Component

Human SGLT1 and SGLT2 transport activity

Species, preparation, dose and limitations are retained on linked claims.

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.

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 acts on it

  1. Phlorizin inhibited human SGLT2 more strongly than SGLT1 in HEK293T electrophysiology, with reported Ki values of 11 and 140 nM, respectively.

    Phlorizin → Human SGLT1 and SGLT2 transport activity source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    dose
    Phlorizin concentration-response
    duration
    Acute
    evidence_access
    Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    evidence_scope
    literature_reviewed; model-specific source-derived curation
    experimental_model
    HEK293T cells expressing human SGLT2 or SGLT1
    limitations
    The indexed article has an erratum notice; the exact correction was not recovered in this curation and the numerical values require rechecking before quantitative reuse.
    nutrient_topic
    Phlorizin chapter; interacting nutrients, drugs, peptides and proteins retain their experimental settings. · Phlorizin
    organism
    HEK293T cells expressing human SGLT2 or SGLT1
    plain_language
    Phlorizin inhibited human SGLT2 more strongly than SGLT1 in HEK293T electrophysiology, with reported Ki values of 11 and 140 nM, respectively.
    primary_references
    Glucose transport by human renal Na+/D-glucose cotransporters SGLT1 and SGLT2. (2011). https://pubmed.ncbi.nlm.nih.gov/20980548/ DOI: 10.1152/ajpcell.00388.2010
    route
    In vitro
    tissue
    Whole-cell sodium/glucose cotransport current
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Phlorizin: mechanism of action and interactions (2026-09-20) · lines 22–31

    Original AI-assisted source-specific curation with primary-study citations, model, exposure, route, duration, negative findings and limitations preserved. Not publisher full text. · supports · HEK293T cells expressing human SGLT2 or SGLT1 · source_derived_draft · unverified_draft

    ## phlorizin-sglt1-sglt2-affinity Phlorizin inhibited human SGLT2 more strongly than SGLT1 in HEK293T electrophysiology, with reported Ki values of 11 and 140 nM, respectively. Model/species: HEK293T cells expressing human SGLT2 or SGLT1 Tissue/system: Whole-cell sodium/glucose cotransport current Exposure: Phlorizin concentration-response Route: In vitro Duration: Acute Limits: The indexed article has an erratum notice; the exact correction was not recovered in this curation and the numerical values require rechecking before quantitative reuse. Primary reference: Glucose transport by human renal Na+/D-glucose cotransporters SGLT1 and SGLT2. (2011). https://pubmed.ncbi.nlm.nih.gov/20980548/ DOI: 10.1152/ajpcell.00388.2010 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    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