Component

17-beta-Estradiol

17-beta-Estradiol. Species, exposure and limitations are retained in each linked claim.

4 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

What it acts on

  1. The increased PEMT message was accompanied by higher protein expression and enzyme activity in the hepatocyte study.

    17-beta-Estradiol → Human hepatocyte PEMT enzyme activity source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/choline-research/17456783.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d3585209a8c4db7cfe8b93aa2587fdd570f5e5c42bd3ea8f6195feb60b23b9da", "start_char": 0, "end_char": 1399, "text_sha256": "d3585209a8c4db7cfe8b93aa2587fdd570f5e5c42bd3ea8f6195feb60b23b9da"}
    experimental_model
    Primary-hepatocyte estrogen exposure
    exposure
    17-beta-estradiol treatment for 24 hours
    limitations
    Culture regulation supports a mechanism but does not set requirements for every person or justify hormone treatment.
    nutrient_topic
    Choline research collection; topical membership is not evidence of a direct dietary effect. · Choline
    organism
    Human primary hepatocytes
    plain_language
    The response extended beyond an RNA measurement.
    primary_references
    [choline-p17456783] Phosphatidylethanolamine N-methyltransferase (PEMT) gene expression is induced by estrogen in human and mouse primary hepatocytes. (2007). https://pubmed.ncbi.nlm.nih.gov/17456783/ DOI: 10.1096/fj.07-8227com
    tissue_or_cell_type
    Primary hepatocytes

    Choline: metabolism, signaling and nutrient connections (2026-09-17) · lines 841–852

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Primary-hepatocyte estrogen exposure · source_derived_draft · unverified_draft

    ### choline-estrogen-pemt-activity The increased PEMT message was accompanied by higher protein expression and enzyme activity in the hepatocyte study. Condition category: normal nutrient_topic: Choline research collection; topical membership is not evidence of a direct dietary effect. plain_language: The response extended beyond an RNA measurement. organism: Human primary hepatocytes tissue_or_cell_type: Primary hepatocytes experimental_model: Primary-hepatocyte estrogen exposure limitations: Culture regulation supports a mechanism but does not set requirements for every person or justify hormone treatment. exposure: 17-beta-estradiol treatment for 24 hours evidence_span: {"source_cache": "artifacts/choline-research/17456783.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d3585209a8c4db7cfe8b93aa2587fdd570f5e5c42bd3ea8f6195feb60b23b9da", "start_char": 0, "end_char": 1399, "text_sha256": "d3585209a8c4db7cfe8b93aa2587fdd570f5e5c42bd3ea8f6195feb60b23b9da"} [choline-p17456783] Phosphatidylethanolamine N-methyltransferase (PEMT) gene expression is induced by estrogen in human and mouse primary hepatocytes. (2007). https://pubmed.ncbi.nlm.nih.gov/17456783/ DOI: 10.1096/fj.07-8227com
    Complete structured claim and evidence

  2. Estradiol increased PEMT transcription in primary human hepatocytes in a dose-dependent manner.

    17-beta-Estradiol → Human hepatocyte PEMT transcription source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/choline-research/17456783.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d3585209a8c4db7cfe8b93aa2587fdd570f5e5c42bd3ea8f6195feb60b23b9da", "start_char": 0, "end_char": 1399, "text_sha256": "d3585209a8c4db7cfe8b93aa2587fdd570f5e5c42bd3ea8f6195feb60b23b9da"}
    experimental_model
    Primary-hepatocyte estrogen exposure
    exposure
    17-beta-estradiol treatment for 24 hours
    limitations
    Culture regulation supports a mechanism but does not set requirements for every person or justify hormone treatment.
    nutrient_topic
    Choline research collection; topical membership is not evidence of a direct dietary effect. · Choline
    organism
    Human primary hepatocytes
    plain_language
    Hormone status can affect endogenous choline-headgroup synthesis.
    primary_references
    [choline-p17456783] Phosphatidylethanolamine N-methyltransferase (PEMT) gene expression is induced by estrogen in human and mouse primary hepatocytes. (2007). https://pubmed.ncbi.nlm.nih.gov/17456783/ DOI: 10.1096/fj.07-8227com
    tissue_or_cell_type
    Primary hepatocytes

    Choline: metabolism, signaling and nutrient connections (2026-09-17) · lines 828–839

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Primary-hepatocyte estrogen exposure · source_derived_draft · unverified_draft

    ### choline-estrogen-pemt-transcription Estradiol increased PEMT transcription in primary human hepatocytes in a dose-dependent manner. Condition category: normal nutrient_topic: Choline research collection; topical membership is not evidence of a direct dietary effect. plain_language: Hormone status can affect endogenous choline-headgroup synthesis. organism: Human primary hepatocytes tissue_or_cell_type: Primary hepatocytes experimental_model: Primary-hepatocyte estrogen exposure limitations: Culture regulation supports a mechanism but does not set requirements for every person or justify hormone treatment. exposure: 17-beta-estradiol treatment for 24 hours evidence_span: {"source_cache": "artifacts/choline-research/17456783.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d3585209a8c4db7cfe8b93aa2587fdd570f5e5c42bd3ea8f6195feb60b23b9da", "start_char": 0, "end_char": 1399, "text_sha256": "d3585209a8c4db7cfe8b93aa2587fdd570f5e5c42bd3ea8f6195feb60b23b9da"} [choline-p17456783] Phosphatidylethanolamine N-methyltransferase (PEMT) gene expression is induced by estrogen in human and mouse primary hepatocytes. (2007). https://pubmed.ncbi.nlm.nih.gov/17456783/ DOI: 10.1096/fj.07-8227com
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. DIM inhibited estradiol-induced MCF-7 proliferation in the tested estrogen-stimulated system.

