Nutrient chapter

Sucrose

Context-specific entity; species, compartment and exposure are stated on each claim.

53 recorded mechanisms · 3 availability situations · 5 preserved sources. Draft and verified records are labeled separately.

Read recorded mechanisms Open recursive mind map

The mechanisms

What the sources say this nutrient does, one relationship at a time. Plain wording comes first; the technical statement follows.

Human sucrase-isomaltase hydrolyzes sucrose, releasing its glucose moiety.
Human sucrase-isomaltase / SI → D-glucose source_derived_draftungraded
Experimental context and source evidence
dose
75 mM sucrose for expressed-SI activity; 0.7 mM added glucose in brush-border kinetic experiments
duration
1 hour at 37 C for expressed-enzyme activity; kinetic series for product inhibition
evidence_access
Selected primary full-text sections inspected via indexed PMC page; local XML has abstract only.
evidence_scope
literature_reviewed; source-specific curation
experimental_model
Human SI expressed in COS-1 cells; isolated human intestinal brush border
exposure_scope
Human enzyme mechanism
limitations
Glucose feedback was measured in an enzyme preparation, not demonstrated as a whole-body blood-glucose control mechanism. Selected full-text methods/results inspected; archived PubMed/PMC XML contains abstract only.
nutrient_topic
Sucrose chapter; direct sucrose observations are distinguished from shared component metabolism. · Sucrose
organism
Human SI expressed in COS-1 cells; isolated human intestinal brush border
plain_language
Human sucrase-isomaltase hydrolyzes sucrose, releasing its glucose moiety.
primary_references
Structure-function analysis of human sucrase-isomaltase identifies key residues required for catalytic activity. (2017). https://pubmed.ncbi.nlm.nih.gov/28522605/ DOI: 10.1074/jbc.M117.791939
route
In vitro enzyme/substrate incubation
tissue
Brush-border carbohydrate digestion
Sucrose: mechanism of action and metabolic impact (2026-09-20) · lines 19–29
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 · Human SI expressed in COS-1 cells; isolated human intestinal brush border · source_derived_draft · unverified_draft
## sucrose-hydrolysis-glucose Human sucrase-isomaltase hydrolyzes sucrose, releasing its glucose moiety. Model/species: Human SI expressed in COS-1 cells; isolated human intestinal brush border Tissue: Brush-border carbohydrate digestion Exposure: 75 mM sucrose for expressed-SI activity; 0.7 mM added glucose in brush-border kinetic experiments Route: In vitro enzyme/substrate incubation Duration: 1 hour at 37 C for expressed-enzyme activity; kinetic series for product inhibition Exposure scope: Human enzyme mechanism Limits: Glucose feedback was measured in an enzyme preparation, not demonstrated as a whole-body blood-glucose control mechanism. Selected full-text methods/results inspected; archived PubMed/PMC XML contains abstract only. Reference: Structure-function analysis of human sucrase-isomaltase identifies key residues required for catalytic activity. (2017). https://pubmed.ncbi.nlm.nih.gov/28522605/ DOI: 10.1074/jbc.M117.791939 Access: Selected primary full-text sections inspected via indexed PMC page; local XML has abstract only.
Complete structured claim and evidence
Cleavage of sucrose by human sucrase-isomaltase also releases fructose.
Human sucrase-isomaltase / SI → Fructose source_derived_draftungraded
Experimental context and source evidence
dose
75 mM sucrose for expressed-SI activity; 0.7 mM added glucose in brush-border kinetic experiments
duration
1 hour at 37 C for expressed-enzyme activity; kinetic series for product inhibition
evidence_access
Selected primary full-text sections inspected via indexed PMC page; local XML has abstract only.
evidence_scope
literature_reviewed; source-specific curation
experimental_model
Human SI expressed in COS-1 cells; isolated human intestinal brush border
exposure_scope
Human enzyme mechanism
limitations
Glucose feedback was measured in an enzyme preparation, not demonstrated as a whole-body blood-glucose control mechanism. Selected full-text methods/results inspected; archived PubMed/PMC XML contains abstract only.
nutrient_topic
Sucrose chapter; direct sucrose observations are distinguished from shared component metabolism. · Sucrose
organism
Human SI expressed in COS-1 cells; isolated human intestinal brush border
plain_language
Cleavage of sucrose by human sucrase-isomaltase also releases fructose.
