Component
SLC5A11 (human SMIT2)
SLC5A11 (human SMIT2). Species, exposure and limitations are retained in each linked claim.
4 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 it acts on
Human SMIT2 expression increased D-chiro-inositol uptake 159-fold in rat L6 cells.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/inositol-research/19032932.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4fdc565b9aa26ef5f2d083c539a1b0367403b39f0c75d3ea1b194bf6fa525242", "start_char": 0, "end_char": 1164, "text_sha256": "4fdc565b9aa26ef5f2d083c539a1b0367403b39f0c75d3ea1b194bf6fa525242"}
- experimental_model
- Human SMIT2 overexpression and radiotracer uptake
- exposure
- Overexpression, glucose competition and insulin exposure
- limitations
- Overexpression is not normal transporter abundance. Insulin experiments used untransfected rat cells; changes in human diabetes are proposed, not demonstrated here.
- nutrient_topic
- Inositol research collection; topical membership is not evidence of a direct dietary effect. · Inositol (stereoisomer family)
- organism
- Human transporter in rat L6 myoblasts
- plain_language
- The transporter can carry a second inositol stereoisomer.
- primary_references
- [ino-p19032932] Human sodium/inositol cotransporter 2 (SMIT2) transports inositols but not glucose in L6 cells. (2009). https://pubmed.ncbi.nlm.nih.gov/19032932/ DOI: 10.1016/j.abb.2008.11.008
- tissue_or_cell_type
- Skeletal-muscle cell model
- transport_effect
- raises Expression increased D-chiro-inositol uptake 159-fold.
- transport_pool
- the expressing cell Expression increased D-chiro-inositol uptake 159-fold.
Inositol: synthesis, signaling, mineral interactions and conditional deficiency (2026-09-17) · lines 301–312
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human SMIT2 overexpression and radiotracer uptake · source_derived_draft · unverified_draft
### ino-smit2-dci Human SMIT2 expression increased D-chiro-inositol uptake 159-fold in rat L6 cells. Condition category: normal nutrient_topic: Inositol research collection; topical membership is not evidence of a direct dietary effect. plain_language: The transporter can carry a second inositol stereoisomer. organism: Human transporter in rat L6 myoblasts tissue_or_cell_type: Skeletal-muscle cell model experimental_model: Human SMIT2 overexpression and radiotracer uptake limitations: Overexpression is not normal transporter abundance. Insulin experiments used untransfected rat cells; changes in human diabetes are proposed, not demonstrated here. exposure: Overexpression, glucose competition and insulin exposure evidence_span: {"source_cache": "artifacts/inositol-research/19032932.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4fdc565b9aa26ef5f2d083c539a1b0367403b39f0c75d3ea1b194bf6fa525242", "start_char": 0, "end_char": 1164, "text_sha256": "4fdc565b9aa26ef5f2d083c539a1b0367403b39f0c75d3ea1b194bf6fa525242"} [ino-p19032932] Human sodium/inositol cotransporter 2 (SMIT2) transports inositols but not glucose in L6 cells. (2009). https://pubmed.ncbi.nlm.nih.gov/19032932/ DOI: 10.1016/j.abb.2008.11.008
Complete structured claim and evidenceHuman SMIT2 expression increased myo-inositol uptake 37-fold relative to vector control in rat L6 cells.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/inositol-research/19032932.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4fdc565b9aa26ef5f2d083c539a1b0367403b39f0c75d3ea1b194bf6fa525242", "start_char": 0, "end_char": 1164, "text_sha256": "4fdc565b9aa26ef5f2d083c539a1b0367403b39f0c75d3ea1b194bf6fa525242"}
- experimental_model
- Human SMIT2 overexpression and radiotracer uptake
- exposure
- Overexpression, glucose competition and insulin exposure
- limitations
- Overexpression is not normal transporter abundance. Insulin experiments used untransfected rat cells; changes in human diabetes are proposed, not demonstrated here.
