Component

Human hepatic lipid content measured by imaging

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. The HFCS group showed a 0.4 +/- 0.2 percentage-point increase in hepatic lipid from baseline; its direct contrast with aspartame was not significant.

    HFCS-55 → Human hepatic lipid content measured by imaging source_derived_draftungraded
    Experimental context and source evidence
    dose
    HFCS-55 or sucrose at 25% energy requirement versus aspartame; HFCS n=28, sucrose n=24, control n=23
    duration
    16 days of beverages, approximately 2 weeks
    evidence_access
    Primary full-text methods/results and metadata inspected.
    evidence_scope
    literature_reviewed; source-specific curation
    experimental_model
    75 adults in nonrandomized double-blinded matched beverage groups
    exposure_scope
    Direct HFCS-55 comparison
    limitations
    No random assignment; 66 paired MRI scans, including 23 HFCS. Liver-fat HFCS significance was versus baseline, not established versus aspartame. No detected HFCS-sucrose difference is not universal equivalence. HFCS/control lipid data overlap PMID 25904601.
    nutrient_topic
    HFCS chapter: actual formulation studies, component biochemistry and interventions are explicitly distinguished. · High-Fructose Corn Syrup / HFCS
    organism
    75 adults in nonrandomized double-blinded matched beverage groups
    plain_language
    The HFCS group showed a 0.4 +/- 0.2 percentage-point increase in hepatic lipid from baseline; its direct contrast with aspartame was not significant.
    primary_references
    Consuming Sucrose- or HFCS-sweetened Beverages Increases Hepatic Lipid and Decreases Insulin Sensitivity in Adults. (2021). https://pubmed.ncbi.nlm.nih.gov/34265055/ DOI: 10.1210/clinem/dgab508
    route
    Oral 3 servings/day; usual diet outpatient, isocaloric substitutions during inpatient testing
    tissue
    MRI liver fat, oral-glucose-derived sensitivity, plasma markers

    High-Fructose Corn Syrup: mechanism of action and metabolic impact (2026-09-20) · lines 317–327

    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 · 75 adults in nonrandomized double-blinded matched beverage groups · source_derived_draft · unverified_draft

    ## hfcs-liver-fat The HFCS group showed a 0.4 +/- 0.2 percentage-point increase in hepatic lipid from baseline; its direct contrast with aspartame was not significant. Model/species: 75 adults in nonrandomized double-blinded matched beverage groups Tissue: MRI liver fat, oral-glucose-derived sensitivity, plasma markers Exposure: HFCS-55 or sucrose at 25% energy requirement versus aspartame; HFCS n=28, sucrose n=24, control n=23 Route: Oral 3 servings/day; usual diet outpatient, isocaloric substitutions during inpatient testing Duration: 16 days of beverages, approximately 2 weeks Exposure scope: Direct HFCS-55 comparison Limits: No random assignment; 66 paired MRI scans, including 23 HFCS. Liver-fat HFCS significance was versus baseline, not established versus aspartame. No detected HFCS-sucrose difference is not universal equivalence. HFCS/control lipid data overlap PMID 25904601. Reference: Consuming Sucrose- or HFCS-sweetened Beverages Increases Hepatic Lipid and Decreases Insulin Sensitivity in Adults. (2021). https://pubmed.ncbi.nlm.nih.gov/34265055/ DOI: 10.1210/clinem/dgab508 Access: Primary full-text methods/results and metadata inspected.
    Complete structured claim and evidence

