Component

D-Fructose 1-phosphate

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

5 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 acts on it

  1. Wild-type recombinant human aldolase B had catalytic activity toward fructose 1-phosphate.

    Human aldolase B / ALDOB → D-Fructose 1-phosphate source_derived_draftungraded
    Experimental context and source evidence
    dose
    Wild-type versus hereditary-fructose-intolerance-associated variants; exact substrate series not in abstract
    duration
    Assay duration not recovered
    evidence_access
    Primary abstract/metadata; unrecovered methods explicitly retained.
    evidence_scope
    literature_reviewed; source-specific curation
    experimental_model
    Recombinant wild-type and Arg303Trp human ALDOB
    exposure_scope
    Human genetic machinery / fructose component
    limitations
    A mutation-specific activity defect is not ordinary dietary intolerance or a population toxicity threshold. Full article is scanned; abstract kinetics used.
    nutrient_topic
    HFCS chapter: actual formulation studies, component biochemistry and interventions are explicitly distinguished. · High-Fructose Corn Syrup / HFCS
    organism
    Recombinant wild-type and Arg303Trp human ALDOB
    plain_language
    Wild-type recombinant human aldolase B had catalytic activity toward fructose 1-phosphate.
    primary_references
    Functional and molecular modelling studies of two hereditary fructose intolerance-causing mutations at arginine 303 in human liver aldolase. (2000). https://pubmed.ncbi.nlm.nih.gov/10970798/
    route
    In vitro recombinant enzyme assay
    tissue
    Fructose-1-phosphate enzyme assay

    High-Fructose Corn Syrup: mechanism of action and metabolic impact (2026-09-20) · lines 113–123

    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 · Recombinant wild-type and Arg303Trp human ALDOB · source_derived_draft · unverified_draft

    ## hfcs-aldob-activity Wild-type recombinant human aldolase B had catalytic activity toward fructose 1-phosphate. Model/species: Recombinant wild-type and Arg303Trp human ALDOB Tissue: Fructose-1-phosphate enzyme assay Exposure: Wild-type versus hereditary-fructose-intolerance-associated variants; exact substrate series not in abstract Route: In vitro recombinant enzyme assay Duration: Assay duration not recovered Exposure scope: Human genetic machinery / fructose component Limits: A mutation-specific activity defect is not ordinary dietary intolerance or a population toxicity threshold. Full article is scanned; abstract kinetics used. Reference: Functional and molecular modelling studies of two hereditary fructose intolerance-causing mutations at arginine 303 in human liver aldolase. (2000). https://pubmed.ncbi.nlm.nih.gov/10970798/ Access: Primary abstract/metadata; unrecovered methods explicitly retained.
    Complete structured claim and evidence

  2. The human ALDOB Arg303Trp variant had no detectable fructose-1-phosphate activity in the reported assay.

    Human ALDOB Arg303Trp variant → D-Fructose 1-phosphate source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    dose
    Wild-type versus hereditary-fructose-intolerance-associated variants; exact substrate series not in abstract
    duration
    Assay duration not recovered
    evidence_access
    Primary abstract/metadata; unrecovered methods explicitly retained.
    evidence_scope
    literature_reviewed; source-specific curation
    experimental_model
    Recombinant wild-type and Arg303Trp human ALDOB
    exposure_scope
    Human genetic machinery / fructose component
    limitations
    A mutation-specific activity defect is not ordinary dietary intolerance or a population toxicity threshold. Full article is scanned; abstract kinetics used.
    nutrient_topic
    HFCS chapter: actual formulation studies, component biochemistry and interventions are explicitly distinguished. · High-Fructose Corn Syrup / HFCS
    organism
    Recombinant wild-type and Arg303Trp human ALDOB
    plain_language
    The human ALDOB Arg303Trp variant had no detectable fructose-1-phosphate activity in the reported assay.
    primary_references
    Functional and molecular modelling studies of two hereditary fructose intolerance-causing mutations at arginine 303 in human liver aldolase. (2000). https://pubmed.ncbi.nlm.nih.gov/10970798/
    route
    In vitro recombinant enzyme assay
    tissue
    Fructose-1-phosphate enzyme assay
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    High-Fructose Corn Syrup: mechanism of action and metabolic impact (2026-09-20) · lines 125–135

    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 · Recombinant wild-type and Arg303Trp human ALDOB · source_derived_draft · unverified_draft