primary_references
Structure-function analysis of human sucrase-isomaltase identifies key residues required for catalytic activity. (2017). https://pubmed.ncbi.nlm.nih.gov/28522605/ DOI: 10.1074/jbc.M117.791939
route
In vitro enzyme/substrate incubation
tissue
Brush-border carbohydrate digestion
Sucrose: mechanism of action and metabolic impact (2026-09-20) · lines 31–41
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 · Human SI expressed in COS-1 cells; isolated human intestinal brush border · source_derived_draft · unverified_draft
## sucrose-hydrolysis-fructose Cleavage of sucrose by human sucrase-isomaltase also releases fructose. Model/species: Human SI expressed in COS-1 cells; isolated human intestinal brush border Tissue: Brush-border carbohydrate digestion Exposure: 75 mM sucrose for expressed-SI activity; 0.7 mM added glucose in brush-border kinetic experiments Route: In vitro enzyme/substrate incubation Duration: 1 hour at 37 C for expressed-enzyme activity; kinetic series for product inhibition Exposure scope: Human enzyme mechanism Limits: Glucose feedback was measured in an enzyme preparation, not demonstrated as a whole-body blood-glucose control mechanism. Selected full-text methods/results inspected; archived PubMed/PMC XML contains abstract only. Reference: Structure-function analysis of human sucrase-isomaltase identifies key residues required for catalytic activity. (2017). https://pubmed.ncbi.nlm.nih.gov/28522605/ DOI: 10.1074/jbc.M117.791939 Access: Selected primary full-text sections inspected via indexed PMC page; local XML has abstract only.
Complete structured claim and evidence
Adding 0.7 mM glucose partially inhibited sucrose hydrolysis in the human intestinal brush-border enzyme preparation.
D-glucose → Human sucrase-isomaltase / SI source_derived_draftungraded
Experimental context and source evidence
dose
75 mM sucrose for expressed-SI activity; 0.7 mM added glucose in brush-border kinetic experiments
duration
1 hour at 37 C for expressed-enzyme activity; kinetic series for product inhibition
evidence_access
Selected primary full-text sections inspected via indexed PMC page; local XML has abstract only.
evidence_scope
literature_reviewed; source-specific curation
experimental_model
Human SI expressed in COS-1 cells; isolated human intestinal brush border
exposure_scope
Human enzyme mechanism
limitations
Glucose feedback was measured in an enzyme preparation, not demonstrated as a whole-body blood-glucose control mechanism. Selected full-text methods/results inspected; archived PubMed/PMC XML contains abstract only.
nutrient_topic
Sucrose chapter; direct sucrose observations are distinguished from shared component metabolism. · Sucrose
organism
Human SI expressed in COS-1 cells; isolated human intestinal brush border
plain_language
Adding 0.7 mM glucose partially inhibited sucrose hydrolysis in the human intestinal brush-border enzyme preparation.
primary_references
Structure-function analysis of human sucrase-isomaltase identifies key residues required for catalytic activity. (2017). https://pubmed.ncbi.nlm.nih.gov/28522605/ DOI: 10.1074/jbc.M117.791939
route
In vitro enzyme/substrate incubation
tissue
Brush-border carbohydrate digestion
Sucrose: mechanism of action and metabolic impact (2026-09-20) · lines 43–53
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 · Human SI expressed in COS-1 cells; isolated human intestinal brush border · source_derived_draft · unverified_draft
## sucrose-glucose-feedback Adding 0.7 mM glucose partially inhibited sucrose hydrolysis in the human intestinal brush-border enzyme preparation. Model/species: Human SI expressed in COS-1 cells; isolated human intestinal brush border Tissue: Brush-border carbohydrate digestion Exposure: 75 mM sucrose for expressed-SI activity; 0.7 mM added glucose in brush-border kinetic experiments Route: In vitro enzyme/substrate incubation Duration: 1 hour at 37 C for expressed-enzyme activity; kinetic series for product inhibition Exposure scope: Human enzyme mechanism Limits: Glucose feedback was measured in an enzyme preparation, not demonstrated as a whole-body blood-glucose control mechanism. Selected full-text methods/results inspected; archived PubMed/PMC XML contains abstract only. Reference: Structure-function analysis of human sucrase-isomaltase identifies key residues required for catalytic activity. (2017). https://pubmed.ncbi.nlm.nih.gov/28522605/ DOI: 10.1074/jbc.M117.791939 Access: Selected primary full-text sections inspected via indexed PMC page; local XML has abstract only.
Complete structured claim and evidence
Sucrose elicited a calcium response in cells coexpressing human TAS1R2 and TAS1R3, but not either subunit alone.
Sucrose → Human sweet taste receptor TAS1R2/TAS1R3 source_derived_draftungraded
Experimental context and source evidence
dose
300 mM sucrose with or without 1.25 mM lactisole
duration
Acute calcium response
evidence_access
Selected primary full-text sections inspected via indexed PMC page; local XML has abstract only.
evidence_scope
literature_reviewed; source-specific curation
experimental_model
Human TAS1R2/TAS1R3 coexpressed with engineered G-alpha15 in HEK-derived cells
exposure_scope
Human receptor in an expression system
limitations
Engineered coupling and high assay concentration do not measure human dietary absorption. Rat lactisole sensitivity differs. Selected full-text sections inspected; archived XML is abstract only.
nutrient_topic
Sucrose chapter; direct sucrose observations are distinguished from shared component metabolism. · Sucrose
organism
Human TAS1R2/TAS1R3 coexpressed with engineered G-alpha15 in HEK-derived cells
plain_language
Sucrose elicited a calcium response in cells coexpressing human TAS1R2 and TAS1R3, but not either subunit alone.
