Component

Delivery of intestinal copper to peripheral tissues

Delivery of intestinal copper to peripheral tissues. Species, exposure and limitations are retained in each linked claim.

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. Oral elesclomol without extra copper supplementation rescued neonatal mortality in intestine-specific Ctr1 knockout mice.

    Elesclomol → Delivery of intestinal copper to peripheral tissues source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/copper-research/35433682.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6ebf1fdc967be53f455383e4edc79468266a5685db3867ca04ce2e2ccc4f2617", "start_char": 0, "end_char": 1449, "text_sha256": "6ebf1fdc967be53f455383e4edc79468266a5685db3867ca04ce2e2ccc4f2617"}
    experimental_model
    Oral elesclomol in genetically copper-transport-defective animals
    exposure
    Oral drug exposure without additional copper supplementation
    limitations
    Animal rescue does not establish safety or efficacy in people. Intestinal CTR1 loss is a different block from mitochondrial SLC25A3 loss.
    nutrient_topic
    Copper research collection; topical membership is not evidence of a direct dietary effect. · Copper
    organism
    Mouse; separate Caenorhabditis elegans experiments
    plain_language
    The drug helped use existing dietary copper despite a missing intestinal entry route.
    primary_references
    [copper-p35433682] Oral Elesclomol Treatment Alleviates Copper Deficiency in Animal Models. (2022). https://pubmed.ncbi.nlm.nih.gov/35433682/ DOI: 10.3389/fcell.2022.856300
    tissue_or_cell_type
    Intestine and whole-animal development
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Copper: transport, cuproenzymes, deficiency, excess and nutrient interactions (2026-09-17) · lines 598–609

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Oral elesclomol in genetically copper-transport-defective animals · source_derived_draft · unverified_draft

    ### copper-elesclomol-intestinal-bypass Oral elesclomol without extra copper supplementation rescued neonatal mortality in intestine-specific Ctr1 knockout mice. Condition category: machinery_impairment nutrient_topic: Copper research collection; topical membership is not evidence of a direct dietary effect. plain_language: The drug helped use existing dietary copper despite a missing intestinal entry route. organism: Mouse; separate Caenorhabditis elegans experiments tissue_or_cell_type: Intestine and whole-animal development experimental_model: Oral elesclomol in genetically copper-transport-defective animals limitations: Animal rescue does not establish safety or efficacy in people. Intestinal CTR1 loss is a different block from mitochondrial SLC25A3 loss. exposure: Oral drug exposure without additional copper supplementation evidence_span: {"source_cache": "artifacts/copper-research/35433682.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6ebf1fdc967be53f455383e4edc79468266a5685db3867ca04ce2e2ccc4f2617", "start_char": 0, "end_char": 1449, "text_sha256": "6ebf1fdc967be53f455383e4edc79468266a5685db3867ca04ce2e2ccc4f2617"} [copper-p35433682] Oral Elesclomol Treatment Alleviates Copper Deficiency in Animal Models. (2022). https://pubmed.ncbi.nlm.nih.gov/35433682/ DOI: 10.3389/fcell.2022.856300
    Complete structured claim and evidence

  2. A single postnatal copper administration partially rescued growth and viability in intestinal Ctr1 knockout mice.

    Copper → Delivery of intestinal copper to peripheral tissues source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/copper-research/16950140.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "08532f69fd9530033f8d9afcece9249fc50dd425f57313e120f55ea81cee8f98", "start_char": 0, "end_char": 1026, "text_sha256": "08532f69fd9530033f8d9afcece9249fc50dd425f57313e120f55ea81cee8f98"}
    experimental_model
    Intestinal epithelial Ctr1 knockout mice
    exposure
    Intestinal Ctr1 deletion; postnatal copper rescue
    limitations
    Genetic intestinal transport failure differs from low dietary intake. The indexed abstract does not establish the administration route of the rescue dose.
    nutrient_topic
    Copper research collection; topical membership is not evidence of a direct dietary effect. · Copper
    organism
    Mouse
    plain_language
    Some consequences of the transport defect could be bypassed in this animal experiment.
    primary_references
    [copper-p16950140] Ctr1 drives intestinal copper absorption and is essential for growth, iron metabolism, and neonatal cardiac function. (2006). https://pubmed.ncbi.nlm.nih.gov/16950140/ DOI: 10.1016/j.cmet.2006.08.009
    tissue_or_cell_type
    Intestine and peripheral organs
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Copper: transport, cuproenzymes, deficiency, excess and nutrient interactions (2026-09-17) · lines 338–349

