Component

Serum iron concentration

Independent biological entity. Read linked claims for experimental scope and context.

4 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. After cobalamin therapy, mean serum iron fell from 126.4 to 59.1 micrograms/dL, ferritin from 192.5 to 44.9 ng/mL and transferrin saturation from 47.2% to 17.5%.

    Vitamin B12 (cobalamins) → Serum iron concentration source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    cross_nutrient
    B12-associated ineffective blood-cell production can complicate iron-status interpretation.
    experimental_model
    Before/after series of 75 patients diagnosed with cobalamin deficiency.
    exposure
    Blood counts and iron-status measurements before and after cobalamin therapy; regimen is not extracted from the abstract.
    limitations
    Before/after observations cannot isolate iron utilization from all other changes.
    nutrient_topic
    Vitamin B12 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B12 (cobalamins)
    organism
    Homo sapiens
    plain_language
    Restoring B12 changed how the blood iron results looked.
    primary_references
    [b12-solmaz2015] Cobalamin deficiency can mask depleted body iron reserves (2015). https://pubmed.ncbi.nlm.nih.gov/25825568/ DOI: 10.1007/s12288-014-0417-x
    tissue_or_cell_type
    Human blood or whole-person endpoints
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Vitamin B12: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1585–1596

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Before/after series of 75 patients diagnosed with cobalamin deficiency. · source_derived_draft · unverified_draft

    ### b12-repletion-iron-readouts After cobalamin therapy, mean serum iron fell from 126.4 to 59.1 micrograms/dL, ferritin from 192.5 to 44.9 ng/mL and transferrin saturation from 47.2% to 17.5%. Condition category: nutrient_deficiency nutrient_topic: Vitamin B12 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Restoring B12 changed how the blood iron results looked. organism: Homo sapiens tissue_or_cell_type: Human blood or whole-person endpoints experimental_model: Before/after series of 75 patients diagnosed with cobalamin deficiency. limitations: Before/after observations cannot isolate iron utilization from all other changes. exposure: Blood counts and iron-status measurements before and after cobalamin therapy; regimen is not extracted from the abstract. cross_nutrient: B12-associated ineffective blood-cell production can complicate iron-status interpretation. [b12-solmaz2015] Cobalamin deficiency can mask depleted body iron reserves (2015). https://pubmed.ncbi.nlm.nih.gov/25825568/ DOI: 10.1007/s12288-014-0417-x
    Complete structured claim and evidence

  2. Intestinal Hif2a deletion lowered serum and liver iron and markedly reduced liver hepcidin expression.

    Mouse hypoxia-inducible factor 2 alpha / Epas1 → Serum iron concentration source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/iron-research/19352007.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "623fedcdd407c02879254b087510cff95b61336f7605c2430f51ab75ac550040", "start_char": 0, "end_char": 1411, "text_sha256": "623fedcdd407c02879254b087510cff95b61336f7605c2430f51ab75ac550040"}
    experimental_model
    Conditional intestinal Hif1a/Hif2a knockout
    exposure
    Separate Hif1a versus Hif2a deletion
    limitations
    HIF isoforms were not interchangeable in this mouse experiment.
    nutrient_topic
    Iron research collection; topical membership is not evidence of a direct dietary effect. · Iron
    organism
    Mice
    plain_language
    A hormonal attempt to increase iron availability did not replace the missing intestinal regulator.
    primary_references
    [iron-p19352007] HIF-2alpha, but not HIF-1alpha, promotes iron absorption in mice. (2009). https://pubmed.ncbi.nlm.nih.gov/19352007/ DOI: 10.1172/jci38499
    tissue_or_cell_type
    Duodenal epithelium and systemic iron
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Iron: absorption, trafficking, iron-dependent enzymes and nutrient interactions (2026-09-17) · lines 862–873

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Conditional intestinal Hif1a/Hif2a knockout · source_derived_draft · unverified_draft

    ### iron-hif2-loss Intestinal Hif2a deletion lowered serum and liver iron and markedly reduced liver hepcidin expression. Condition category: machinery_impairment nutrient_topic: Iron research collection; topical membership is not evidence of a direct dietary effect. plain_language: A hormonal attempt to increase iron availability did not replace the missing intestinal regulator. organism: Mice tissue_or_cell_type: Duodenal epithelium and systemic iron experimental_model: Conditional intestinal Hif1a/Hif2a knockout limitations: HIF isoforms were not interchangeable in this mouse experiment. exposure: Separate Hif1a versus Hif2a deletion evidence_span: {"source_cache": "artifacts/iron-research/19352007.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "623fedcdd407c02879254b087510cff95b61336f7605c2430f51ab75ac550040", "start_char": 0, "end_char": 1411, "text_sha256": "623fedcdd407c02879254b087510cff95b61336f7605c2430f51ab75ac550040"} [iron-p19352007] HIF-2alpha, but not HIF-1alpha, promotes iron absorption in mice. (2009). https://pubmed.ncbi.nlm.nih.gov/19352007/ DOI: 10.1172/jci38499
    Complete structured claim and evidence