primary_references
Human receptors for sweet and umami taste. (2002). https://pubmed.ncbi.nlm.nih.gov/11917125/ DOI: 10.1073/pnas.072090199
route
In vitro receptor stimulation
tissue
Recombinant sweet-receptor calcium-response assay
Sucrose: mechanism of action and metabolic impact (2026-09-20) · lines 55–65
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 · Human TAS1R2/TAS1R3 coexpressed with engineered G-alpha15 in HEK-derived cells · source_derived_draft · unverified_draft
## sucrose-sweet-receptor Sucrose elicited a calcium response in cells coexpressing human TAS1R2 and TAS1R3, but not either subunit alone. Model/species: Human TAS1R2/TAS1R3 coexpressed with engineered G-alpha15 in HEK-derived cells Tissue: Recombinant sweet-receptor calcium-response assay Exposure: 300 mM sucrose with or without 1.25 mM lactisole Route: In vitro receptor stimulation Duration: Acute calcium response Exposure scope: Human receptor in an expression system Limits: Engineered coupling and high assay concentration do not measure human dietary absorption. Rat lactisole sensitivity differs. Selected full-text sections inspected; archived XML is abstract only. Reference: Human receptors for sweet and umami taste. (2002). https://pubmed.ncbi.nlm.nih.gov/11917125/ DOI: 10.1073/pnas.072090199 Access: Selected primary full-text sections inspected via indexed PMC page; local XML has abstract only.
Complete structured claim and evidence
Lactisole inhibited the sucrose-evoked response of expressed human TAS1R2/TAS1R3.
Lactisole → Human sweet taste receptor TAS1R2/TAS1R3 source_derived_draftungraded
Experimental context and source evidence
dose
300 mM sucrose with or without 1.25 mM lactisole
duration
Acute calcium response
evidence_access
Selected primary full-text sections inspected via indexed PMC page; local XML has abstract only.
evidence_scope
literature_reviewed; source-specific curation
experimental_model
Human TAS1R2/TAS1R3 coexpressed with engineered G-alpha15 in HEK-derived cells
exposure_scope
Human receptor in an expression system
limitations
Engineered coupling and high assay concentration do not measure human dietary absorption. Rat lactisole sensitivity differs. Selected full-text sections inspected; archived XML is abstract only.
nutrient_topic
Sucrose chapter; direct sucrose observations are distinguished from shared component metabolism. · Sucrose
organism
Human TAS1R2/TAS1R3 coexpressed with engineered G-alpha15 in HEK-derived cells
plain_language
Lactisole inhibited the sucrose-evoked response of expressed human TAS1R2/TAS1R3.
primary_references
Human receptors for sweet and umami taste. (2002). https://pubmed.ncbi.nlm.nih.gov/11917125/ DOI: 10.1073/pnas.072090199
route
In vitro receptor stimulation
tissue
Recombinant sweet-receptor calcium-response assay
Sucrose: mechanism of action and metabolic impact (2026-09-20) · lines 67–77
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 · Human TAS1R2/TAS1R3 coexpressed with engineered G-alpha15 in HEK-derived cells · source_derived_draft · unverified_draft
## sucrose-lactisole-receptor Lactisole inhibited the sucrose-evoked response of expressed human TAS1R2/TAS1R3. Model/species: Human TAS1R2/TAS1R3 coexpressed with engineered G-alpha15 in HEK-derived cells Tissue: Recombinant sweet-receptor calcium-response assay Exposure: 300 mM sucrose with or without 1.25 mM lactisole Route: In vitro receptor stimulation Duration: Acute calcium response Exposure scope: Human receptor in an expression system Limits: Engineered coupling and high assay concentration do not measure human dietary absorption. Rat lactisole sensitivity differs. Selected full-text sections inspected; archived XML is abstract only. Reference: Human receptors for sweet and umami taste. (2002). https://pubmed.ncbi.nlm.nih.gov/11917125/ DOI: 10.1073/pnas.072090199 Access: Selected primary full-text sections inspected via indexed PMC page; local XML has abstract only.
Complete structured claim and evidence
Coapplied MSG attenuated the sucrose-evoked calcium response in cells expressing human TAS1R2/TAS1R3.
Monosodium L-glutamate → Human sweet taste receptor TAS1R2/TAS1R3 source_derived_draftungraded
Experimental context and source evidence
dose
Sucrose concentration series up to 150 mM; MSG or Glu-Glu/Glu-Asp concentration series; mutant imaging used 100 mM sucrose with 1 mM Glu-Glu or 50 mM MSG
duration
120-second fluorescence acquisition; imaging at 30 seconds
evidence_access
Primary full-text methods/results and metadata inspected.
evidence_scope
literature_reviewed; source-specific curation
experimental_model
Human TAS1R2/TAS1R3 in Flp-In 293 cells
exposure_scope
Nutrient and peptide modulation of human sweet receptor
limitations
Cellular response, not a direct binding assay or a demonstration that every food tastes less sweet. pH/osmolarity controls and agonist-specific responses limit interpretation. Doses differ among panels.
nutrient_topic
Sucrose chapter; direct sucrose observations are distinguished from shared component metabolism. · Sucrose
organism
Human TAS1R2/TAS1R3 in Flp-In 293 cells
plain_language
Coapplied MSG attenuated the sucrose-evoked calcium response in cells expressing human TAS1R2/TAS1R3.