    ## hfcs-aldob-variant The human ALDOB Arg303Trp variant had no detectable fructose-1-phosphate activity in the reported assay. Model/species: Recombinant wild-type and Arg303Trp human ALDOB Tissue: Fructose-1-phosphate enzyme assay Exposure: Wild-type versus hereditary-fructose-intolerance-associated variants; exact substrate series not in abstract Route: In vitro recombinant enzyme assay Duration: Assay duration not recovered Exposure scope: Human genetic machinery / fructose component Limits: A mutation-specific activity defect is not ordinary dietary intolerance or a population toxicity threshold. Full article is scanned; abstract kinetics used. Reference: Functional and molecular modelling studies of two hereditary fructose intolerance-causing mutations at arginine 303 in human liver aldolase. (2000). https://pubmed.ncbi.nlm.nih.gov/10970798/ Access: Primary abstract/metadata; unrecovered methods explicitly retained.
    Complete structured claim and evidence

  3. Purified human liver ketohexokinase catalyzed the ATP-dependent phosphorylation of fructose.

    Human ketohexokinase / KHK → D-Fructose 1-phosphate source_derived_draftungraded
    Experimental context and source evidence
    dose
    Fructose substrate and ATP-dependent enzyme characterization; exact concentrations not in abstract
    duration
    Assay duration not recovered
    evidence_access
    Primary abstract/metadata; unrecovered methods explicitly retained.
    evidence_scope
    literature_reviewed; source-specific curation
    experimental_model
    Ketohexokinase purified from human liver
    exposure_scope
    Human component biochemistry
    limitations
    Isoform unresolved; enzyme chemistry does not quantify whole-body flux after ordinary HFCS intake. Only abstract/metadata recovered for this scanned article.
    nutrient_topic
    HFCS chapter: actual formulation studies, component biochemistry and interventions are explicitly distinguished. · High-Fructose Corn Syrup / HFCS
    organism
    Ketohexokinase purified from human liver
    plain_language
    Purified human liver ketohexokinase catalyzed the ATP-dependent phosphorylation of fructose.
    primary_references
    The purification and properties of human liver ketohexokinase. A role for ketohexokinase and fructose-bisphosphate aldolase in the metabolic production of oxalate from xylitol. (1985). https://pubmed.ncbi.nlm.nih.gov/2996495/ DOI: 10.1042/bj2300053
    route
    In vitro enzyme/substrate incubation
    tissue
    Cell-free enzyme kinetics

    High-Fructose Corn Syrup: mechanism of action and metabolic impact (2026-09-20) · lines 101–111

    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 · Ketohexokinase purified from human liver · source_derived_draft · unverified_draft

    ## hfcs-khk-phosphorylation Purified human liver ketohexokinase catalyzed the ATP-dependent phosphorylation of fructose. Model/species: Ketohexokinase purified from human liver Tissue: Cell-free enzyme kinetics Exposure: Fructose substrate and ATP-dependent enzyme characterization; exact concentrations not in abstract Route: In vitro enzyme/substrate incubation Duration: Assay duration not recovered Exposure scope: Human component biochemistry Limits: Isoform unresolved; enzyme chemistry does not quantify whole-body flux after ordinary HFCS intake. Only abstract/metadata recovered for this scanned article. Reference: The purification and properties of human liver ketohexokinase. A role for ketohexokinase and fructose-bisphosphate aldolase in the metabolic production of oxalate from xylitol. (1985). https://pubmed.ncbi.nlm.nih.gov/2996495/ DOI: 10.1042/bj2300053 Access: Primary abstract/metadata; unrecovered methods explicitly retained.
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. The intravenous fructose bolus acutely lowered hepatic inorganic phosphate as sugar phosphates accumulated.

