Component

Human sodium/glucose cotransporter SGLT1 / SLC5A1

Human sodium/glucose cotransporter SGLT1 / SLC5A1. Species, exposure and limitations are retained in each linked claim.

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

Read recorded mechanisms Open recursive mind map

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. Normal intestinal SGLT1 couples glucose entry to the inward sodium electrochemical gradient.

    Human sodium/glucose cotransporter SGLT1 / SLC5A1 → D-glucose source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/sodium-research/2008213.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ba4e32dc5111895acfe9e109cf57a7e07bc3c4e07e82ad3b4f7715cfaf10af74", "start_char": 0, "end_char": 1357, "text_sha256": "ba4e32dc5111895acfe9e109cf57a7e07bc3c4e07e82ad3b4f7715cfaf10af74"}
    experimental_model
    Family segregation and Xenopus oocyte transport assay
    exposure
    Disease-associated SGLT1 missense variant versus normal transporter
    limitations
    A genetic transporter defect is not sodium dietary deficiency; the sugar-malabsorption phenotype must not be presented as a reason to add salt.
    nutrient_topic
    Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
    organism
    Human SGLT1 expressed in frog oocytes
    plain_language
    A sodium gradient helps intestinal cells take up glucose.
    primary_references
    [sodium-p2008213] Glucose/galactose malabsorption caused by a defect in the Na+/glucose cotransporter. (1991). https://pubmed.ncbi.nlm.nih.gov/2008213/ DOI: 10.1038/350354a0
    tissue_or_cell_type
    Intestinal brush border
    transport_effect
    raises Couples glucose entry to the inward sodium electrochemical gradient.
    transport_pool
    the enterocyte interior Couples glucose entry to the inward sodium electrochemical gradient.

    Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 291–302

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Family segregation and Xenopus oocyte transport assay · source_derived_draft · unverified_draft

    ### sodium-sglt1-gradient Normal intestinal SGLT1 couples glucose entry to the inward sodium electrochemical gradient. Condition category: normal nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A sodium gradient helps intestinal cells take up glucose. organism: Human SGLT1 expressed in frog oocytes tissue_or_cell_type: Intestinal brush border experimental_model: Family segregation and Xenopus oocyte transport assay limitations: A genetic transporter defect is not sodium dietary deficiency; the sugar-malabsorption phenotype must not be presented as a reason to add salt. exposure: Disease-associated SGLT1 missense variant versus normal transporter evidence_span: {"source_cache": "artifacts/sodium-research/2008213.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ba4e32dc5111895acfe9e109cf57a7e07bc3c4e07e82ad3b4f7715cfaf10af74", "start_char": 0, "end_char": 1357, "text_sha256": "ba4e32dc5111895acfe9e109cf57a7e07bc3c4e07e82ad3b4f7715cfaf10af74"} [sodium-p2008213] Glucose/galactose malabsorption caused by a defect in the Na+/glucose cotransporter. (1991). https://pubmed.ncbi.nlm.nih.gov/2008213/ DOI: 10.1038/350354a0
    Complete structured claim and evidence

  2. The familial SGLT1 missense variant abolished sodium-dependent glucose transport in injected oocytes.

    Human sodium/glucose cotransporter SGLT1 / SLC5A1 → Intestinal epithelial glucose uptake source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/sodium-research/2008213.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ba4e32dc5111895acfe9e109cf57a7e07bc3c4e07e82ad3b4f7715cfaf10af74", "start_char": 0, "end_char": 1357, "text_sha256": "ba4e32dc5111895acfe9e109cf57a7e07bc3c4e07e82ad3b4f7715cfaf10af74"}
    experimental_model
    Family segregation and Xenopus oocyte transport assay
    exposure
    Disease-associated SGLT1 missense variant versus normal transporter
    limitations
    A genetic transporter defect is not sodium dietary deficiency; the sugar-malabsorption phenotype must not be presented as a reason to add salt.
    nutrient_topic
    Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
    organism
    Human SGLT1 expressed in frog oocytes
    plain_language
    The transport protein itself can be the limiting step.
    primary_references
    [sodium-p2008213] Glucose/galactose malabsorption caused by a defect in the Na+/glucose cotransporter. (1991). https://pubmed.ncbi.nlm.nih.gov/2008213/ DOI: 10.1038/350354a0
    tissue_or_cell_type
    Intestinal brush border
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 304–315

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Family segregation and Xenopus oocyte transport assay · source_derived_draft · unverified_draft