primary_references
Modulation of sweet taste by umami compounds via sweet taste receptor subunit hT1R2. (2015). https://pubmed.ncbi.nlm.nih.gov/25853419/ DOI: 10.1371/journal.pone.0124030
route
In vitro coapplication
tissue
Sweet-receptor calcium signaling
Sucrose: mechanism of action and metabolic impact (2026-09-20) · lines 79–89
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 · Human TAS1R2/TAS1R3 in Flp-In 293 cells · source_derived_draft · unverified_draft
## sucrose-msg-receptor Coapplied MSG attenuated the sucrose-evoked calcium response in cells expressing human TAS1R2/TAS1R3. Model/species: Human TAS1R2/TAS1R3 in Flp-In 293 cells Tissue: Sweet-receptor calcium signaling Exposure: Sucrose concentration series up to 150 mM; MSG or Glu-Glu/Glu-Asp concentration series; mutant imaging used 100 mM sucrose with 1 mM Glu-Glu or 50 mM MSG Route: In vitro coapplication Duration: 120-second fluorescence acquisition; imaging at 30 seconds Exposure scope: Nutrient and peptide modulation of human sweet receptor Limits: Cellular response, not a direct binding assay or a demonstration that every food tastes less sweet. pH/osmolarity controls and agonist-specific responses limit interpretation. Doses differ among panels. Reference: Modulation of sweet taste by umami compounds via sweet taste receptor subunit hT1R2. (2015). https://pubmed.ncbi.nlm.nih.gov/25853419/ DOI: 10.1371/journal.pone.0124030 Access: Primary full-text methods/results and metadata inspected.
Complete structured claim and evidence
Coapplied Glu-Glu attenuated the sucrose-evoked calcium response in cells expressing human TAS1R2/TAS1R3.
L-Glutamyl-L-glutamate / Glu-Glu → Human sweet taste receptor TAS1R2/TAS1R3 source_derived_draftungraded
Experimental context and source evidence
dose
Sucrose concentration series up to 150 mM; MSG or Glu-Glu/Glu-Asp concentration series; mutant imaging used 100 mM sucrose with 1 mM Glu-Glu or 50 mM MSG
duration
120-second fluorescence acquisition; imaging at 30 seconds
evidence_access
Primary full-text methods/results and metadata inspected.
evidence_scope
literature_reviewed; source-specific curation
experimental_model
Human TAS1R2/TAS1R3 in Flp-In 293 cells
exposure_scope
Nutrient and peptide modulation of human sweet receptor
limitations
Cellular response, not a direct binding assay or a demonstration that every food tastes less sweet. pH/osmolarity controls and agonist-specific responses limit interpretation. Doses differ among panels.
nutrient_topic
Sucrose chapter; direct sucrose observations are distinguished from shared component metabolism. · Sucrose
organism
Human TAS1R2/TAS1R3 in Flp-In 293 cells
plain_language
Coapplied Glu-Glu attenuated the sucrose-evoked calcium response in cells expressing human TAS1R2/TAS1R3.
primary_references
Modulation of sweet taste by umami compounds via sweet taste receptor subunit hT1R2. (2015). https://pubmed.ncbi.nlm.nih.gov/25853419/ DOI: 10.1371/journal.pone.0124030
route
In vitro coapplication
tissue
Sweet-receptor calcium signaling
Sucrose: mechanism of action and metabolic impact (2026-09-20) · lines 91–101
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 · Human TAS1R2/TAS1R3 in Flp-In 293 cells · source_derived_draft · unverified_draft
## sucrose-gluglu-receptor Coapplied Glu-Glu attenuated the sucrose-evoked calcium response in cells expressing human TAS1R2/TAS1R3. Model/species: Human TAS1R2/TAS1R3 in Flp-In 293 cells Tissue: Sweet-receptor calcium signaling Exposure: Sucrose concentration series up to 150 mM; MSG or Glu-Glu/Glu-Asp concentration series; mutant imaging used 100 mM sucrose with 1 mM Glu-Glu or 50 mM MSG Route: In vitro coapplication Duration: 120-second fluorescence acquisition; imaging at 30 seconds Exposure scope: Nutrient and peptide modulation of human sweet receptor Limits: Cellular response, not a direct binding assay or a demonstration that every food tastes less sweet. pH/osmolarity controls and agonist-specific responses limit interpretation. Doses differ among panels. Reference: Modulation of sweet taste by umami compounds via sweet taste receptor subunit hT1R2. (2015). https://pubmed.ncbi.nlm.nih.gov/25853419/ DOI: 10.1371/journal.pone.0124030 Access: Primary full-text methods/results and metadata inspected.
Complete structured claim and evidence
Coapplied Glu-Asp attenuated the sucrose-evoked calcium response in cells expressing human TAS1R2/TAS1R3.
