Component

Mouse ketohexokinase C isoform / Khk-C

Species, exposure, manipulation and evidence limits are specified on each linked claim.

1 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.

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. Deleting intestinal Khk-C increased fructose spillover and hepatic lipogenesis during sucrose feeding in mice.

    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    dose
    10% sucrose in drinking water
    duration
    8 weeks
    evidence_access
    Primary full-text methods/results and metadata inspected.
    evidence_scope
    literature_reviewed; source-specific curation
    experimental_model
    Intestine-specific Khk-C knockout mice and littermate controls
    exposure_scope
    Sucrose / fructose-component mechanism
    limitations
    Tissue-specific deletion differs from systemic KHK inhibition. Source is sucrose exposure, not an HFCS trial; mouse intake patterns are not a human safety threshold.
    nutrient_topic
    HFCS chapter: actual formulation studies, component biochemistry and interventions are explicitly distinguished. · High-Fructose Corn Syrup / HFCS
    organism
    Intestine-specific Khk-C knockout mice and littermate controls
    plain_language
    Deleting intestinal Khk-C increased fructose spillover and hepatic lipogenesis during sucrose feeding in mice.
    primary_references
    The small intestine shields the liver from fructose-induced steatosis. (2020). https://pubmed.ncbi.nlm.nih.gov/32694791/ DOI: 10.1038/s42255-020-0222-9
    route
    Oral ad libitum sucrose with genetic deletion
    tissue
    Intestinal clearance and liver lipid metabolism
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    High-Fructose Corn Syrup: mechanism of action and metabolic impact (2026-09-20) · lines 185–195

    Original AI-assisted curation of twenty primary studies and official FDA composition information, with one reused canonical glucose-transport claim. Study-specific citations, negative findings and limitations retained. Not publisher full text. · supports · Intestine-specific Khk-C knockout mice and littermate controls · source_derived_draft · unverified_draft

    ## hfcs-intestinal-khk-deletion Deleting intestinal Khk-C increased fructose spillover and hepatic lipogenesis during sucrose feeding in mice. Model/species: Intestine-specific Khk-C knockout mice and littermate controls Tissue: Intestinal clearance and liver lipid metabolism Exposure: 10% sucrose in drinking water Route: Oral ad libitum sucrose with genetic deletion Duration: 8 weeks Exposure scope: Sucrose / fructose-component mechanism Limits: Tissue-specific deletion differs from systemic KHK inhibition. Source is sucrose exposure, not an HFCS trial; mouse intake patterns are not a human safety threshold. Reference: The small intestine shields the liver from fructose-induced steatosis. (2020). https://pubmed.ncbi.nlm.nih.gov/32694791/ DOI: 10.1038/s42255-020-0222-9 Access: Primary full-text methods/results and metadata inspected.
    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