  2. PF-06835919 at 300 mg/day reduced liver fat relative to placebo by a reported 18.73% after six weeks.

    PF-06835919 → Human hepatic lipid content measured by imaging source_derived_draftungraded
    Experimental context and source evidence
    dose
    PF-06835919 75 or 300 mg once daily versus placebo
    duration
    6 weeks
    evidence_access
    Primary abstract/metadata; unrecovered methods explicitly retained.
    evidence_scope
    literature_reviewed; source-specific curation
    experimental_model
    53 randomized adults with NAFLD; 48 completed phase 2a trial
    exposure_scope
    Fructose-pathway intervention, not an HFCS challenge
    limitations
    Small Pfizer-sponsored trial; 300 mg change was relative liver fat, not 18.73 percentage points. Not evidence of an approved drug or proof that HFCS caused each participant's disease.
    nutrient_topic
    HFCS chapter: actual formulation studies, component biochemistry and interventions are explicitly distinguished. · High-Fructose Corn Syrup / HFCS
    organism
    53 randomized adults with NAFLD; 48 completed phase 2a trial
    plain_language
    PF-06835919 at 300 mg/day reduced liver fat relative to placebo by a reported 18.73% after six weeks.
    primary_references
    Inhibition of ketohexokinase in adults with NAFLD reduces liver fat and inflammatory markers: A randomized phase 2 trial. (2021). https://pubmed.ncbi.nlm.nih.gov/35590219/ DOI: 10.1016/j.medj.2021.04.007
    route
    Oral drug; no controlled HFCS exposure
    tissue
    MRI proton-density liver fat

    High-Fructose Corn Syrup: mechanism of action and metabolic impact (2026-09-20) · lines 593–603

    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 · 53 randomized adults with NAFLD; 48 completed phase 2a trial · source_derived_draft · unverified_draft

    ## hfcs-pf-human-liver PF-06835919 at 300 mg/day reduced liver fat relative to placebo by a reported 18.73% after six weeks. Model/species: 53 randomized adults with NAFLD; 48 completed phase 2a trial Tissue: MRI proton-density liver fat Exposure: PF-06835919 75 or 300 mg once daily versus placebo Route: Oral drug; no controlled HFCS exposure Duration: 6 weeks Exposure scope: Fructose-pathway intervention, not an HFCS challenge Limits: Small Pfizer-sponsored trial; 300 mg change was relative liver fat, not 18.73 percentage points. Not evidence of an approved drug or proof that HFCS caused each participant's disease. Reference: Inhibition of ketohexokinase in adults with NAFLD reduces liver fat and inflammatory markers: A randomized phase 2 trial. (2021). https://pubmed.ncbi.nlm.nih.gov/35590219/ DOI: 10.1016/j.medj.2021.04.007 Access: Primary abstract/metadata; unrecovered methods explicitly retained.
    Complete structured claim and evidence

  3. The 75 mg/day PF-06835919 arm did not show a significant liver-fat reduction versus placebo.

    PF-06835919 → Human hepatic lipid content measured by imaging source_derived_draftungraded
    Experimental context and source evidence
    dose
    PF-06835919 75 or 300 mg once daily versus placebo
    duration
    6 weeks
    evidence_access
    Primary abstract/metadata; unrecovered methods explicitly retained.
    evidence_scope
    literature_reviewed; source-specific curation
    experimental_model
    53 randomized adults with NAFLD; 48 completed phase 2a trial
    exposure_scope
    Fructose-pathway intervention, not an HFCS challenge
    limitations
    Small Pfizer-sponsored trial; 300 mg change was relative liver fat, not 18.73 percentage points. Not evidence of an approved drug or proof that HFCS caused each participant's disease.
    nutrient_topic
    HFCS chapter: actual formulation studies, component biochemistry and interventions are explicitly distinguished. · High-Fructose Corn Syrup / HFCS
    organism
    53 randomized adults with NAFLD; 48 completed phase 2a trial
    plain_language
    The 75 mg/day PF-06835919 arm did not show a significant liver-fat reduction versus placebo.
    primary_references
    Inhibition of ketohexokinase in adults with NAFLD reduces liver fat and inflammatory markers: A randomized phase 2 trial. (2021). https://pubmed.ncbi.nlm.nih.gov/35590219/ DOI: 10.1016/j.medj.2021.04.007
    route
    Oral drug; no controlled HFCS exposure
    tissue
    MRI proton-density liver fat