    ### sodium-sglt1-loss The familial SGLT1 missense variant abolished sodium-dependent glucose transport in injected oocytes. Condition category: machinery_impairment nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The transport protein itself can be the limiting step. organism: Human SGLT1 expressed in frog oocytes tissue_or_cell_type: Intestinal brush border experimental_model: Family segregation and Xenopus oocyte transport assay limitations: A genetic transporter defect is not sodium dietary deficiency; the sugar-malabsorption phenotype must not be presented as a reason to add salt. exposure: Disease-associated SGLT1 missense variant versus normal transporter evidence_span: {"source_cache": "artifacts/sodium-research/2008213.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ba4e32dc5111895acfe9e109cf57a7e07bc3c4e07e82ad3b4f7715cfaf10af74", "start_char": 0, "end_char": 1357, "text_sha256": "ba4e32dc5111895acfe9e109cf57a7e07bc3c4e07e82ad3b4f7715cfaf10af74"} [sodium-p2008213] Glucose/galactose malabsorption caused by a defect in the Na+/glucose cotransporter. (1991). https://pubmed.ncbi.nlm.nih.gov/2008213/ DOI: 10.1038/350354a0
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Upper small-intestinal metformin restored SGLT1 expression and glucose sensing in high-fat-diet rats, triggering an SGLT1-dependent pathway that lowered glucose production.

    Metformin → Upper small-intestinal glucose sensing source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/metformin-research/29056513.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a04767b5cd42e2e3e3eced3fc1f6bc2c20d8c71adb044483fe8443ef1c59fc97", "start_char": 0, "end_char": 1110, "text_sha256": "a04767b5cd42e2e3e3eced3fc1f6bc2c20d8c71adb044483fe8443ef1c59fc97"}
    experimental_model
    Rat upper small-intestinal infusion, microbiota transplantation and SGLT1 measurements
    exposure
    Upper small-intestinal metformin in high-fat-diet rats
    limitations
    A regional intestinal mechanism in rats. Transplantation between rats supports the microbial step; human relevance is not established here.
    nutrient_topic
    Metformin research collection; topical membership is not evidence of a direct clinical effect, and pharmacological exposure is not dietary intake. · Metformin
    organism
    Rat
    plain_language
    A sensor in the upper gut tells the liver to make less glucose, and the drug restores it.
    primary_references
    [metformin-p29056513] Metformin Alters Upper Small Intestinal Microbiota that Impact a Glucose-SGLT1-Sensing Glucoregulatory Pathway. (2018). https://pubmed.ncbi.nlm.nih.gov/29056513/ DOI: 10.1016/j.cmet.2017.09.019
    tissue_or_cell_type
    Upper small intestine

    Metformin: transport, molecular targets, gut mechanisms and nutrient interactions (2026-09-19) · lines 970–981

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rat upper small-intestinal infusion, microbiota transplantation and SGLT1 measurements · source_derived_draft · unverified_draft

    ### metformin-sglt1-sensing Upper small-intestinal metformin restored SGLT1 expression and glucose sensing in high-fat-diet rats, triggering an SGLT1-dependent pathway that lowered glucose production. Condition category: normal nutrient_topic: Metformin research collection; topical membership is not evidence of a direct clinical effect, and pharmacological exposure is not dietary intake. plain_language: A sensor in the upper gut tells the liver to make less glucose, and the drug restores it. organism: Rat tissue_or_cell_type: Upper small intestine experimental_model: Rat upper small-intestinal infusion, microbiota transplantation and SGLT1 measurements limitations: A regional intestinal mechanism in rats. Transplantation between rats supports the microbial step; human relevance is not established here. exposure: Upper small-intestinal metformin in high-fat-diet rats evidence_span: {"source_cache": "artifacts/metformin-research/29056513.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a04767b5cd42e2e3e3eced3fc1f6bc2c20d8c71adb044483fe8443ef1c59fc97", "start_char": 0, "end_char": 1110, "text_sha256": "a04767b5cd42e2e3e3eced3fc1f6bc2c20d8c71adb044483fe8443ef1c59fc97"} [metformin-p29056513] Metformin Alters Upper Small Intestinal Microbiota that Impact a Glucose-SGLT1-Sensing Glucoregulatory Pathway. (2018). https://pubmed.ncbi.nlm.nih.gov/29056513/ DOI: 10.1016/j.cmet.2017.09.019
    Complete structured claim and evidence

  2. 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.

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