Component
Human adenosine A1 receptor / ADORA1
Study-scoped entity; inspect species, exposure, model and limitations on each claim.
2 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
Caffeine displaced 5–44% of the A1 PET ligand signal; modeled half-maximal displacement corresponded to plasma caffeine of 67 micromolar.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- 15 adults; 0.5–4.3 mg/kg intravenous caffeine after at least 36 hours abstinence; one vehicle subject.
- limitations
- PET occupancy does not establish that A1 alone mediates wakefulness or a universal oral-dose threshold.
- nutrient_topic
- Caffeine collection; salts, coffee, species and coexposure contexts retain their identities. · Caffeine
- plain_language
- Caffeine reached and occupied adenosine receptors in the human brain.
- primary_references
- Caffeine occupancy of human cerebral A1 adenosine receptors: in vivo quantification with 18F-CPFPX and PET. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22966134/ · DOI 10.2967/jnumed.112.105114
Caffeine: receptors, metabolism, nutrient interactions, adaptation and discovery questions (2026-09-18) · lines 20–26
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · 15 adults; 0.5–4.3 mg/kg intravenous caffeine after at least 36 hours abstinence; one vehicle subject. · source_derived_draft · unverified_draft
## caf-human-a1 Caffeine reached and occupied adenosine receptors in the human brain. Caffeine displaced 5–44% of the A1 PET ligand signal; modeled half-maximal displacement corresponded to plasma caffeine of 67 micromolar. Model: 15 adults; 0.5–4.3 mg/kg intravenous caffeine after at least 36 hours abstinence; one vehicle subject. Limitations: PET occupancy does not establish that A1 alone mediates wakefulness or a universal oral-dose threshold. Evidence access: Primary abstract Caffeine occupancy of human cerebral A1 adenosine receptors: in vivo quantification with 18F-CPFPX and PET. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22966134/ · DOI 10.2967/jnumed.112.105114
Complete structured claim and evidence
Where it participates (unsigned role)
Adenosine signalling contributed to ethanol-induced fatty liver in mice, with the effect traced through adenosine receptors and the equilibrative nucleoside transporter.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/alcohol-research/19221436.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "21c9018b01ea529427ab3e8f55fd2f561e0a9ba03c22788fb1875609bf9d4312", "start_char": 0, "end_char": 1663, "text_sha256": "21c9018b01ea529427ab3e8f55fd2f561e0a9ba03c22788fb1875609bf9d4312"}
- experimental_model
- Ethanol-fed mice with adenosine receptor and transporter deletion
- exposure
- Chronic ethanol feeding in Ent1-null and adenosine receptor-null mice
- limitations
- Connects the adenosine target to an organ outcome using genetic deletion, which is stronger than correlation.
- nutrient_topic
- Alcohol research collection; topical membership is not evidence of a direct clinical effect, and ethanol is recorded separately from the acetaldehyde it becomes. · Ethanol
- organism
- Mouse
- plain_language
- The same adenosine rise that sedates the brain also drives fat into the liver.
- primary_references
- [alcohol-p19221436] Adenosine signaling contributes to ethanol-induced fatty liver in mice. (2009). https://pubmed.ncbi.nlm.nih.gov/19221436/ DOI: 10.1172/jci37409
- tissue_or_cell_type
- Liver
Alcohol: ethanol clearance, acetaldehyde, the channels it binds, organ injury and nutrient collisions (2026-09-21) · lines 449–460
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Ethanol-fed mice with adenosine receptor and transporter deletion · source_derived_draft · unverified_draft
### alcohol-adenosine-fatty-liver Adenosine signalling contributed to ethanol-induced fatty liver in mice, with the effect traced through adenosine receptors and the equilibrative nucleoside transporter. Condition category: normal nutrient_topic: Alcohol research collection; topical membership is not evidence of a direct clinical effect, and ethanol is recorded separately from the acetaldehyde it becomes. plain_language: The same adenosine rise that sedates the brain also drives fat into the liver. organism: Mouse tissue_or_cell_type: Liver experimental_model: Ethanol-fed mice with adenosine receptor and transporter deletion limitations: Connects the adenosine target to an organ outcome using genetic deletion, which is stronger than correlation. exposure: Chronic ethanol feeding in Ent1-null and adenosine receptor-null mice evidence_span: {"source_cache": "artifacts/alcohol-research/19221436.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "21c9018b01ea529427ab3e8f55fd2f561e0a9ba03c22788fb1875609bf9d4312", "start_char": 0, "end_char": 1663, "text_sha256": "21c9018b01ea529427ab3e8f55fd2f561e0a9ba03c22788fb1875609bf9d4312"} [alcohol-p19221436] Adenosine signaling contributes to ethanol-induced fatty liver in mice. (2009). https://pubmed.ncbi.nlm.nih.gov/19221436/ DOI: 10.1172/jci37409
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.