- nutrient_topic
- Inositol research collection; topical membership is not evidence of a direct dietary effect. · Inositol (stereoisomer family)
- organism
- Human transporter in rat L6 myoblasts
- plain_language
- SMIT2 can bring free myo-inositol into cells.
- primary_references
- [ino-p19032932] Human sodium/inositol cotransporter 2 (SMIT2) transports inositols but not glucose in L6 cells. (2009). https://pubmed.ncbi.nlm.nih.gov/19032932/ DOI: 10.1016/j.abb.2008.11.008
- tissue_or_cell_type
- Skeletal-muscle cell model
- transport_effect
- raises Expression increased myo-inositol uptake 37-fold against vector control.
- transport_pool
- the expressing cell Expression increased myo-inositol uptake 37-fold against vector control.
Inositol: synthesis, signaling, mineral interactions and conditional deficiency (2026-09-17) · lines 288–299
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human SMIT2 overexpression and radiotracer uptake · source_derived_draft · unverified_draft
### ino-smit2-myo Human SMIT2 expression increased myo-inositol uptake 37-fold relative to vector control in rat L6 cells. Condition category: normal nutrient_topic: Inositol research collection; topical membership is not evidence of a direct dietary effect. plain_language: SMIT2 can bring free myo-inositol into cells. organism: Human transporter in rat L6 myoblasts tissue_or_cell_type: Skeletal-muscle cell model experimental_model: Human SMIT2 overexpression and radiotracer uptake limitations: Overexpression is not normal transporter abundance. Insulin experiments used untransfected rat cells; changes in human diabetes are proposed, not demonstrated here. exposure: Overexpression, glucose competition and insulin exposure evidence_span: {"source_cache": "artifacts/inositol-research/19032932.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4fdc565b9aa26ef5f2d083c539a1b0367403b39f0c75d3ea1b194bf6fa525242", "start_char": 0, "end_char": 1164, "text_sha256": "4fdc565b9aa26ef5f2d083c539a1b0367403b39f0c75d3ea1b194bf6fa525242"} [ino-p19032932] Human sodium/inositol cotransporter 2 (SMIT2) transports inositols but not glucose in L6 cells. (2009). https://pubmed.ncbi.nlm.nih.gov/19032932/ DOI: 10.1016/j.abb.2008.11.008
Complete structured claim and evidence
What acts on it
A fitted five-state model of human SMIT2 currents included cooperative Na+ binding and a likely rate-limiting return of empty transporter.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/inositol-research/24944204.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "12216ce12672706d91e22c9fbc1ebc5dbe77444e9869048f8a0d456f621cb41e", "start_char": 0, "end_char": 1647, "text_sha256": "12216ce12672706d91e22c9fbc1ebc5dbe77444e9869048f8a0d456f621cb41e"}
- experimental_model
- Voltage clamp and kinetic model fitting
- exposure
- Sodium and voltage manipulations
- limitations
- Cooperative sodium binding and turnover were model-derived; this is not a clinical sodium recommendation.
- nutrient_topic
- Inositol research collection; topical membership is not evidence of a direct dietary effect. · Inositol (stereoisomer family)
- organism
- Human SMIT2 in Xenopus oocytes
- plain_language
- The sodium gradient is part of the transport machinery, rather than inositol moving independently of ions.
