Component
PTH-(1–34) experimental peptide
PTH-(1–34) experimental peptide. Species, exposure and limitations are retained in each linked claim.
2 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
PTH-(1–34) induced NaPi-IIa internalization in both wild-type and Nherf1-deficient mice.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/phosphorus-research/16987995.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c5a055252ffc61da98e24d1de3a1733ee7aea678aded8cbdf071d18ad707d0bc", "start_char": 0, "end_char": 1699, "text_sha256": "c5a055252ffc61da98e24d1de3a1733ee7aea678aded8cbdf071d18ad707d0bc"}
- experimental_model
- Receptor-fragment stimulation, knockout and signaling-bypass experiments
- exposure
- PTH-(1–34), apically selective PTH-(3–34), PKC/PKA pathway stimulation
- limitations
- Apical and basolateral receptor routes differ. Loss of one scaffold does not eliminate every PTH response.
- nutrient_topic
- Phosphorus research collection; topical membership is not evidence of a direct dietary effect. · Phosphorus
- organism
- Mouse
- plain_language
- PTH could remove the transporter from the brush border even when one scaffold was absent.
- primary_references
- [phosphorus-p16987995] Defective coupling of apical PTH receptors to phospholipase C prevents internalization of the Na+-phosphate cotransporter NaPi-IIa in Nherf1-deficient mice. (2007). https://pubmed.ncbi.nlm.nih.gov/16987995/ DOI: 10.1152/ajpcell.00126.2006
- tissue_or_cell_type
- Renal proximal tubule brush-border membrane
Phosphorus: metabolism, signaling and nutrient connections (2026-09-17) · lines 399–410
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Receptor-fragment stimulation, knockout and signaling-bypass experiments · source_derived_draft · unverified_draft
### phosphorus-pth-internalization PTH-(1–34) induced NaPi-IIa internalization in both wild-type and Nherf1-deficient mice. Condition category: normal nutrient_topic: Phosphorus research collection; topical membership is not evidence of a direct dietary effect. plain_language: PTH could remove the transporter from the brush border even when one scaffold was absent. organism: Mouse tissue_or_cell_type: Renal proximal tubule brush-border membrane experimental_model: Receptor-fragment stimulation, knockout and signaling-bypass experiments limitations: Apical and basolateral receptor routes differ. Loss of one scaffold does not eliminate every PTH response. exposure: PTH-(1–34), apically selective PTH-(3–34), PKC/PKA pathway stimulation evidence_span: {"source_cache": "artifacts/phosphorus-research/16987995.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c5a055252ffc61da98e24d1de3a1733ee7aea678aded8cbdf071d18ad707d0bc", "start_char": 0, "end_char": 1699, "text_sha256": "c5a055252ffc61da98e24d1de3a1733ee7aea678aded8cbdf071d18ad707d0bc"} [phosphorus-p16987995] Defective coupling of apical PTH receptors to phospholipase C prevents internalization of the Na+-phosphate cotransporter NaPi-IIa in Nherf1-deficient mice. (2007). https://pubmed.ncbi.nlm.nih.gov/16987995/ DOI: 10.1152/ajpcell.00126.2006
Complete structured claim and evidence
Where it participates (unsigned role)
Antibiotic-depleted or germ-free female mice lost the bone-anabolic response to intermittent PTH; restoring physiological butyrate levels restored the response.
Experimental context and source evidence
- availability_state
- nutrient_deficiency Imported condition classification; unverified.
- evidence_access
- Primary abstract and full-text intervention methods
- experimental_model
- Female mice; microbial depletion, daily subcutaneous human PTH(1-34) at 80 micrograms/kg for four weeks; 5 mM butyrate repletion in drinking water.
- limitations
- Not proof that human PTH treatment failure is usually butyrate deficiency, or that butyrate replaces PTH, calcium or vitamin D.
- nutrient_topic
- Butyrate collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Butyrate
- plain_language
- In this mouse model, the hormone response depended on a microbial metabolite.
- primary_references
- Parathyroid hormone-dependent bone formation requires butyrate production by intestinal microbiota. · 2020 · https://pubmed.ncbi.nlm.nih.gov/31917685/ · DOI 10.1172/JCI133473
- trigger_kind
- nutrient_deficiency Imported condition classification; unverified.
Butyrate: microbial production, fuel use, signaling and nutrient interactions (2026-09-19) · lines 486–492
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Female mice; microbial depletion, daily subcutaneous human PTH(1-34) at 80 micrograms/kg for four weeks; 5 mM butyrate repletion in drinking water. · source_derived_draft · unverified_draft
## butyrate-pth-microbial-depletion In this mouse model, the hormone response depended on a microbial metabolite. Antibiotic-depleted or germ-free female mice lost the bone-anabolic response to intermittent PTH; restoring physiological butyrate levels restored the response. Model: Female mice; microbial depletion, daily subcutaneous human PTH(1-34) at 80 micrograms/kg for four weeks; 5 mM butyrate repletion in drinking water. Limitations: Not proof that human PTH treatment failure is usually butyrate deficiency, or that butyrate replaces PTH, calcium or vitamin D. Evidence access: Primary abstract and full-text intervention methods Parathyroid hormone-dependent bone formation requires butyrate production by intestinal microbiota. · 2020 · https://pubmed.ncbi.nlm.nih.gov/31917685/ · DOI 10.1172/JCI133473
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.