L-Glutamyl-L-aspartate / Glu-Asp → Human sweet taste receptor TAS1R2/TAS1R3 source_derived_draftungraded
Experimental context and source evidence
dose
Sucrose concentration series up to 150 mM; MSG or Glu-Glu/Glu-Asp concentration series; mutant imaging used 100 mM sucrose with 1 mM Glu-Glu or 50 mM MSG
duration
120-second fluorescence acquisition; imaging at 30 seconds
evidence_access
Primary full-text methods/results and metadata inspected.
evidence_scope
literature_reviewed; source-specific curation
experimental_model
Human TAS1R2/TAS1R3 in Flp-In 293 cells
exposure_scope
Nutrient and peptide modulation of human sweet receptor
limitations
Cellular response, not a direct binding assay or a demonstration that every food tastes less sweet. pH/osmolarity controls and agonist-specific responses limit interpretation. Doses differ among panels.
nutrient_topic
Sucrose chapter; direct sucrose observations are distinguished from shared component metabolism. · Sucrose
organism
Human TAS1R2/TAS1R3 in Flp-In 293 cells
plain_language
Coapplied Glu-Asp attenuated the sucrose-evoked calcium response in cells expressing human TAS1R2/TAS1R3.
primary_references
Modulation of sweet taste by umami compounds via sweet taste receptor subunit hT1R2. (2015). https://pubmed.ncbi.nlm.nih.gov/25853419/ DOI: 10.1371/journal.pone.0124030
route
In vitro coapplication
tissue
Sweet-receptor calcium signaling
Sucrose: mechanism of action and metabolic impact (2026-09-20) · lines 103–113
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 · Human TAS1R2/TAS1R3 in Flp-In 293 cells · source_derived_draft · unverified_draft
## sucrose-gluasp-receptor Coapplied Glu-Asp attenuated the sucrose-evoked calcium response in cells expressing human TAS1R2/TAS1R3. Model/species: Human TAS1R2/TAS1R3 in Flp-In 293 cells Tissue: Sweet-receptor calcium signaling Exposure: Sucrose concentration series up to 150 mM; MSG or Glu-Glu/Glu-Asp concentration series; mutant imaging used 100 mM sucrose with 1 mM Glu-Glu or 50 mM MSG Route: In vitro coapplication Duration: 120-second fluorescence acquisition; imaging at 30 seconds Exposure scope: Nutrient and peptide modulation of human sweet receptor Limits: Cellular response, not a direct binding assay or a demonstration that every food tastes less sweet. pH/osmolarity controls and agonist-specific responses limit interpretation. Doses differ among panels. Reference: Modulation of sweet taste by umami compounds via sweet taste receptor subunit hT1R2. (2015). https://pubmed.ncbi.nlm.nih.gov/25853419/ DOI: 10.1371/journal.pone.0124030 Access: Primary full-text methods/results and metadata inspected.
Complete structured claim and evidence
Adding 60 ppm lactisole to the sucrose drink increased subsequent breakfast energy intake by 12.9 +/- 5.8% in the male crossover study.
Lactisole → Human subsequent meal energy intake after sucrose with lactisole source_derived_draftungraded
Experimental context and source evidence
dose
300 mL of 10% w/v sucrose with or without 60 ppm lactisole; parallel glucose conditions
duration
120 minutes; breakfast at 2 hours
evidence_access
Primary full-text methods/results and metadata inspected.
evidence_scope
literature_reviewed; source-specific curation
experimental_model
27 healthy men in randomized single-blinded crossover
exposure_scope
Sucrose and taste antagonist
limitations
Acute experiment in men; peripheral serotonin is not brain serotonin. Receptor mediation and binding-affinity explanation were not directly established; no long-term weight outcome.
nutrient_topic
Sucrose chapter; direct sucrose observations are distinguished from shared component metabolism. · Sucrose
organism
27 healthy men in randomized single-blinded crossover
plain_language
Adding 60 ppm lactisole to the sucrose drink increased subsequent breakfast energy intake by 12.9 +/- 5.8% in the male crossover study.
primary_references
Sweet Taste Antagonist Lactisole Administered in Combination with Sucrose, But Not Glucose, Increases Energy Intake and Decreases Peripheral Serotonin in Male Subjects. (2020). https://pubmed.ncbi.nlm.nih.gov/33066498/ DOI: 10.3390/nu12103133
route
Oral test drink after overnight fast
tissue
Subsequent food intake and peripheral hormone measurements
Sucrose: mechanism of action and metabolic impact (2026-09-20) · lines 115–125
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 · 27 healthy men in randomized single-blinded crossover · source_derived_draft · unverified_draft
## sucrose-lactisole-intake Adding 60 ppm lactisole to the sucrose drink increased subsequent breakfast energy intake by 12.9 +/- 5.8% in the male crossover study. Model/species: 27 healthy men in randomized single-blinded crossover Tissue: Subsequent food intake and peripheral hormone measurements Exposure: 300 mL of 10% w/v sucrose with or without 60 ppm lactisole; parallel glucose conditions Route: Oral test drink after overnight fast Duration: 120 minutes; breakfast at 2 hours Exposure scope: Sucrose and taste antagonist Limits: Acute experiment in men; peripheral serotonin is not brain serotonin. Receptor mediation and binding-affinity explanation were not directly established; no long-term weight outcome. Reference: Sweet Taste Antagonist Lactisole Administered in Combination with Sucrose, But Not Glucose, Increases Energy Intake and Decreases Peripheral Serotonin in Male Subjects. (2020). https://pubmed.ncbi.nlm.nih.gov/33066498/ DOI: 10.3390/nu12103133 Access: Primary full-text methods/results and metadata inspected.
