Component
Human monocarboxylate transporter 1 / SLC16A1
Context-specific entity; species, compartment and exposure are stated on each claim.
3 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
After preincubation with 2 mM sodium butyrate, AA/C1 cells increased the maximal butyrate uptake rate about fivefold without a significant change in apparent Km.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Human colonic-cell radiotracer uptake.
- limitations
- An adaptive culture response does not establish oral bioavailability.
- nutrient_topic
- Butyrate collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Butyrate
- plain_language
- Transport capacity increased rather than measured substrate affinity.
- primary_references
- Substrate-induced regulation of the human colonic monocarboxylate transporter, MCT1. · 2002 · https://pubmed.ncbi.nlm.nih.gov/11882670/ · DOI 10.1113/jphysiol.2001.014241
Butyrate: microbial production, fuel use, signaling and nutrient interactions (2026-09-19) · lines 134–140
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human colonic-cell radiotracer uptake. · source_derived_draft · unverified_draft
## butyrate-mct1-capacity Transport capacity increased rather than measured substrate affinity. After preincubation with 2 mM sodium butyrate, AA/C1 cells increased the maximal butyrate uptake rate about fivefold without a significant change in apparent Km. Model: Human colonic-cell radiotracer uptake. Limitations: An adaptive culture response does not establish oral bioavailability. Evidence access: Primary abstract Substrate-induced regulation of the human colonic monocarboxylate transporter, MCT1. · 2002 · https://pubmed.ncbi.nlm.nih.gov/11882670/ · DOI 10.1113/jphysiol.2001.014241
Complete structured claim and evidence
What acts on it
At 2 mM sodium butyrate, human AA/C1 colonic cells increased MCT1 mRNA and protein through transcription and greater mRNA stability.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Human colonic epithelial AA/C1 cultures.
- limitations
- Acetate and propionate did not reproduce this response; exposure and cell state matter.
- nutrient_topic
- Butyrate collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Butyrate
- plain_language
- Butyrate increased the capacity of one of its own uptake routes.
- primary_references
- Substrate-induced regulation of the human colonic monocarboxylate transporter, MCT1. · 2002 · https://pubmed.ncbi.nlm.nih.gov/11882670/ · DOI 10.1113/jphysiol.2001.014241
Butyrate: microbial production, fuel use, signaling and nutrient interactions (2026-09-19) · lines 126–132
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human colonic epithelial AA/C1 cultures. · source_derived_draft · unverified_draft
## butyrate-mct1-expression Butyrate increased the capacity of one of its own uptake routes. At 2 mM sodium butyrate, human AA/C1 colonic cells increased MCT1 mRNA and protein through transcription and greater mRNA stability. Model: Human colonic epithelial AA/C1 cultures. Limitations: Acetate and propionate did not reproduce this response; exposure and cell state matter. Evidence access: Primary abstract Substrate-induced regulation of the human colonic monocarboxylate transporter, MCT1. · 2002 · https://pubmed.ncbi.nlm.nih.gov/11882670/ · DOI 10.1113/jphysiol.2001.014241
Complete structured claim and evidence
Where it participates (unsigned role)
Butyrate restored MCT1 and IL-18 expression in challenged human epithelial organoids, but did not suppress their pro-inflammatory gene expression as it did in mononuclear-cell experiments.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Human organoids, mucosa and mononuclear-cell comparisons.
- limitations
- MCT1 recovery and immune-cell cytokine suppression are separate endpoints.
- nutrient_topic
- Butyrate collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Butyrate
- plain_language
- Cell identity changed which effects were seen.
- primary_references
- Butyrate suppresses mucosal inflammation in inflammatory bowel disease primarily through HDAC3 inhibition in monocytes and macrophages. · 2025 · https://pubmed.ncbi.nlm.nih.gov/41110099/ · DOI 10.1111/febs.70289
Butyrate: microbial production, fuel use, signaling and nutrient interactions (2026-09-19) · lines 422–428
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human organoids, mucosa and mononuclear-cell comparisons. · source_derived_draft · unverified_draft
## butyrate-ibd-epithelial-limit Cell identity changed which effects were seen. Butyrate restored MCT1 and IL-18 expression in challenged human epithelial organoids, but did not suppress their pro-inflammatory gene expression as it did in mononuclear-cell experiments. Model: Human organoids, mucosa and mononuclear-cell comparisons. Limitations: MCT1 recovery and immune-cell cytokine suppression are separate endpoints. Evidence access: Primary abstract Butyrate suppresses mucosal inflammation in inflammatory bowel disease primarily through HDAC3 inhibition in monocytes and macrophages. · 2025 · https://pubmed.ncbi.nlm.nih.gov/41110099/ · DOI 10.1111/febs.70289
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.