    High-Fructose Corn Syrup: mechanism of action and metabolic impact (2026-09-20) · lines 605–615

    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 · 53 randomized adults with NAFLD; 48 completed phase 2a trial · source_derived_draft · unverified_draft

    ## hfcs-pf-low-dose-null The 75 mg/day PF-06835919 arm did not show a significant liver-fat reduction versus placebo. Model/species: 53 randomized adults with NAFLD; 48 completed phase 2a trial Tissue: MRI proton-density liver fat Exposure: PF-06835919 75 or 300 mg once daily versus placebo Route: Oral drug; no controlled HFCS exposure Duration: 6 weeks Exposure scope: Fructose-pathway intervention, not an HFCS challenge Limits: Small Pfizer-sponsored trial; 300 mg change was relative liver fat, not 18.73 percentage points. Not evidence of an approved drug or proof that HFCS caused each participant's disease. Reference: Inhibition of ketohexokinase in adults with NAFLD reduces liver fat and inflammatory markers: A randomized phase 2 trial. (2021). https://pubmed.ncbi.nlm.nih.gov/35590219/ DOI: 10.1016/j.medj.2021.04.007 Access: Primary abstract/metadata; unrecovered methods explicitly retained.
    Complete structured claim and evidence

  4. Sucrose beverages increased hepatic lipid by 0.6 +/- 0.2 percentage points from baseline, with a significant contrast against aspartame.

    Sucrose → Human hepatic lipid content measured by imaging source_derived_draftungraded
    Experimental context and source evidence
    dose
    Sucrose or HFCS beverages at 25% of energy requirement versus aspartame, 3 servings/day
    duration
    16 days, approximately two weeks
    evidence_access
    Primary full-text methods/results and metadata inspected.
    evidence_scope
    literature_reviewed; source-specific curation
    experimental_model
    75 adults in nonrandomized double-blind matched groups; sucrose n=24, HFCS n=28, aspartame n=23
    exposure_scope
    Direct sucrose beverage comparison
    limitations
    Nonrandomized; paired MRI n=23 sucrose, 23 HFCS, 20 control. Outpatient calories not clamped; weight adjustment does not establish calorie independence. HFCS/control participants and some plasma outcomes overlap PMID 25904601. Short biomarkers are not clinical disease incidence.
    nutrient_topic
    Sucrose chapter; direct sucrose observations are distinguished from shared component metabolism. · Sucrose
    organism
    75 adults in nonrandomized double-blind matched groups; sucrose n=24, HFCS n=28, aspartame n=23
    plain_language
    Sucrose beverages increased hepatic lipid by 0.6 +/- 0.2 percentage points from baseline, with a significant contrast against aspartame.
    primary_references
    Consuming Sucrose- or HFCS-sweetened Beverages Increases Hepatic Lipid and Decreases Insulin Sensitivity in Adults. (2021). https://pubmed.ncbi.nlm.nih.gov/34265055/ DOI: 10.1210/clinem/dgab508
    route
    Oral beverages; outpatient usual diet, controlled inpatient meal substitutions
    tissue
    MRI liver fat, OGTT-derived insulin sensitivity and plasma markers

    Sucrose: mechanism of action and metabolic impact (2026-09-20) · lines 331–341

    Original AI-assisted source-specific sucrose curation with shared canonical claims retained by identity. Primary-study citations, negative findings, exposure details and limitations preserved. Not publisher full text. · supports · 75 adults in nonrandomized double-blind matched groups; sucrose n=24, HFCS n=28, aspartame n=23 · source_derived_draft · unverified_draft