Complete structured claim and evidence
Adding lactisole to sucrose lowered the plasma serotonin change at 30 minutes relative to sucrose alone.
Lactisole → Human postprandial plasma serotonin response source_derived_draftungraded
Experimental context and source evidence
dose
300 mL of 10% w/v sucrose with or without 60 ppm lactisole; parallel glucose conditions
duration
120 minutes; breakfast at 2 hours
evidence_access
Primary full-text methods/results and metadata inspected.
evidence_scope
literature_reviewed; source-specific curation
experimental_model
27 healthy men in randomized single-blinded crossover
exposure_scope
Sucrose and taste antagonist
limitations
Acute experiment in men; peripheral serotonin is not brain serotonin. Receptor mediation and binding-affinity explanation were not directly established; no long-term weight outcome.
nutrient_topic
Sucrose chapter; direct sucrose observations are distinguished from shared component metabolism. · Sucrose
organism
27 healthy men in randomized single-blinded crossover
plain_language
Adding lactisole to sucrose lowered the plasma serotonin change at 30 minutes relative to sucrose alone.
primary_references
Sweet Taste Antagonist Lactisole Administered in Combination with Sucrose, But Not Glucose, Increases Energy Intake and Decreases Peripheral Serotonin in Male Subjects. (2020). https://pubmed.ncbi.nlm.nih.gov/33066498/ DOI: 10.3390/nu12103133
route
Oral test drink after overnight fast
tissue
Subsequent food intake and peripheral hormone measurements
Sucrose: mechanism of action and metabolic impact (2026-09-20) · lines 127–137
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 · 27 healthy men in randomized single-blinded crossover · source_derived_draft · unverified_draft
## sucrose-lactisole-serotonin Adding lactisole to sucrose lowered the plasma serotonin change at 30 minutes relative to sucrose alone. Model/species: 27 healthy men in randomized single-blinded crossover Tissue: Subsequent food intake and peripheral hormone measurements Exposure: 300 mL of 10% w/v sucrose with or without 60 ppm lactisole; parallel glucose conditions Route: Oral test drink after overnight fast Duration: 120 minutes; breakfast at 2 hours Exposure scope: Sucrose and taste antagonist Limits: Acute experiment in men; peripheral serotonin is not brain serotonin. Receptor mediation and binding-affinity explanation were not directly established; no long-term weight outcome. Reference: Sweet Taste Antagonist Lactisole Administered in Combination with Sucrose, But Not Glucose, Increases Energy Intake and Decreases Peripheral Serotonin in Male Subjects. (2020). https://pubmed.ncbi.nlm.nih.gov/33066498/ DOI: 10.3390/nu12103133 Access: Primary full-text methods/results and metadata inspected.
Complete structured claim and evidence
Adding lactisole to sucrose did not significantly change postprandial plasma CCK.
Lactisole → Human plasma cholecystokinin response source_derived_draftungraded
Experimental context and source evidence
dose
300 mL of 10% w/v sucrose with or without 60 ppm lactisole; parallel glucose conditions
duration
120 minutes; breakfast at 2 hours
evidence_access
Primary full-text methods/results and metadata inspected.
evidence_scope
literature_reviewed; source-specific curation
experimental_model
27 healthy men in randomized single-blinded crossover
exposure_scope
Sucrose and taste antagonist
limitations
Acute experiment in men; peripheral serotonin is not brain serotonin. Receptor mediation and binding-affinity explanation were not directly established; no long-term weight outcome.
nutrient_topic
Sucrose chapter; direct sucrose observations are distinguished from shared component metabolism. · Sucrose
organism
27 healthy men in randomized single-blinded crossover
plain_language
Adding lactisole to sucrose did not significantly change postprandial plasma CCK.
primary_references
Sweet Taste Antagonist Lactisole Administered in Combination with Sucrose, But Not Glucose, Increases Energy Intake and Decreases Peripheral Serotonin in Male Subjects. (2020). https://pubmed.ncbi.nlm.nih.gov/33066498/ DOI: 10.3390/nu12103133
route
Oral test drink after overnight fast
tissue
Subsequent food intake and peripheral hormone measurements
Sucrose: mechanism of action and metabolic impact (2026-09-20) · lines 139–149
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 · 27 healthy men in randomized single-blinded crossover · source_derived_draft · unverified_draft
## sucrose-lactisole-cck-null Adding lactisole to sucrose did not significantly change postprandial plasma CCK. Model/species: 27 healthy men in randomized single-blinded crossover Tissue: Subsequent food intake and peripheral hormone measurements Exposure: 300 mL of 10% w/v sucrose with or without 60 ppm lactisole; parallel glucose conditions Route: Oral test drink after overnight fast Duration: 120 minutes; breakfast at 2 hours Exposure scope: Sucrose and taste antagonist Limits: Acute experiment in men; peripheral serotonin is not brain serotonin. Receptor mediation and binding-affinity explanation were not directly established; no long-term weight outcome. Reference: Sweet Taste Antagonist Lactisole Administered in Combination with Sucrose, But Not Glucose, Increases Energy Intake and Decreases Peripheral Serotonin in Male Subjects. (2020). https://pubmed.ncbi.nlm.nih.gov/33066498/ DOI: 10.3390/nu12103133 Access: Primary full-text methods/results and metadata inspected.
