Component

SLC34A3-associated phosphate wasting in the 2016 ATP-flux patient

SLC34A3-associated phosphate wasting in the 2016 ATP-flux patient. Species, exposure and limitations are retained in each linked claim.

1 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

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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.

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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 it acts on

  1. The patient with SLC34A3-associated chronic hypophosphatemia had approximately 50% lower serum phosphate and muscle ATP synthetic flux.

    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/phosphorus-research/27338702.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "634bc9a26ebb8d6a911692bcb98a05432db2bc08455c0a02f1ef5e4b953150fe", "start_char": 0, "end_char": 1786, "text_sha256": "634bc9a26ebb8d6a911692bcb98a05432db2bc08455c0a02f1ef5e4b953150fe"}
    experimental_model
    31P-MRS ATP-flux measurements, repletion and cellular/mitochondrial experiments
    exposure
    Diet-induced low phosphate, NaPi-IIa knockout, phosphate repletion; one SLC34A3-associated human case
    limitations
    ATP synthetic flux is not ATP pool size or direct proof that all measured flux is mitochondrial oxidative phosphorylation. One human case cannot define a population threshold.
    nutrient_topic
    Phosphorus research collection; topical membership is not evidence of a direct dietary effect. · Phosphorus
    organism
    Human
    plain_language
    The study found a similar pattern in one person with inherited renal phosphate wasting.
    primary_references
    [phosphorus-p27338702] Hypophosphatemia promotes lower rates of muscle ATP synthesis. (2016). https://pubmed.ncbi.nlm.nih.gov/27338702/ DOI: 10.1096/fj.201600473r
    tissue_or_cell_type
    Skeletal muscle
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Phosphorus: metabolism, signaling and nutrient connections (2026-09-17) · lines 607–618

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · 31P-MRS ATP-flux measurements, repletion and cellular/mitochondrial experiments · source_derived_draft · unverified_draft

    ### phosphorus-human-atp-defect The patient with SLC34A3-associated chronic hypophosphatemia had approximately 50% lower serum phosphate and muscle ATP synthetic flux. Condition category: machinery_impairment nutrient_topic: Phosphorus research collection; topical membership is not evidence of a direct dietary effect. plain_language: The study found a similar pattern in one person with inherited renal phosphate wasting. organism: Human tissue_or_cell_type: Skeletal muscle experimental_model: 31P-MRS ATP-flux measurements, repletion and cellular/mitochondrial experiments limitations: ATP synthetic flux is not ATP pool size or direct proof that all measured flux is mitochondrial oxidative phosphorylation. One human case cannot define a population threshold. exposure: Diet-induced low phosphate, NaPi-IIa knockout, phosphate repletion; one SLC34A3-associated human case evidence_span: {"source_cache": "artifacts/phosphorus-research/27338702.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "634bc9a26ebb8d6a911692bcb98a05432db2bc08455c0a02f1ef5e4b953150fe", "start_char": 0, "end_char": 1786, "text_sha256": "634bc9a26ebb8d6a911692bcb98a05432db2bc08455c0a02f1ef5e4b953150fe"} [phosphorus-p27338702] Hypophosphatemia promotes lower rates of muscle ATP synthesis. (2016). https://pubmed.ncbi.nlm.nih.gov/27338702/ DOI: 10.1096/fj.201600473r
    Complete structured claim and evidence

In the sources

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