Component

Propranolol

Propranolol. Species, exposure and limitations are retained in each linked claim.

3 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. With propranolol, caffeine-associated insulin and C-peptide responses resembled placebo.

    Propranolol → Insulin response during an oral glucose tolerance test source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Seven healthy men; 5 mg/kg caffeine, 80 mg propranolol, combination or placebo before an oral glucose tolerance test.
    limitations
    Small acute experiment. Beta blockade supports an adrenergic contribution, not proof that it is the only mechanism or that a blocker should be used to counter caffeine.
    nutrient_topic
    Caffeine collection; salts, coffee, species and coexposure contexts retain their identities. · Caffeine
    plain_language
    Blocking beta-adrenergic signaling removed the response in this test.
    primary_references
    Caffeine-induced impairment of glucose tolerance is abolished by beta-adrenergic receptor blockade in humans. · 2002 · https://pubmed.ncbi.nlm.nih.gov/12015346/ · DOI 10.1152/japplphysiol.01229.2001

    Caffeine: receptors, metabolism, nutrient interactions, adaptation and discovery questions (2026-09-18) · lines 500–506

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Seven healthy men; 5 mg/kg caffeine, 80 mg propranolol, combination or placebo before an oral glucose tolerance test. · source_derived_draft · unverified_draft

    ## caf-beta-block Blocking beta-adrenergic signaling removed the response in this test. With propranolol, caffeine-associated insulin and C-peptide responses resembled placebo. Model: Seven healthy men; 5 mg/kg caffeine, 80 mg propranolol, combination or placebo before an oral glucose tolerance test. Limitations: Small acute experiment. Beta blockade supports an adrenergic contribution, not proof that it is the only mechanism or that a blocker should be used to counter caffeine. Evidence access: Primary abstract Caffeine-induced impairment of glucose tolerance is abolished by beta-adrenergic receptor blockade in humans. · 2002 · https://pubmed.ncbi.nlm.nih.gov/12015346/ · DOI 10.1152/japplphysiol.01229.2001
    Complete structured claim and evidence

What acts on it

  1. CYP1A2 contributed prominently to propranolol N-desisopropylation.

    Human cytochrome P450 1A2 → Propranolol source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/dim-research/7640150.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "368198090ed645914a14e9d365b48030bcfd8a67e4d5bc4f9f6d1476e8340247", "start_char": 0, "end_char": 2428, "text_sha256": "368198090ed645914a14e9d365b48030bcfd8a67e4d5bc4f9f6d1476e8340247"}
    experimental_model
    Human microsomes and recombinant enzyme phenotyping
    exposure
    N-desisopropylation versus ring hydroxylation
    limitations
    Route- and enantiomer-specific biochemistry; total propranolol exposure cannot be predicted from one route.
    nutrient_topic
    Diindolylmethane (DIM) research collection; topical membership is not evidence of a direct dietary effect. · 3,3'-Diindolylmethane / DIM
    organism
    Human CYP isoforms
    plain_language
    This is one route through a drug with several clearance mechanisms.
    primary_references
    [dim-p7640150] Identification of human CYP isoforms involved in the metabolism of propranolol enantiomers--N-desisopropylation is mediated mainly by CYP1A2. (1995). https://pubmed.ncbi.nlm.nih.gov/7640150/ DOI: 10.1111/j.1365-2125.1995.tb04472.x
    tissue_or_cell_type
    Propranolol enantiomer metabolism

    Diindolylmethane (DIM): formation, receptor signaling, metabolism and drug interactions (2026-09-17) · lines 909–920

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human microsomes and recombinant enzyme phenotyping · source_derived_draft · unverified_draft