- primary_references
- [ino-p24944204] The transport mechanism of the human sodium/myo-inositol transporter 2 (SMIT2/SGLT6), a member of the LeuT structural family. (2014). https://pubmed.ncbi.nlm.nih.gov/24944204/ DOI: 10.1152/ajpcell.00054.2014
- tissue_or_cell_type
- Heterologous membrane transport
Inositol: synthesis, signaling, mineral interactions and conditional deficiency (2026-09-17) · lines 340–351
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Voltage clamp and kinetic model fitting · source_derived_draft · unverified_draft
### ino-smit2-sodium A fitted five-state model of human SMIT2 currents included cooperative Na+ binding and a likely rate-limiting return of empty transporter. Condition category: normal nutrient_topic: Inositol research collection; topical membership is not evidence of a direct dietary effect. plain_language: The sodium gradient is part of the transport machinery, rather than inositol moving independently of ions. organism: Human SMIT2 in Xenopus oocytes tissue_or_cell_type: Heterologous membrane transport experimental_model: Voltage clamp and kinetic model fitting limitations: Cooperative sodium binding and turnover were model-derived; this is not a clinical sodium recommendation. exposure: Sodium and voltage manipulations evidence_span: {"source_cache": "artifacts/inositol-research/24944204.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "12216ce12672706d91e22c9fbc1ebc5dbe77444e9869048f8a0d456f621cb41e", "start_char": 0, "end_char": 1647, "text_sha256": "12216ce12672706d91e22c9fbc1ebc5dbe77444e9869048f8a0d456f621cb41e"} [ino-p24944204] The transport mechanism of the human sodium/myo-inositol transporter 2 (SMIT2/SGLT6), a member of the LeuT structural family. (2014). https://pubmed.ncbi.nlm.nih.gov/24944204/ DOI: 10.1152/ajpcell.00054.2014
Complete structured claim and evidence
Where it participates (unsigned role)
Glucose competed for D-chiro-inositol uptake with a reported Ki of 6.1 mM in the SMIT2 expression system, without evidence that SMIT2 transported glucose in those assays.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/inositol-research/19032932.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4fdc565b9aa26ef5f2d083c539a1b0367403b39f0c75d3ea1b194bf6fa525242", "start_char": 0, "end_char": 1164, "text_sha256": "4fdc565b9aa26ef5f2d083c539a1b0367403b39f0c75d3ea1b194bf6fa525242"}
- experimental_model
- Human SMIT2 overexpression and radiotracer uptake
- exposure
- Overexpression, glucose competition and insulin exposure
- limitations
- Overexpression is not normal transporter abundance. Insulin experiments used untransfected rat cells; changes in human diabetes are proposed, not demonstrated here.
- nutrient_topic
- Inositol research collection; topical membership is not evidence of a direct dietary effect. · Inositol (stereoisomer family)
- organism
- Human transporter in rat L6 myoblasts
- plain_language
- Glucose competed for entry without itself becoming demonstrated cargo of this transporter.
- primary_references
- [ino-p19032932] Human sodium/inositol cotransporter 2 (SMIT2) transports inositols but not glucose in L6 cells. (2009). https://pubmed.ncbi.nlm.nih.gov/19032932/ DOI: 10.1016/j.abb.2008.11.008
- tissue_or_cell_type
- Skeletal-muscle cell model
Inositol: synthesis, signaling, mineral interactions and conditional deficiency (2026-09-17) · lines 314–325
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human SMIT2 overexpression and radiotracer uptake · source_derived_draft · unverified_draft
### ino-smit2-glucose Glucose competed for D-chiro-inositol uptake with a reported Ki of 6.1 mM in the SMIT2 expression system, without evidence that SMIT2 transported glucose in those assays. Condition category: normal nutrient_topic: Inositol research collection; topical membership is not evidence of a direct dietary effect. plain_language: Glucose competed for entry without itself becoming demonstrated cargo of this transporter. organism: Human transporter in rat L6 myoblasts tissue_or_cell_type: Skeletal-muscle cell model experimental_model: Human SMIT2 overexpression and radiotracer uptake limitations: Overexpression is not normal transporter abundance. Insulin experiments used untransfected rat cells; changes in human diabetes are proposed, not demonstrated here. exposure: Overexpression, glucose competition and insulin exposure evidence_span: {"source_cache": "artifacts/inositol-research/19032932.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4fdc565b9aa26ef5f2d083c539a1b0367403b39f0c75d3ea1b194bf6fa525242", "start_char": 0, "end_char": 1164, "text_sha256": "4fdc565b9aa26ef5f2d083c539a1b0367403b39f0c75d3ea1b194bf6fa525242"} [ino-p19032932] Human sodium/inositol cotransporter 2 (SMIT2) transports inositols but not glucose in L6 cells. (2009). https://pubmed.ncbi.nlm.nih.gov/19032932/ DOI: 10.1016/j.abb.2008.11.008
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.