Component
Trabecular bone mineral density
Imaging-derived trabecular mineral density in a specified skeletal site.
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 acts on it
Prolonged low-potassium feeding reduced trabecular bone mineral density in the male-mouse study.
Experimental context and source evidence
- availability_state
- nutrient_deficiency Imported condition classification; unverified.
- cross_nutrient
- Dietary potassium restriction altered renal calcium balance, circulating PTH and trabecular mineral density; each endpoint is recorded independently.
- endpoint
- Prolonged low-potassium feeding reduced trabecular bone mineral density in the male-mouse study.
- experimental-exposure
- Male mice; two-week potassium-free discovery study and four/eight-week low-potassium study; urine/plasma minerals, renal proteomics, skeletal imaging, and constitutively active SPAK model.
- experimental_model
- Male mice; two-week potassium-free discovery study and four/eight-week low-potassium study; urine/plasma minerals, renal proteomics, skeletal imaging, and constitutively active SPAK model.
- limitations
- Male mouse model; co-occurring renal transporter and endocrine changes do not prove a complete causal chain or a human fracture effect. NCC-specific mediation is incompletely isolated.
- nutrient_topic
- Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
- organism
- Mus musculus
- plain_language
- The mineral imbalance extended to a measured skeletal endpoint.
- primary_references
- [murali-2026-calcium] Dietary potassium restriction causes hypercalciuria, hypocalcemia, and bone loss in male mice (2026). https://insight.jci.org/articles/view/196339 DOI: 10.1172/jci.insight.196339
- tissue_or_cell_type
- kidney, blood and trabecular skeleton
- trigger_kind
- nutrient_deficiency Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1330–1342
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Male mice; two-week potassium-free discovery study and four/eight-week low-potassium study; urine/plasma minerals, renal proteomics, skeletal imaging, and constitutively active SPAK model. · source_derived_draft · unverified_draft
### mouse-k-restriction-trabecular-bone Prolonged low-potassium feeding reduced trabecular bone mineral density in the male-mouse study. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The mineral imbalance extended to a measured skeletal endpoint. organism: Mus musculus tissue_or_cell_type: kidney, blood and trabecular skeleton experimental_model: Male mice; two-week potassium-free discovery study and four/eight-week low-potassium study; urine/plasma minerals, renal proteomics, skeletal imaging, and constitutively active SPAK model. limitations: Male mouse model; co-occurring renal transporter and endocrine changes do not prove a complete causal chain or a human fracture effect. NCC-specific mediation is incompletely isolated. cross_nutrient: Dietary potassium restriction altered renal calcium balance, circulating PTH and trabecular mineral density; each endpoint is recorded independently. experimental-exposure: Male mice; two-week potassium-free discovery study and four/eight-week low-potassium study; urine/plasma minerals, renal proteomics, skeletal imaging, and constitutively active SPAK model. endpoint: Prolonged low-potassium feeding reduced trabecular bone mineral density in the male-mouse study. [murali-2026-calcium] Dietary potassium restriction causes hypercalciuria, hypocalcemia, and bone loss in male mice (2026). https://insight.jci.org/articles/view/196339 DOI: 10.1172/jci.insight.196339
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.