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Intestinal epithelial Ctr1 knockout mice · source_derived_draft · unverified_draft

    ### copper-intestinal-ctr1-copper-rescue A single postnatal copper administration partially rescued growth and viability in intestinal Ctr1 knockout mice. Condition category: machinery_impairment nutrient_topic: Copper research collection; topical membership is not evidence of a direct dietary effect. plain_language: Some consequences of the transport defect could be bypassed in this animal experiment. organism: Mouse tissue_or_cell_type: Intestine and peripheral organs experimental_model: Intestinal epithelial Ctr1 knockout mice limitations: Genetic intestinal transport failure differs from low dietary intake. The indexed abstract does not establish the administration route of the rescue dose. exposure: Intestinal Ctr1 deletion; postnatal copper rescue evidence_span: {"source_cache": "artifacts/copper-research/16950140.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "08532f69fd9530033f8d9afcece9249fc50dd425f57313e120f55ea81cee8f98", "start_char": 0, "end_char": 1026, "text_sha256": "08532f69fd9530033f8d9afcece9249fc50dd425f57313e120f55ea81cee8f98"} [copper-p16950140] Ctr1 drives intestinal copper absorption and is essential for growth, iron metabolism, and neonatal cardiac function. (2006). https://pubmed.ncbi.nlm.nih.gov/16950140/ DOI: 10.1016/j.cmet.2006.08.009
    Complete structured claim and evidence

  3. Intestinal Ctr1 deletion reduced peripheral copper availability and caused neonatal growth failure and cardiac hypertrophy in mice.

    Mouse copper transporter Ctr1 / Slc31a1 → Delivery of intestinal copper to peripheral tissues source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/copper-research/16950140.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "08532f69fd9530033f8d9afcece9249fc50dd425f57313e120f55ea81cee8f98", "start_char": 0, "end_char": 1026, "text_sha256": "08532f69fd9530033f8d9afcece9249fc50dd425f57313e120f55ea81cee8f98"}
    experimental_model
    Intestinal epithelial Ctr1 knockout mice
    exposure
    Intestinal Ctr1 deletion; postnatal copper rescue
    limitations
    Genetic intestinal transport failure differs from low dietary intake. The indexed abstract does not establish the administration route of the rescue dose.
    nutrient_topic
    Copper research collection; topical membership is not evidence of a direct dietary effect. · Copper
    organism
    Mouse
    plain_language
    Copper in food is not enough if the intestine cannot deliver it to the body.
    primary_references
    [copper-p16950140] Ctr1 drives intestinal copper absorption and is essential for growth, iron metabolism, and neonatal cardiac function. (2006). https://pubmed.ncbi.nlm.nih.gov/16950140/ DOI: 10.1016/j.cmet.2006.08.009
    tissue_or_cell_type
    Intestine and peripheral organs
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Copper: transport, cuproenzymes, deficiency, excess and nutrient interactions (2026-09-17) · lines 312–323

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Intestinal epithelial Ctr1 knockout mice · source_derived_draft · unverified_draft

    ### copper-intestinal-ctr1-systemic Intestinal Ctr1 deletion reduced peripheral copper availability and caused neonatal growth failure and cardiac hypertrophy in mice. Condition category: machinery_impairment nutrient_topic: Copper research collection; topical membership is not evidence of a direct dietary effect. plain_language: Copper in food is not enough if the intestine cannot deliver it to the body. organism: Mouse tissue_or_cell_type: Intestine and peripheral organs experimental_model: Intestinal epithelial Ctr1 knockout mice limitations: Genetic intestinal transport failure differs from low dietary intake. The indexed abstract does not establish the administration route of the rescue dose. exposure: Intestinal Ctr1 deletion; postnatal copper rescue evidence_span: {"source_cache": "artifacts/copper-research/16950140.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "08532f69fd9530033f8d9afcece9249fc50dd425f57313e120f55ea81cee8f98", "start_char": 0, "end_char": 1026, "text_sha256": "08532f69fd9530033f8d9afcece9249fc50dd425f57313e120f55ea81cee8f98"} [copper-p16950140] Ctr1 drives intestinal copper absorption and is essential for growth, iron metabolism, and neonatal cardiac function. (2006). https://pubmed.ncbi.nlm.nih.gov/16950140/ DOI: 10.1016/j.cmet.2006.08.009
    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