Complete structured claim and evidence
Adding lactisole to sucrose did not significantly change postprandial plasma ghrelin.
Lactisole → Human postprandial plasma ghrelin response source_derived_draftungraded
Experimental context and source evidence
dose
300 mL of 10% w/v sucrose with or without 60 ppm lactisole; parallel glucose conditions
duration
120 minutes; breakfast at 2 hours
evidence_access
Primary full-text methods/results and metadata inspected.
evidence_scope
literature_reviewed; source-specific curation
experimental_model
27 healthy men in randomized single-blinded crossover
exposure_scope
Sucrose and taste antagonist
limitations
Acute experiment in men; peripheral serotonin is not brain serotonin. Receptor mediation and binding-affinity explanation were not directly established; no long-term weight outcome.
nutrient_topic
Sucrose chapter; direct sucrose observations are distinguished from shared component metabolism. · Sucrose
organism
27 healthy men in randomized single-blinded crossover
plain_language
Adding lactisole to sucrose did not significantly change postprandial plasma ghrelin.
primary_references
Sweet Taste Antagonist Lactisole Administered in Combination with Sucrose, But Not Glucose, Increases Energy Intake and Decreases Peripheral Serotonin in Male Subjects. (2020). https://pubmed.ncbi.nlm.nih.gov/33066498/ DOI: 10.3390/nu12103133
route
Oral test drink after overnight fast
tissue
Subsequent food intake and peripheral hormone measurements
Sucrose: mechanism of action and metabolic impact (2026-09-20) · lines 151–161
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 · 27 healthy men in randomized single-blinded crossover · source_derived_draft · unverified_draft
## sucrose-lactisole-ghrelin-null Adding lactisole to sucrose did not significantly change postprandial plasma ghrelin. Model/species: 27 healthy men in randomized single-blinded crossover Tissue: Subsequent food intake and peripheral hormone measurements Exposure: 300 mL of 10% w/v sucrose with or without 60 ppm lactisole; parallel glucose conditions Route: Oral test drink after overnight fast Duration: 120 minutes; breakfast at 2 hours Exposure scope: Sucrose and taste antagonist Limits: Acute experiment in men; peripheral serotonin is not brain serotonin. Receptor mediation and binding-affinity explanation were not directly established; no long-term weight outcome. Reference: Sweet Taste Antagonist Lactisole Administered in Combination with Sucrose, But Not Glucose, Increases Energy Intake and Decreases Peripheral Serotonin in Male Subjects. (2020). https://pubmed.ncbi.nlm.nih.gov/33066498/ DOI: 10.3390/nu12103133 Access: Primary full-text methods/results and metadata inspected.
Complete structured claim and evidence
Sacrosidase, with or without milk, reduced breath hydrogen after sucrose compared with placebo in children with CSID.
Sacrosidase → Human sucrose malabsorption assessed by breath hydrogen source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
dose
Yeast sucrase preparation, 6000 IU/mg protein; full strength and 1:10, 1:100, 1:1000 dilutions; >15 kg received 2 mL; lower-weight dose volume missing from accessed abstract
duration
Single-dose breath tests; four 10-day dose periods
evidence_access
Primary abstract/metadata; unrecovered methods explicitly retained.
evidence_scope
literature_reviewed; source-specific curation
experimental_model
28 children aged 5 months to 11 years with congenital sucrase-isomaltase deficiency; randomized double-blind trial
exposure_scope
Drug rescue of human genetic digestive impairment
limitations
Enzyme replacement in diagnosed CSID, not sucrose supplementation for a nutrient deficiency. Exact sucrose challenge amount and lower-weight volume unrecovered. Vomiting did not differ; wheezing occurred in one child with asthma. Not prescribing guidance.
nutrient_topic
Sucrose chapter; direct sucrose observations are distinguished from shared component metabolism. · Sucrose
organism
28 children aged 5 months to 11 years with congenital sucrase-isomaltase deficiency; randomized double-blind trial
plain_language
Sacrosidase, with or without milk, reduced breath hydrogen after sucrose compared with placebo in children with CSID.
primary_references
Sacrosidase therapy for congenital sucrase-isomaltase deficiency. (1999). https://pubmed.ncbi.nlm.nih.gov/9932843/ DOI: 10.1097/00005176-199902000-00008
route
Oral enzyme with sucrose challenge or normal carbohydrate-containing diet
tissue
Intestinal sucrose handling and stool/symptom outcomes
trigger_kind
machinery_impairment Imported condition classification; unverified.