    ### dim-propranolol-1a2 CYP1A2 contributed prominently to propranolol N-desisopropylation. Condition category: normal nutrient_topic: Diindolylmethane (DIM) research collection; topical membership is not evidence of a direct dietary effect. plain_language: This is one route through a drug with several clearance mechanisms. organism: Human CYP isoforms tissue_or_cell_type: Propranolol enantiomer metabolism experimental_model: Human microsomes and recombinant enzyme phenotyping limitations: Route- and enantiomer-specific biochemistry; total propranolol exposure cannot be predicted from one route. exposure: N-desisopropylation versus ring hydroxylation evidence_span: {"source_cache": "artifacts/dim-research/7640150.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "368198090ed645914a14e9d365b48030bcfd8a67e4d5bc4f9f6d1476e8340247", "start_char": 0, "end_char": 2428, "text_sha256": "368198090ed645914a14e9d365b48030bcfd8a67e4d5bc4f9f6d1476e8340247"} [dim-p7640150] Identification of human CYP isoforms involved in the metabolism of propranolol enantiomers--N-desisopropylation is mediated mainly by CYP1A2. (1995). https://pubmed.ncbi.nlm.nih.gov/7640150/ DOI: 10.1111/j.1365-2125.1995.tb04472.x
    Complete structured claim and evidence

  2. CYP2D6 was a major catalyst of propranolol ring 4-hydroxylation.

    Human cytochrome P450 2D6 → Propranolol source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/dim-research/7640150.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "368198090ed645914a14e9d365b48030bcfd8a67e4d5bc4f9f6d1476e8340247", "start_char": 0, "end_char": 2428, "text_sha256": "368198090ed645914a14e9d365b48030bcfd8a67e4d5bc4f9f6d1476e8340247"}
    experimental_model
    Human microsomes and recombinant enzyme phenotyping
    exposure
    N-desisopropylation versus ring hydroxylation
    limitations
    Route- and enantiomer-specific biochemistry; total propranolol exposure cannot be predicted from one route.
    nutrient_topic
    Diindolylmethane (DIM) research collection; topical membership is not evidence of a direct dietary effect. · 3,3'-Diindolylmethane / DIM
    organism
    Human CYP isoforms
    plain_language
    A separate enzyme supports a different transformation of the same drug.
    primary_references
    [dim-p7640150] Identification of human CYP isoforms involved in the metabolism of propranolol enantiomers--N-desisopropylation is mediated mainly by CYP1A2. (1995). https://pubmed.ncbi.nlm.nih.gov/7640150/ DOI: 10.1111/j.1365-2125.1995.tb04472.x
    tissue_or_cell_type
    Propranolol enantiomer metabolism

    Diindolylmethane (DIM): formation, receptor signaling, metabolism and drug interactions (2026-09-17) · lines 922–933

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human microsomes and recombinant enzyme phenotyping · source_derived_draft · unverified_draft

    ### dim-propranolol-2d6 CYP2D6 was a major catalyst of propranolol ring 4-hydroxylation. Condition category: normal nutrient_topic: Diindolylmethane (DIM) research collection; topical membership is not evidence of a direct dietary effect. plain_language: A separate enzyme supports a different transformation of the same drug. organism: Human CYP isoforms tissue_or_cell_type: Propranolol enantiomer metabolism experimental_model: Human microsomes and recombinant enzyme phenotyping limitations: Route- and enantiomer-specific biochemistry; total propranolol exposure cannot be predicted from one route. exposure: N-desisopropylation versus ring hydroxylation evidence_span: {"source_cache": "artifacts/dim-research/7640150.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "368198090ed645914a14e9d365b48030bcfd8a67e4d5bc4f9f6d1476e8340247", "start_char": 0, "end_char": 2428, "text_sha256": "368198090ed645914a14e9d365b48030bcfd8a67e4d5bc4f9f6d1476e8340247"} [dim-p7640150] Identification of human CYP isoforms involved in the metabolism of propranolol enantiomers--N-desisopropylation is mediated mainly by CYP1A2. (1995). https://pubmed.ncbi.nlm.nih.gov/7640150/ DOI: 10.1111/j.1365-2125.1995.tb04472.x
    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