Component
Patients with recessive SECISBP2 defects
Human genetic disease cohort reported by Dumitrescu et al., 2005; not an ordinary nutritional deficiency state.
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.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
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.
What it acts on
Fibroblasts from affected siblings with a recessive SECISBP2 defect had reduced DIO2 activity; linkage did not map the defect to DIO2 itself.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- cross_nutrient
- Selenium-incorporation machinery is required for hormone-processing selenoproteins; this is not dietary selenium deficiency.
- evidence_locator
- Primary abstract
- evidence_spans
- [{"source_document": "artifacts/iodine-metabolism-sources/16228000.json", "source_field": "resultList.result[0].abstractText", "start_char": 0, "end_char": 1084}]
- experimental_model
- Two human families with recessive SECISBP2 variants; patient fibroblast enzyme assays and linkage analysis
- exposure
- Inherited SECISBP2 variants; no dietary deprivation exposure.
- limitations
- Abstract-only; variant-specific kinetics and dietary rescue were not established.
- nutrient_topic
- Iodine research collection; topical membership is not evidence of a direct dietary effect. · Iodine
- organism
- Homo sapiens
- plain_language
- A defect in selenium-incorporation machinery can impair thyroid-hormone processing even when the deiodinase gene is not the cause.
- primary_references
- [i-met-16228000] Mutations in SECISBP2 result in abnormal thyroid hormone metabolism. (2005). https://pubmed.ncbi.nlm.nih.gov/16228000/ DOI: 10.1038/ng1654
- tissue_or_cell_type
- Patient fibroblasts
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Iodine: thyroid hormone production, deficiency, excess and nutrient interactions (2026-09-17) · lines 1099–1112
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Two human families with recessive SECISBP2 variants; patient fibroblast enzyme assays and linkage analysis · source_derived_draft · unverified_draft
### i-met-secisbp2-fibroblast-dio2 Fibroblasts from affected siblings with a recessive SECISBP2 defect had reduced DIO2 activity; linkage did not map the defect to DIO2 itself. Condition category: machinery_impairment nutrient_topic: Iodine research collection; topical membership is not evidence of a direct dietary effect. plain_language: A defect in selenium-incorporation machinery can impair thyroid-hormone processing even when the deiodinase gene is not the cause. organism: Homo sapiens tissue_or_cell_type: Patient fibroblasts experimental_model: Two human families with recessive SECISBP2 variants; patient fibroblast enzyme assays and linkage analysis limitations: Abstract-only; variant-specific kinetics and dietary rescue were not established. exposure: Inherited SECISBP2 variants; no dietary deprivation exposure. cross_nutrient: Selenium-incorporation machinery is required for hormone-processing selenoproteins; this is not dietary selenium deficiency. evidence_locator: Primary abstract evidence_spans: [{"source_document": "artifacts/iodine-metabolism-sources/16228000.json", "source_field": "resultList.result[0].abstractText", "start_char": 0, "end_char": 1084}] [i-met-16228000] Mutations in SECISBP2 result in abnormal thyroid hormone metabolism. (2005). https://pubmed.ncbi.nlm.nih.gov/16228000/ DOI: 10.1038/ng1654
Complete structured claim and evidence
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.