Component

Blood manganese concentration (specimen not further specified)

Blood manganese concentration (specimen not further specified). Read the linked claim for experimental scope.

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.

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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

Where it participates (unsigned role)

  1. The genetic investigation linked SLC39A8 variants, very low blood manganese and type II glycosylation abnormalities.

    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    Human ZIP8 (SLC39A8) (affected_protein); Blood manganese concentration (specimen not further specified) (low_marker); UDP-galactose (related_substrate)
    evidence_span
    {"source_cache": "artifacts/manganese-clinical-sources/park2015.abstract.txt", "locator": "Indexed primary abstract", "file_sha256": "c4e7009c947d1854370f8c9f62c206a8c2190b2e23099a5b991b01465321023d", "start_char": 0, "end_char": 1348, "text_sha256": "c4e7009c947d1854370f8c9f62c206a8c2190b2e23099a5b991b01465321023d", "text_characters": 1348}
    experimental_model
    Genetic investigation of two individuals with SLC39A8-CDG
    exposure
    Affected individuals with compound heterozygous SLC39A8 variants.
    limitations
    Inherited transport failure is distinct from dietary shortage. The study supports hypogalactosylation but does not directly measure activity of every manganese enzyme in every tissue.
    nutrient_topic
    Manganese research collection; topical membership is not evidence of a direct dietary effect. · Manganese
    organism
    Homo sapiens
    plain_language
    A transport defect can deprive sugar-building enzymes of manganese.
    primary_references
    [mn-clin-park2015] SLC39A8 Deficiency: A Disorder of Manganese Transport and Glycosylation. (2015). https://pubmed.ncbi.nlm.nih.gov/26637979/ DOI: 10.1016/j.ajhg.2015.11.003
    tissue_or_cell_type
    Blood manganese and serum glycoproteins
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Manganese: enzyme cofactors, glycosylation, transport and nutrient interactions (2026-09-17) · lines 1174–1186

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Genetic investigation of two individuals with SLC39A8-CDG · source_derived_draft · unverified_draft

    ### mn-clin-zip8-glycosylation The genetic investigation linked SLC39A8 variants, very low blood manganese and type II glycosylation abnormalities. Condition category: machinery_impairment nutrient_topic: Manganese research collection; topical membership is not evidence of a direct dietary effect. plain_language: A transport defect can deprive sugar-building enzymes of manganese. organism: Homo sapiens tissue_or_cell_type: Blood manganese and serum glycoproteins experimental_model: Genetic investigation of two individuals with SLC39A8-CDG limitations: Inherited transport failure is distinct from dietary shortage. The study supports hypogalactosylation but does not directly measure activity of every manganese enzyme in every tissue. exposure: Affected individuals with compound heterozygous SLC39A8 variants. cross_nutrient: Human ZIP8 (SLC39A8) (affected_protein); Blood manganese concentration (specimen not further specified) (low_marker); UDP-galactose (related_substrate) evidence_span: {"source_cache": "artifacts/manganese-clinical-sources/park2015.abstract.txt", "locator": "Indexed primary abstract", "file_sha256": "c4e7009c947d1854370f8c9f62c206a8c2190b2e23099a5b991b01465321023d", "start_char": 0, "end_char": 1348, "text_sha256": "c4e7009c947d1854370f8c9f62c206a8c2190b2e23099a5b991b01465321023d", "text_characters": 1348} [mn-clin-park2015] SLC39A8 Deficiency: A Disorder of Manganese Transport and Glycosylation. (2015). https://pubmed.ncbi.nlm.nih.gov/26637979/ DOI: 10.1016/j.ajhg.2015.11.003
    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.

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