Component

Mouse sodium/glucose cotransporter SGLT2 / Slc5a2

Mouse sodium/glucose cotransporter SGLT2 / Slc5a2. 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.

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.

Recorded relationships

What it acts on

  1. Early proximal glucose reabsorption was 78 ± 6% in wild-type mice and absent in Sglt2-null mice.

    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/sodium-research/20616166.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0596ceea07c063931780bf6128a238c81622461ed65dd5b0d382f0202e1626f9", "start_char": 0, "end_char": 1704, "text_sha256": "0596ceea07c063931780bf6128a238c81622461ed65dd5b0d382f0202e1626f9"}
    experimental_model
    Sglt2-null mice, localization, clearance and micropuncture
    exposure
    Genetic Slc5a2 deletion
    limitations
    Renal glucose reabsorption and water output changed, but the knockout did not show the measured signs of volume depletion. Genetic deletion is not a dietary experiment.
    nutrient_topic
    Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
    organism
    Mouse
    plain_language
    The early kidney tubule uses a specific sodium/glucose transporter to reclaim filtered glucose.
    primary_references
    [sodium-p20616166] SGLT2 mediates glucose reabsorption in the early proximal tubule. (2011). https://pubmed.ncbi.nlm.nih.gov/20616166/ DOI: 10.1681/asn.2010030246
    tissue_or_cell_type
    Renal early proximal tubule
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 317–328

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Sglt2-null mice, localization, clearance and micropuncture · source_derived_draft · unverified_draft

    ### sodium-sglt2-early Early proximal glucose reabsorption was 78 ± 6% in wild-type mice and absent in Sglt2-null mice. Condition category: machinery_impairment nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The early kidney tubule uses a specific sodium/glucose transporter to reclaim filtered glucose. organism: Mouse tissue_or_cell_type: Renal early proximal tubule experimental_model: Sglt2-null mice, localization, clearance and micropuncture limitations: Renal glucose reabsorption and water output changed, but the knockout did not show the measured signs of volume depletion. Genetic deletion is not a dietary experiment. exposure: Genetic Slc5a2 deletion evidence_span: {"source_cache": "artifacts/sodium-research/20616166.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0596ceea07c063931780bf6128a238c81622461ed65dd5b0d382f0202e1626f9", "start_char": 0, "end_char": 1704, "text_sha256": "0596ceea07c063931780bf6128a238c81622461ed65dd5b0d382f0202e1626f9"} [sodium-p20616166] SGLT2 mediates glucose reabsorption in the early proximal tubule. (2011). https://pubmed.ncbi.nlm.nih.gov/20616166/ DOI: 10.1681/asn.2010030246
    Complete structured claim and evidence
  2. Sglt2-null mice had glucosuria and polyuria without differences in plasma glucose or GFR versus controls.

    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/sodium-research/20616166.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0596ceea07c063931780bf6128a238c81622461ed65dd5b0d382f0202e1626f9", "start_char": 0, "end_char": 1704, "text_sha256": "0596ceea07c063931780bf6128a238c81622461ed65dd5b0d382f0202e1626f9"}
    experimental_model
    Sglt2-null mice, localization, clearance and micropuncture
    exposure
    Genetic Slc5a2 deletion
    limitations
    Renal glucose reabsorption and water output changed, but the knockout did not show the measured signs of volume depletion. Genetic deletion is not a dietary experiment.
    nutrient_topic
    Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
    organism
    Mouse
    plain_language
    Losing this transporter sends glucose into urine; it does not mean the blood glucose must be high.
    primary_references
    [sodium-p20616166] SGLT2 mediates glucose reabsorption in the early proximal tubule. (2011). https://pubmed.ncbi.nlm.nih.gov/20616166/ DOI: 10.1681/asn.2010030246
    tissue_or_cell_type
    Renal early proximal tubule
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 330–341

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Sglt2-null mice, localization, clearance and micropuncture · source_derived_draft · unverified_draft

    ### sodium-sglt2-urine Sglt2-null mice had glucosuria and polyuria without differences in plasma glucose or GFR versus controls. Condition category: machinery_impairment nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Losing this transporter sends glucose into urine; it does not mean the blood glucose must be high. organism: Mouse tissue_or_cell_type: Renal early proximal tubule experimental_model: Sglt2-null mice, localization, clearance and micropuncture limitations: Renal glucose reabsorption and water output changed, but the knockout did not show the measured signs of volume depletion. Genetic deletion is not a dietary experiment. exposure: Genetic Slc5a2 deletion evidence_span: {"source_cache": "artifacts/sodium-research/20616166.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0596ceea07c063931780bf6128a238c81622461ed65dd5b0d382f0202e1626f9", "start_char": 0, "end_char": 1704, "text_sha256": "0596ceea07c063931780bf6128a238c81622461ed65dd5b0d382f0202e1626f9"} [sodium-p20616166] SGLT2 mediates glucose reabsorption in the early proximal tubule. (2011). https://pubmed.ncbi.nlm.nih.gov/20616166/ DOI: 10.1681/asn.2010030246
    Complete structured claim and evidence

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

    Evidence, AI assistance and curation standards