    3,3'-Diindolylmethane / DIM → Cell proliferation source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/dim-research/9771935.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2f0967e62f0757c6ff4e68f7f7f673b6ba12ec581cbc7bd5c5594bdbf1964799", "start_char": 0, "end_char": 1556, "text_sha256": "2f0967e62f0757c6ff4e68f7f7f673b6ba12ec581cbc7bd5c5594bdbf1964799"}
    experimental_model
    Ligand binding, nuclear complex, transcription and growth assays
    exposure
    DIM 10-50 micromolar in cells; rodent dosing separately
    limitations
    Preclinical evidence. Estrogen exposure, tissue and concentrations affect the response; no human cancer-treatment efficacy established.
    nutrient_topic
    Diindolylmethane (DIM) research collection; topical membership is not evidence of a direct dietary effect. · 3,3'-Diindolylmethane / DIM
    organism
    Human MCF-7 cells and rat mammary-tumor model
    plain_language
    Its effect depended on the hormonal conditions being tested.
    primary_references
    [dim-p9771935] Aryl hydrocarbon receptor-mediated antiestrogenic and antitumorigenic activity of diindolylmethane. (1998). https://pubmed.ncbi.nlm.nih.gov/9771935/ DOI: 10.1093/carcin/19.9.1631
    tissue_or_cell_type
    AhR and estrogen-responsive signaling

    Diindolylmethane (DIM): formation, receptor signaling, metabolism and drug interactions (2026-09-17) · lines 311–322

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Ligand binding, nuclear complex, transcription and growth assays · source_derived_draft · unverified_draft

    ### dim-estrogen-growth-inhibition DIM inhibited estradiol-induced MCF-7 proliferation in the tested estrogen-stimulated system. Condition category: normal nutrient_topic: Diindolylmethane (DIM) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Its effect depended on the hormonal conditions being tested. organism: Human MCF-7 cells and rat mammary-tumor model tissue_or_cell_type: AhR and estrogen-responsive signaling experimental_model: Ligand binding, nuclear complex, transcription and growth assays limitations: Preclinical evidence. Estrogen exposure, tissue and concentrations affect the response; no human cancer-treatment efficacy established. exposure: DIM 10-50 micromolar in cells; rodent dosing separately evidence_span: {"source_cache": "artifacts/dim-research/9771935.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2f0967e62f0757c6ff4e68f7f7f673b6ba12ec581cbc7bd5c5594bdbf1964799", "start_char": 0, "end_char": 1556, "text_sha256": "2f0967e62f0757c6ff4e68f7f7f673b6ba12ec581cbc7bd5c5594bdbf1964799"} [dim-p9771935] Aryl hydrocarbon receptor-mediated antiestrogenic and antitumorigenic activity of diindolylmethane. (1998). https://pubmed.ncbi.nlm.nih.gov/9771935/ DOI: 10.1093/carcin/19.9.1631
    Complete structured claim and evidence

  2. Resveratrol bound ERalpha and ERbeta with comparable affinity, approximately 7,000-fold weaker than estradiol in the reported assays.

    trans-Resveratrol → Human estrogen receptor alpha / ESR1 source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Receptor binding and CHO-K1 reporter experiments.
    limitations
    No demonstrated hormone normalization in humans.
    nutrient_topic
    Resveratrol collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Resveratrol
    plain_language
    It can interact with hormone receptors, but weak affinity matters.
    primary_references
    Resveratrol acts as a mixed agonist/antagonist for estrogen receptors alpha and beta. · 2000 · https://pubmed.ncbi.nlm.nih.gov/11014220/ · DOI 10.1210/endo.141.10.7721

    Resveratrol: metabolites, target selectivity and cross-nutrient mechanisms (2026-09-19) · lines 398–404

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Receptor binding and CHO-K1 reporter experiments. · source_derived_draft · unverified_draft

    ## resveratrol-er-binding It can interact with hormone receptors, but weak affinity matters. Resveratrol bound ERalpha and ERbeta with comparable affinity, approximately 7,000-fold weaker than estradiol in the reported assays. Model: Receptor binding and CHO-K1 reporter experiments. Limitations: No demonstrated hormone normalization in humans. Evidence access: Primary abstract Resveratrol acts as a mixed agonist/antagonist for estrogen receptors alpha and beta. · 2000 · https://pubmed.ncbi.nlm.nih.gov/11014220/ · DOI 10.1210/endo.141.10.7721
    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.

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