Component
Intestinal epithelial glucose uptake
Intestinal epithelial glucose uptake. Species, exposure and limitations are retained in each linked claim.
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.
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 acts on it
The familial SGLT1 missense variant abolished sodium-dependent glucose transport in injected oocytes.
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
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.