Component

Serum zinc concentration

Measured circulating zinc concentration.

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. Intestinal Trpm7 deletion reduced circulating zinc in early postnatal mice.

    Intestine-specific Trpm7-null mouse genotype → Serum zinc concentration source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    Shared intestinal TRPM7 machinery links zinc and magnesium availability; Mg deficiency as the cause of Zn deficiency was not demonstrated.
    evidence-system
    Conditional intestinal knockout and mineral phenotyping
    experimental_model
    Conditional intestinal knockout and mineral phenotyping
    limitations
    Not evidence that magnesium supplementation universally increases zinc absorption.
    nutrient_topic
    Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
    organism
    Mouse
    plain_language
    A single epithelial machinery defect depleted zinc along with magnesium.
    primary_references
    [mittermeier-2019-trpm7] TRPM7 is the central gatekeeper of intestinal mineral absorption essential for postnatal survival (2019). https://pubmed.ncbi.nlm.nih.gov/30770447/ DOI: 10.1073/pnas.1810633116
    tissue
    Intestine; serum
    tissue_or_cell_type
    Intestine; serum
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1002–1014

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

    ### intestinal-trpm7-loss-zinc Intestinal Trpm7 deletion reduced circulating zinc in early postnatal mice. Condition category: machinery_impairment nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A single epithelial machinery defect depleted zinc along with magnesium. organism: Mouse tissue_or_cell_type: Intestine; serum experimental_model: Conditional intestinal knockout and mineral phenotyping limitations: Not evidence that magnesium supplementation universally increases zinc absorption. cross_nutrient: Shared intestinal TRPM7 machinery links zinc and magnesium availability; Mg deficiency as the cause of Zn deficiency was not demonstrated. evidence-system: Conditional intestinal knockout and mineral phenotyping tissue: Intestine; serum [mittermeier-2019-trpm7] TRPM7 is the central gatekeeper of intestinal mineral absorption essential for postnatal survival (2019). https://pubmed.ncbi.nlm.nih.gov/30770447/ DOI: 10.1073/pnas.1810633116
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Serum ceruloplasmin was unchanged in both intervention groups despite lower erythrocyte Cu/Zn-superoxide dismutase activity; serum zinc rose in both groups.

    Zinc gluconate → Serum ceruloplasmin concentration source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    Copper (affected_nutrient); Serum zinc concentration (increased_marker); Erythrocyte copper/zinc superoxide dismutase activity (decreased_marker)
    evidence_location
    Indexed primary abstract.
    evidence_span
    {"source_cache": "artifacts/zinc-clinical-sources/yadrick1989.abstract.txt", "locator": "Primary indexed abstract; complete local file", "file_sha256": "e2d70d43dded75edb026cac237f238d9e59399db6094098796e169f20e819443", "utf8_bytes": 969}
    experimental_model
    Ten-week zinc or zinc-plus-iron intervention in adult women
    exposure
    50 mg elemental zinc/day as gluconate, with or without 50 mg iron/day as ferrous sulfate monohydrate.
    limitations
    Reported comparisons are within-group pretreatment versus 10 weeks, not placebo-adjusted effects. ESOD is a functional biomarker, not a diagnosis of symptomatic copper deficiency.
    nutrient_topic
    Zinc research collection; topical membership is not evidence of a direct dietary effect. · Zinc
    organism
    Homo sapiens
    plain_language
    A rising zinc blood level and unchanged ceruloplasmin did not capture every functional change.
    primary_references
    [zn-clin-yadrick1989] Iron, copper, and zinc status: response to supplementation with zinc or zinc and iron in adult females. (1989). https://pubmed.ncbi.nlm.nih.gov/2912000/ DOI: 10.1093/ajcn/49.1.145
    tissue_or_cell_type
    Blood and erythrocytes

    Zinc: transport, enzyme loading, deficiency and nutrient interactions (2026-09-17) · lines 1211–1224

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Ten-week zinc or zinc-plus-iron intervention in adult women · source_derived_draft · unverified_draft