  3. The IL-6–hepcidin axis mediated inflammation-associated hypoferremia in the studied systems.

    Hepcidin → Serum iron concentration source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    biomarker_context Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/iron-research/15124018.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f2ed307ef57c255917685bb7bfb1f02f3a6481c732cc2ee41ad1f338e2a2a830", "start_char": 0, "end_char": 578, "text_sha256": "f2ed307ef57c255917685bb7bfb1f02f3a6481c732cc2ee41ad1f338e2a2a830"}
    experimental_model
    Human liver-cell, mouse and human-volunteer inflammation experiments
    exposure
    IL-6 and inflammatory stimulation
    limitations
    IL-6 dependence applies to the tested inflammatory models, not every possible inflammatory iron pathway.
    nutrient_topic
    Iron research collection; topical membership is not evidence of a direct dietary effect. · Iron
    organism
    Humans and mice
    plain_language
    Low blood iron during inflammation is a distribution response, not by itself proof of low total-body stores.
    primary_references
    [iron-p15124018] IL-6 mediates hypoferremia of inflammation by inducing the synthesis of the iron regulatory hormone hepcidin. (2004). https://pubmed.ncbi.nlm.nih.gov/15124018/ DOI: 10.1172/jci20945
    tissue_or_cell_type
    Liver and circulation
    trigger_kind
    biomarker_context Imported condition classification; unverified.

    Iron: absorption, trafficking, iron-dependent enzymes and nutrient interactions (2026-09-17) · lines 888–899

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human liver-cell, mouse and human-volunteer inflammation experiments · source_derived_draft · unverified_draft

    ### iron-inflammatory-low-serum The IL-6–hepcidin axis mediated inflammation-associated hypoferremia in the studied systems. Condition category: biomarker_context nutrient_topic: Iron research collection; topical membership is not evidence of a direct dietary effect. plain_language: Low blood iron during inflammation is a distribution response, not by itself proof of low total-body stores. organism: Humans and mice tissue_or_cell_type: Liver and circulation experimental_model: Human liver-cell, mouse and human-volunteer inflammation experiments limitations: IL-6 dependence applies to the tested inflammatory models, not every possible inflammatory iron pathway. exposure: IL-6 and inflammatory stimulation evidence_span: {"source_cache": "artifacts/iron-research/15124018.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f2ed307ef57c255917685bb7bfb1f02f3a6481c732cc2ee41ad1f338e2a2a830", "start_char": 0, "end_char": 578, "text_sha256": "f2ed307ef57c255917685bb7bfb1f02f3a6481c732cc2ee41ad1f338e2a2a830"} [iron-p15124018] IL-6 mediates hypoferremia of inflammation by inducing the synthesis of the iron regulatory hormone hepcidin. (2004). https://pubmed.ncbi.nlm.nih.gov/15124018/ DOI: 10.1172/jci20945
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Vitamin A-deficient rats had more splenic iron but lower serum iron and transferrin saturation.

    Vitamin A → Splenic iron storage source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    cross_nutrient
    Vitamin A deficiency -> iron distribution.
    experimental_model
    Controlled rat dietary groups.
    limitations
    Erythrophagocytosis is a proposed explanation, not a fully isolated causal sequence.
    nutrient_topic
    Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
    organism
    Rattus norvegicus
    plain_language
    Iron could be retained in one tissue while circulating availability fell.
    primary_references
    [va-cunha2014] Vitamin A deficiency modulates iron metabolism via ineffective erythropoiesis (2014). https://pubmed.ncbi.nlm.nih.gov/24998947/ DOI: 10.1016/j.jnutbio.2014.05.005
    tissue_or_cell_type
    Spleen and serum
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 1743–1753

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Controlled rat dietary groups. · source_derived_draft · unverified_draft

    ### va-deficiency-iron-sequestration Vitamin A-deficient rats had more splenic iron but lower serum iron and transferrin saturation. Condition category: nutrient_deficiency nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: Iron could be retained in one tissue while circulating availability fell. organism: Rattus norvegicus tissue_or_cell_type: Spleen and serum experimental_model: Controlled rat dietary groups. limitations: Erythrophagocytosis is a proposed explanation, not a fully isolated causal sequence. cross_nutrient: Vitamin A deficiency -> iron distribution. [va-cunha2014] Vitamin A deficiency modulates iron metabolism via ineffective erythropoiesis (2014). https://pubmed.ncbi.nlm.nih.gov/24998947/ DOI: 10.1016/j.jnutbio.2014.05.005
    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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