Component

Equilibrative nucleoside transporter 1 / ENT1 / SLC29A1

Equilibrative nucleoside transporter 1 / ENT1 / SLC29A1. Species, exposure and limitations are retained in each linked claim.

2 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

Where it participates (unsigned role)

  1. Adenosine signalling contributed to ethanol-induced fatty liver in mice, with the effect traced through adenosine receptors and the equilibrative nucleoside transporter.

    Extracellular adenosine concentration → Hepatic steatosis / fatty liver source_derived_draftungraded
    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

  2. Ethanol increased extracellular adenosine by inhibiting adenosine uptake via the nucleoside transporter.

    Ethanol → Cellular adenosine uptake by the nucleoside transporter source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/alcohol-research/2298733.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3933013c774b52112ebb838291e240d625dbf664faa2e94db35204bc38fb73d9", "start_char": 0, "end_char": 1419, "text_sha256": "3933013c774b52112ebb838291e240d625dbf664faa2e94db35204bc38fb73d9"}
    experimental_model
    Nucleoside transport and adenosine measurement in cultured cells during ethanol exposure
    exposure
    Ethanol exposure with adenosine uptake measurement
    limitations
    A transport mechanism for an indirect target: the effect is on adenosine handling, not on a receptor. Cultured cells.
    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
    Cultured cells
    plain_language
    Alcohol raises a natural sedative by blocking its reuptake.
    primary_references
    [alcohol-p2298733] Ethanol increases extracellular adenosine by inhibiting adenosine uptake via the nucleoside transporter. (1990). https://pubmed.ncbi.nlm.nih.gov/2298733/ DOI: 10.1016/s0021-9258(19)39923-5
    tissue_or_cell_type
    Nucleoside transporter

    Alcohol: ethanol clearance, acetaldehyde, the channels it binds, organ injury and nutrient collisions (2026-09-21) · lines 410–421

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Nucleoside transport and adenosine measurement in cultured cells during ethanol exposure · source_derived_draft · unverified_draft

    ### alcohol-ent1-inhibition Ethanol increased extracellular adenosine by inhibiting adenosine uptake via the 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: Alcohol raises a natural sedative by blocking its reuptake. organism: Cultured cells tissue_or_cell_type: Nucleoside transporter experimental_model: Nucleoside transport and adenosine measurement in cultured cells during ethanol exposure limitations: A transport mechanism for an indirect target: the effect is on adenosine handling, not on a receptor. Cultured cells. exposure: Ethanol exposure with adenosine uptake measurement evidence_span: {"source_cache": "artifacts/alcohol-research/2298733.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3933013c774b52112ebb838291e240d625dbf664faa2e94db35204bc38fb73d9", "start_char": 0, "end_char": 1419, "text_sha256": "3933013c774b52112ebb838291e240d625dbf664faa2e94db35204bc38fb73d9"} [alcohol-p2298733] Ethanol increases extracellular adenosine by inhibiting adenosine uptake via the nucleoside transporter. (1990). https://pubmed.ncbi.nlm.nih.gov/2298733/ DOI: 10.1016/s0021-9258(19)39923-5
    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.

    Evidence, AI assistance and curation standards