    Fructose → Human hepatic inorganic phosphate measured by phosphorus MRS source_derived_draftungraded
    Experimental context and source evidence
    dose
    Fructose 250 mg/kg bolus
    duration
    Early 5 min changes; sugar-phosphate recovery within about 20 min
    evidence_access
    Primary abstract/metadata; unrecovered methods explicitly retained.
    evidence_scope
    literature_reviewed; source-specific curation
    experimental_model
    Seven healthy human volunteers
    exposure_scope
    Isolated fructose, intravenous
    limitations
    Injection bypasses the intestine. Magnitude cannot be assigned to a normal oral HFCS serving or to dietary phosphate deficiency.
    nutrient_topic
    HFCS chapter: actual formulation studies, component biochemistry and interventions are explicitly distinguished. · High-Fructose Corn Syrup / HFCS
    organism
    Seven healthy human volunteers
    plain_language
    The intravenous fructose bolus acutely lowered hepatic inorganic phosphate as sugar phosphates accumulated.
    primary_references
    Assessment of human liver metabolism by phosphorus-31 magnetic resonance spectroscopy. (1986). https://pubmed.ncbi.nlm.nih.gov/3730768/ DOI: 10.1259/0007-1285-59-703-695
    route
    Intravenous injection
    tissue
    Liver phosphorus-31 MRS

    High-Fructose Corn Syrup: mechanism of action and metabolic impact (2026-09-20) · lines 245–255

    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 · Seven healthy human volunteers · source_derived_draft · unverified_draft

    ## hfcs-iv-phosphate The intravenous fructose bolus acutely lowered hepatic inorganic phosphate as sugar phosphates accumulated. Model/species: Seven healthy human volunteers Tissue: Liver phosphorus-31 MRS Exposure: Fructose 250 mg/kg bolus Route: Intravenous injection Duration: Early 5 min changes; sugar-phosphate recovery within about 20 min Exposure scope: Isolated fructose, intravenous Limits: Injection bypasses the intestine. Magnitude cannot be assigned to a normal oral HFCS serving or to dietary phosphate deficiency. Reference: Assessment of human liver metabolism by phosphorus-31 magnetic resonance spectroscopy. (1986). https://pubmed.ncbi.nlm.nih.gov/3730768/ DOI: 10.1259/0007-1285-59-703-695 Access: Primary abstract/metadata; unrecovered methods explicitly retained.
    Complete structured claim and evidence

  2. PF-06835919 inhibited labeled fructose-1-phosphate formation in primary human hepatocytes.

    PF-06835919 → Fructose-1-phosphate formation in primary human hepatocytes source_derived_draftungraded
    Experimental context and source evidence
    dose
    PF-06835919 concentration series; 10 mM labeled fructose
    duration
    30 min pretreatment; 20 min fructose reaction
    evidence_access
    Primary full-text methods/results and metadata inspected.
    evidence_scope
    literature_reviewed; source-specific curation
    experimental_model
    Primary human hepatocytes
    exposure_scope
    Isolated fructose / investigational drug
    limitations
    Functional KHK inhibition in cells; PF-06835919 is investigational. Study sponsored/conducted by industry; pharmacological target engagement is not dietary efficacy.
    nutrient_topic
    HFCS chapter: actual formulation studies, component biochemistry and interventions are explicitly distinguished. · High-Fructose Corn Syrup / HFCS
    organism
    Primary human hepatocytes
    plain_language
    PF-06835919 inhibited labeled fructose-1-phosphate formation in primary human hepatocytes.
    primary_references
    Pharmacologic inhibition of ketohexokinase prevents fructose-induced metabolic dysfunction. (2021). https://pubmed.ncbi.nlm.nih.gov/33667726/ DOI: 10.1016/j.molmet.2021.101196
    route
    In vitro inhibitor pretreatment and fructose addition
    tissue
    Labeled fructose-1-phosphate production

    High-Fructose Corn Syrup: mechanism of action and metabolic impact (2026-09-20) · lines 569–579

    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 · Primary human hepatocytes · source_derived_draft · unverified_draft

    ## hfcs-pf-hepatocytes PF-06835919 inhibited labeled fructose-1-phosphate formation in primary human hepatocytes. Model/species: Primary human hepatocytes Tissue: Labeled fructose-1-phosphate production Exposure: PF-06835919 concentration series; 10 mM labeled fructose Route: In vitro inhibitor pretreatment and fructose addition Duration: 30 min pretreatment; 20 min fructose reaction Exposure scope: Isolated fructose / investigational drug Limits: Functional KHK inhibition in cells; PF-06835919 is investigational. Study sponsored/conducted by industry; pharmacological target engagement is not dietary efficacy. Reference: Pharmacologic inhibition of ketohexokinase prevents fructose-induced metabolic dysfunction. (2021). https://pubmed.ncbi.nlm.nih.gov/33667726/ DOI: 10.1016/j.molmet.2021.101196 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