Component
Human SLC30A8 protein-truncating variant carrier state
Human SLC30A8 protein-truncating variant carrier 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
Across approximately 150,000 people, carriers of 12 rare SLC30A8 truncating variants had 65% lower type 2 diabetes risk.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- curation_topic
- zinc · Zinc
- experimental_condition
- Noncarrier Truncating-variant carrier · Human SLC30A8 protein-truncating variant carrier state Condition belongs to the full experimental contrast; do not separate a joint intervention.
- experimental_contrast
- {"intervention": "Truncating-variant carrier", "comparator": "Noncarrier", "endpoint": "T2D risk", "effect_direction": "decrease", "combination": "single", "conditions": [{"entity_slug": "human-slc30a8-truncating-genotype", "state": "Truncating-variant carrier"}]} Explicit extracted experimental comparison; source-derived draft.
- experimental_model
- Human genetic association across five ancestry groups
- limitations
- Publisher abstract reviewed; genetic transporter loss is not dietary zinc restriction or a demonstrated supplement effect.
- primary_references
- Flannick et al. 2014; DOI:10.1038/ng.2915; PMCID:PMC4051628; https://www.nature.com/articles/ng.2915
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Diabetes cascade: targeted primary-source supplement · lines 6–6
See claim-local references; curated paraphrases reviewed 2026-09-20. · supports · Human genetic association across five ancestry groups · source_derived_draft · unverified_draft
Across approximately 150,000 people, carriers of 12 rare SLC30A8 truncating variants had 65% lower type 2 diabetes risk. Model: Human genetic association across five ancestry groups. Limits: Publisher abstract reviewed; genetic transporter loss is not dietary zinc restriction or a demonstrated supplement effect. Primary reference: Flannick et al. 2014; DOI:10.1038/ng.2915; PMCID:PMC4051628; https://www.nature.com/articles/ng.2915
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.