Component

Glucagon

Pancreatic peptide hormone.

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. HCl infusion causing acute mineral acidemia raised plasma potassium in the conscious-dog experiment.

    Hydrochloric acid → Serum or plasma potassium concentration source_derived_draftungraded
    Experimental context and source evidence
    endpoint
    HCl infusion causing acute mineral acidemia raised plasma potassium in the conscious-dog experiment.
    experimental-exposure
    Experimental acute mineral acidemia with hyperkalemia; not potassium deficiency or excessive potassium intake.
    experimental_model
    Twelve conscious dogs with portal/hepatic/systemic sampling; beta-hydroxybutyric acid 7 mEq/kg or HCl 3 mEq/kg infused over 30 minutes; additional anesthetized and obstructed-urinary-tract studies.
    limitations
    Acute HCl infusion, not every acidosis; portal glucagon rose and direct H/K exchange was not isolated.
    nutrient_topic
    Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
    organism
    Canis lupus familiaris
    plain_language
    Acid type affected the potassium response; a rise in blood potassium did not imply excess potassium intake.
    primary_references
    [adrogue-1985-acid-infusion] Role of the endocrine pancreas in the kalemic response to acute metabolic acidosis in conscious dogs (1985). https://www.jci.org/articles/view/111775 DOI: 10.1172/JCI111775
    tissue_or_cell_type
    systemic and splanchnic circulation

    Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1151–1162

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Twelve conscious dogs with portal/hepatic/systemic sampling; beta-hydroxybutyric acid 7 mEq/kg or HCl 3 mEq/kg infused over 30 minutes; additional anesthetized and obstructed-urinary-tract studies. · source_derived_draft · unverified_draft

    ### hcl-acidemia-raises-plasma-k HCl infusion causing acute mineral acidemia raised plasma potassium in the conscious-dog experiment. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Acid type affected the potassium response; a rise in blood potassium did not imply excess potassium intake. organism: Canis lupus familiaris tissue_or_cell_type: systemic and splanchnic circulation experimental_model: Twelve conscious dogs with portal/hepatic/systemic sampling; beta-hydroxybutyric acid 7 mEq/kg or HCl 3 mEq/kg infused over 30 minutes; additional anesthetized and obstructed-urinary-tract studies. limitations: Acute HCl infusion, not every acidosis; portal glucagon rose and direct H/K exchange was not isolated. experimental-exposure: Experimental acute mineral acidemia with hyperkalemia; not potassium deficiency or excessive potassium intake. endpoint: HCl infusion causing acute mineral acidemia raised plasma potassium in the conscious-dog experiment. [adrogue-1985-acid-infusion] Role of the endocrine pancreas in the kalemic response to acute metabolic acidosis in conscious dogs (1985). https://www.jci.org/articles/view/111775 DOI: 10.1172/JCI111775
    Complete structured claim and evidence

  2. Somatostatin suppressed splanchnic glucose output by 50–100% for five hours after a 60-hour fast; the overnight-fast reduction was transient.

    Somatostatin-induced combined insulin and glucagon suppression → Splanchnic glucose output source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Healthy humans; somatostatin, glucose infusion to maintain euglycemia, organ exchange measurements.
    limitations
    Insulin and glucagon were both suppressed. The experiment does not isolate glucagon alone.
    nutrient_topic
    Fasting physiological-state collection; human protocols, cellular deprivation and refeeding are distinguished. · Fasting / abstention from energy intake
    plain_language
    Hormonal control changed with the fasting state.
    primary_references
    Role of basal glucagon levels in the regulation of splanchnic glucose output and ketogenesis in insulin-deficient humans. · 1984 · https://pubmed.ncbi.nlm.nih.gov/6146427/ · DOI 10.1111/j.1475-097x.1984.tb00117.x

    Fasting: fuel switching, nutrient sensing, ketone signaling, nutrient dependencies and refeeding (2026-09-18) · lines 96–102

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Healthy humans; somatostatin, glucose infusion to maintain euglycemia, organ exchange measurements. · source_derived_draft · unverified_draft

    ## fast-hormone-withdrawal Hormonal control changed with the fasting state. Somatostatin suppressed splanchnic glucose output by 50–100% for five hours after a 60-hour fast; the overnight-fast reduction was transient. Model: Healthy humans; somatostatin, glucose infusion to maintain euglycemia, organ exchange measurements. Limitations: Insulin and glucagon were both suppressed. The experiment does not isolate glucagon alone. Evidence access: Primary abstract Role of basal glucagon levels in the regulation of splanchnic glucose output and ketogenesis in insulin-deficient humans. · 1984 · https://pubmed.ncbi.nlm.nih.gov/6146427/ · DOI 10.1111/j.1475-097x.1984.tb00117.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