_cell_type
    Intestine; manganese measured in liver and brain
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Manganese: enzyme cofactors, glycosylation, transport and nutrient interactions (2026-09-17) · lines 227–238

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Intestine-specific Slc39a14 knockout mice · source_derived_draft · unverified_draft

    ### mn-trans-intestinal-zip14-loss-tissue-mn Intestine-specific Zip14 knockout increased liver and brain manganese in mice. Condition category: machinery_impairment nutrient_topic: Manganese research collection; topical membership is not evidence of a direct dietary effect. plain_language: Intestinal ZIP14 loss increased manganese retained in distant tissues. organism: Mus musculus tissue_or_cell_type: Intestine; manganese measured in liver and brain experimental_model: Intestine-specific Slc39a14 knockout mice limitations: Liver and brain are specified outcomes; this statement does not imply every tissue or blood measure rose. exposure: Intestine-specific Slc39a14 knockout versus controls. cross_nutrient: false [mn-trans-31028174] The intestinal metal transporter ZIP14 maintains systemic manganese homeostasis. (2019). https://pubmed.ncbi.nlm.nih.gov/31028174/ DOI: 10.1074/jbc.ra119.008762
    Complete structured claim and evidence

  2. Combined liver and small-intestine Slc30a10 deficiency caused manganese excess that was less severe than in whole-body deficient mice.

    Mouse liver-and-small-intestine Slc30a10 double-knockout genotype → Systemic manganese accumulation source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    false
    experimental_model
    Whole-body and tissue-specific Slc30a10 knockout mice
    exposure
    Liver-and-small-intestine Slc30a10 deficiency compared with controls and whole-body deficiency.
    limitations
    The residual difference suggests other sites or adaptation; it does not identify a specific untested tissue.
    nutrient_topic
    Manganese research collection; topical membership is not evidence of a direct dietary effect. · Manganese
    organism
    Mus musculus
    plain_language
    Deleting the liver and gut exporter did not reproduce the full severity of deleting it everywhere.
    primary_references
    [mn-trans-31527311] Manganese transporter Slc30a10 controls physiological manganese excretion and toxicity. (2019). https://pubmed.ncbi.nlm.nih.gov/31527311/ DOI: 10.1172/jci129710
    tissue_or_cell_type
    Hepatocytes and small-intestinal enterocytes
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Manganese: enzyme cofactors, glycosylation, transport and nutrient interactions (2026-09-17) · lines 279–290

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Whole-body and tissue-specific Slc30a10 knockout mice · source_derived_draft · unverified_draft

    ### mn-trans-slc30a10-double-versus-global Combined liver and small-intestine Slc30a10 deficiency caused manganese excess that was less severe than in whole-body deficient mice. Condition category: machinery_impairment nutrient_topic: Manganese research collection; topical membership is not evidence of a direct dietary effect. plain_language: Deleting the liver and gut exporter did not reproduce the full severity of deleting it everywhere. organism: Mus musculus tissue_or_cell_type: Hepatocytes and small-intestinal enterocytes experimental_model: Whole-body and tissue-specific Slc30a10 knockout mice limitations: The residual difference suggests other sites or adaptation; it does not identify a specific untested tissue. exposure: Liver-and-small-intestine Slc30a10 deficiency compared with controls and whole-body deficiency. cross_nutrient: false [mn-trans-31527311] Manganese transporter Slc30a10 controls physiological manganese excretion and toxicity. (2019). https://pubmed.ncbi.nlm.nih.gov/31527311/ DOI: 10.1172/jci129710
    Complete structured claim and evidence

  3. Combined intestinal and hepatic Zip14 deletion increased systemic manganese burden more than intestinal deletion alone in mice.

    Mouse liver-and-intestine Slc39a14 double-knockout genotype → Systemic manganese accumulation source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    false
    experimental_model
    Single- and double-tissue Slc39a14 knockout mice; ICP-MS
    exposure
    Intestine-and-liver double knockout versus single-tissue knockout and floxed controls.
    limitations
    Supports organ cooperation, not a universal claim that liver-only deletion causes systemic overload.
    nutrient_topic
    Manganese research collection; topical membership is not evidence of a direct dietary effect. · Manganese
    organism
    Mus musculus
    plain_language
    Liver ZIP14 became especially important when intestinal ZIP14 was also absent.
    primary_references
    [mn-trans-35742937] The Combined Inactivation of Intestinal and Hepatic ZIP14 Exacerbates Manganese Overload in Mice. (2022). https://pubmed.ncbi.nlm.nih.gov/35742937/ DOI: 10.3390/ijms23126495
    tissue_or_cell_type
    Intestine, liver and systemic tissue manganese
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Manganese: enzyme cofactors, glycosylation, transport and nutrient interactions (2026-09-17) · lines 357–368

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Single- and double-tissue Slc39a14 knockout mice; ICP-MS · source_derived_draft · unverified_draft

    ### mn-trans-zip14-double-worsens-loading Combined intestinal and hepatic Zip14 deletion increased systemic manganese burden more than intestinal deletion alone in mice. Condition category: machinery_impairment nutrient_topic: Manganese research collection; topical membership is not evidence of a direct dietary effect. plain_language: Liver ZIP14 became especially important when intestinal ZIP14 was also absent. organism: Mus musculus tissue_or_cell_type: Intestine, liver and systemic tissue manganese experimental_model: Single- and double-tissue Slc39a14 knockout mice; ICP-MS limitations: Supports organ cooperation, not a universal claim that liver-only deletion causes systemic overload. exposure: Intestine-and-liver double knockout versus single-tissue knockout and floxed controls. cross_nutrient: false [mn-trans-35742937] The Combined Inactivation of Intestinal and Hepatic ZIP14 Exacerbates Manganese Overload in Mice. (2022). https://pubmed.ncbi.nlm.nih.gov/35742937/ DOI: 10.3390/ijms23126495
    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