    ## sucrose-liver-fat Sucrose beverages increased hepatic lipid by 0.6 +/- 0.2 percentage points from baseline, with a significant contrast against aspartame. Model/species: 75 adults in nonrandomized double-blind matched groups; sucrose n=24, HFCS n=28, aspartame n=23 Tissue: MRI liver fat, OGTT-derived insulin sensitivity and plasma markers Exposure: Sucrose or HFCS beverages at 25% of energy requirement versus aspartame, 3 servings/day Route: Oral beverages; outpatient usual diet, controlled inpatient meal substitutions Duration: 16 days, approximately two weeks Exposure scope: Direct sucrose beverage comparison Limits: Nonrandomized; paired MRI n=23 sucrose, 23 HFCS, 20 control. Outpatient calories not clamped; weight adjustment does not establish calorie independence. HFCS/control participants and some plasma outcomes overlap PMID 25904601. Short biomarkers are not clinical disease incidence. Reference: Consuming Sucrose- or HFCS-sweetened Beverages Increases Hepatic Lipid and Decreases Insulin Sensitivity in Adults. (2021). https://pubmed.ncbi.nlm.nih.gov/34265055/ DOI: 10.1210/clinem/dgab508 Access: Primary full-text methods/results and metadata inspected.
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. No measured metabolic outcome differed significantly between the HFCS and sucrose beverage groups.

    HFCS-55 → Human endocrine responses to HFCS versus sucrose source_derived_draftungraded
    Experimental context and source evidence
    dose
    HFCS-55 or sucrose at 25% energy requirement versus aspartame; HFCS n=28, sucrose n=24, control n=23
    duration
    16 days of beverages, approximately 2 weeks
    evidence_access
    Primary full-text methods/results and metadata inspected.
    evidence_scope
    literature_reviewed; source-specific curation
    experimental_model
    75 adults in nonrandomized double-blinded matched beverage groups
    exposure_scope
    Direct HFCS-55 comparison
    limitations
    No random assignment; 66 paired MRI scans, including 23 HFCS. Liver-fat HFCS significance was versus baseline, not established versus aspartame. No detected HFCS-sucrose difference is not universal equivalence. HFCS/control lipid data overlap PMID 25904601.
    nutrient_topic
    HFCS chapter: actual formulation studies, component biochemistry and interventions are explicitly distinguished. · High-Fructose Corn Syrup / HFCS
    organism
    75 adults in nonrandomized double-blinded matched beverage groups
    plain_language
    No measured metabolic outcome differed significantly between the HFCS and sucrose beverage groups.
    primary_references
    Consuming Sucrose- or HFCS-sweetened Beverages Increases Hepatic Lipid and Decreases Insulin Sensitivity in Adults. (2021). https://pubmed.ncbi.nlm.nih.gov/34265055/ DOI: 10.1210/clinem/dgab508
    route
    Oral 3 servings/day; usual diet outpatient, isocaloric substitutions during inpatient testing
    tissue
    MRI liver fat, oral-glucose-derived sensitivity, plasma markers

    High-Fructose Corn Syrup: mechanism of action and metabolic impact (2026-09-20) · lines 341–351

    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 · 75 adults in nonrandomized double-blinded matched beverage groups · source_derived_draft · unverified_draft

    ## hfcs-sucrose-comparison No measured metabolic outcome differed significantly between the HFCS and sucrose beverage groups. Model/species: 75 adults in nonrandomized double-blinded matched beverage groups Tissue: MRI liver fat, oral-glucose-derived sensitivity, plasma markers Exposure: HFCS-55 or sucrose at 25% energy requirement versus aspartame; HFCS n=28, sucrose n=24, control n=23 Route: Oral 3 servings/day; usual diet outpatient, isocaloric substitutions during inpatient testing Duration: 16 days of beverages, approximately 2 weeks Exposure scope: Direct HFCS-55 comparison Limits: No random assignment; 66 paired MRI scans, including 23 HFCS. Liver-fat HFCS significance was versus baseline, not established versus aspartame. No detected HFCS-sucrose difference is not universal equivalence. HFCS/control lipid data overlap PMID 25904601. Reference: Consuming Sucrose- or HFCS-sweetened Beverages Increases Hepatic Lipid and Decreases Insulin Sensitivity in Adults. (2021). https://pubmed.ncbi.nlm.nih.gov/34265055/ DOI: 10.1210/clinem/dgab508 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