    ### zn-clin-ceruloplasmin-null Serum ceruloplasmin was unchanged in both intervention groups despite lower erythrocyte Cu/Zn-superoxide dismutase activity; serum zinc rose in both groups. Condition category: normal nutrient_topic: Zinc research collection; topical membership is not evidence of a direct dietary effect. plain_language: A rising zinc blood level and unchanged ceruloplasmin did not capture every functional change. organism: Homo sapiens tissue_or_cell_type: Blood and erythrocytes experimental_model: Ten-week zinc or zinc-plus-iron intervention in adult women limitations: Reported comparisons are within-group pretreatment versus 10 weeks, not placebo-adjusted effects. ESOD is a functional biomarker, not a diagnosis of symptomatic copper deficiency. exposure: 50 mg elemental zinc/day as gluconate, with or without 50 mg iron/day as ferrous sulfate monohydrate. cross_nutrient: Copper (affected_nutrient); Serum zinc concentration (increased_marker); Erythrocyte copper/zinc superoxide dismutase activity (decreased_marker) evidence_location: Indexed primary abstract. evidence_span: {"source_cache": "artifacts/zinc-clinical-sources/yadrick1989.abstract.txt", "locator": "Primary indexed abstract; complete local file", "file_sha256": "e2d70d43dded75edb026cac237f238d9e59399db6094098796e169f20e819443", "utf8_bytes": 969} [zn-clin-yadrick1989] Iron, copper, and zinc status: response to supplementation with zinc or zinc and iron in adult females. (1989). https://pubmed.ncbi.nlm.nih.gov/2912000/ DOI: 10.1093/ajcn/49.1.145
    Complete structured claim and evidence

  2. Hepatic zinc content differed across stages of alcoholic liver disease and in patients with chronic active and chronic persistent hepatitis.

    Habitual alcohol consumption → Hepatic zinc content source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/alcohol-research/3192174.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7f6eab91e632a1ddf96193486fc1be8bffa4acb0b48d062fef2b65affe168ca3", "start_char": 0, "end_char": 1588, "text_sha256": "7f6eab91e632a1ddf96193486fc1be8bffa4acb0b48d062fef2b65affe168ca3"}
    experimental_model
    Hepatic zinc measurement across stages of alcoholic liver disease and chronic hepatitis
    exposure
    Staged alcoholic liver disease compared with chronic hepatitis
    limitations
    A human tissue measurement with a disease control group, which separates alcohol from liver disease in general.
    nutrient_topic
    Alcohol research collection; topical membership is not evidence of a direct clinical effect, and ethanol is recorded separately from the acetaldehyde it becomes. · Ethanol
    organism
    Human
    plain_language
    The liver itself holds less zinc as the disease advances.
    primary_references
    [alcohol-p3192174] Hepatic zinc content in patients with various stages of alcoholic liver disease and in patients with chronic active and chronic persistent hepatitis. (1988). https://pubmed.ncbi.nlm.nih.gov/3192174/ DOI: 10.1002/hep.1840080622
    tissue_or_cell_type
    Liver
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Alcohol: ethanol clearance, acetaldehyde, the channels it binds, organ injury and nutrient collisions (2026-09-21) · lines 800–811

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Hepatic zinc measurement across stages of alcoholic liver disease and chronic hepatitis · source_derived_draft · unverified_draft

    ### alcohol-hepatic-zinc-depletion Hepatic zinc content differed across stages of alcoholic liver disease and in patients with chronic active and chronic persistent hepatitis. Condition category: nutrient_deficiency nutrient_topic: Alcohol research collection; topical membership is not evidence of a direct clinical effect, and ethanol is recorded separately from the acetaldehyde it becomes. plain_language: The liver itself holds less zinc as the disease advances. organism: Human tissue_or_cell_type: Liver experimental_model: Hepatic zinc measurement across stages of alcoholic liver disease and chronic hepatitis limitations: A human tissue measurement with a disease control group, which separates alcohol from liver disease in general. exposure: Staged alcoholic liver disease compared with chronic hepatitis evidence_span: {"source_cache": "artifacts/alcohol-research/3192174.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7f6eab91e632a1ddf96193486fc1be8bffa4acb0b48d062fef2b65affe168ca3", "start_char": 0, "end_char": 1588, "text_sha256": "7f6eab91e632a1ddf96193486fc1be8bffa4acb0b48d062fef2b65affe168ca3"} [alcohol-p3192174] Hepatic zinc content in patients with various stages of alcoholic liver disease and in patients with chronic active and chronic persistent hepatitis. (1988). https://pubmed.ncbi.nlm.nih.gov/3192174/ DOI: 10.1002/hep.1840080622
    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