Sucrose: mechanism of action and metabolic impact (2026-09-20) · lines 163–173
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 · 28 children aged 5 months to 11 years with congenital sucrase-isomaltase deficiency; randomized double-blind trial · source_derived_draft · unverified_draft
## sucrose-sacrosidase-hydrogen Sacrosidase, with or without milk, reduced breath hydrogen after sucrose compared with placebo in children with CSID. Model/species: 28 children aged 5 months to 11 years with congenital sucrase-isomaltase deficiency; randomized double-blind trial Tissue: Intestinal sucrose handling and stool/symptom outcomes Exposure: Yeast sucrase preparation, 6000 IU/mg protein; full strength and 1:10, 1:100, 1:1000 dilutions; >15 kg received 2 mL; lower-weight dose volume missing from accessed abstract Route: Oral enzyme with sucrose challenge or normal carbohydrate-containing diet Duration: Single-dose breath tests; four 10-day dose periods Exposure scope: Drug rescue of human genetic digestive impairment Limits: Enzyme replacement in diagnosed CSID, not sucrose supplementation for a nutrient deficiency. Exact sucrose challenge amount and lower-weight volume unrecovered. Vomiting did not differ; wheezing occurred in one child with asthma. Not prescribing guidance. Reference: Sacrosidase therapy for congenital sucrase-isomaltase deficiency. (1999). https://pubmed.ncbi.nlm.nih.gov/9932843/ DOI: 10.1097/00005176-199902000-00008 Access: Primary abstract/metadata; unrecovered methods explicitly retained.
Complete structured claim and evidence
Higher sacrosidase concentrations reduced stool frequency relative to lower concentrations during carbohydrate-containing diets in children with CSID.
Sacrosidase → Stool frequency in children with congenital sucrase-isomaltase deficiency source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
dose
Yeast sucrase preparation, 6000 IU/mg protein; full strength and 1:10, 1:100, 1:1000 dilutions; >15 kg received 2 mL; lower-weight dose volume missing from accessed abstract
duration
Single-dose breath tests; four 10-day dose periods
evidence_access
Primary abstract/metadata; unrecovered methods explicitly retained.
evidence_scope
literature_reviewed; source-specific curation
experimental_model
28 children aged 5 months to 11 years with congenital sucrase-isomaltase deficiency; randomized double-blind trial
exposure_scope
Drug rescue of human genetic digestive impairment
limitations
Enzyme replacement in diagnosed CSID, not sucrose supplementation for a nutrient deficiency. Exact sucrose challenge amount and lower-weight volume unrecovered. Vomiting did not differ; wheezing occurred in one child with asthma. Not prescribing guidance.
nutrient_topic
Sucrose chapter; direct sucrose observations are distinguished from shared component metabolism. · Sucrose
organism
28 children aged 5 months to 11 years with congenital sucrase-isomaltase deficiency; randomized double-blind trial
plain_language
Higher sacrosidase concentrations reduced stool frequency relative to lower concentrations during carbohydrate-containing diets in children with CSID.
primary_references
Sacrosidase therapy for congenital sucrase-isomaltase deficiency. (1999). https://pubmed.ncbi.nlm.nih.gov/9932843/ DOI: 10.1097/00005176-199902000-00008
route
Oral enzyme with sucrose challenge or normal carbohydrate-containing diet
tissue
Intestinal sucrose handling and stool/symptom outcomes
trigger_kind
machinery_impairment Imported condition classification; unverified.
Sucrose: mechanism of action and metabolic impact (2026-09-20) · lines 175–185
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 · 28 children aged 5 months to 11 years with congenital sucrase-isomaltase deficiency; randomized double-blind trial · source_derived_draft · unverified_draft
## sucrose-sacrosidase-stools Higher sacrosidase concentrations reduced stool frequency relative to lower concentrations during carbohydrate-containing diets in children with CSID. Model/species: 28 children aged 5 months to 11 years with congenital sucrase-isomaltase deficiency; randomized double-blind trial Tissue: Intestinal sucrose handling and stool/symptom outcomes Exposure: Yeast sucrase preparation, 6000 IU/mg protein; full strength and 1:10, 1:100, 1:1000 dilutions; >15 kg received 2 mL; lower-weight dose volume missing from accessed abstract Route: Oral enzyme with sucrose challenge or normal carbohydrate-containing diet Duration: Single-dose breath tests; four 10-day dose periods Exposure scope: Drug rescue of human genetic digestive impairment Limits: Enzyme replacement in diagnosed CSID, not sucrose supplementation for a nutrient deficiency. Exact sucrose challenge amount and lower-weight volume unrecovered. Vomiting did not differ; wheezing occurred in one child with asthma. Not prescribing guidance. Reference: Sacrosidase therapy for congenital sucrase-isomaltase deficiency. (1999). https://pubmed.ncbi.nlm.nih.gov/9932843/ DOI: 10.1097/00005176-199902000-00008 Access: Primary abstract/metadata; unrecovered methods explicitly retained.
Complete structured claim and evidence
Higher sacrosidase concentrations reduced gas, cramps and bloating during carbohydrate-containing diets in children with CSID.
Sacrosidase → Gas, cramps and bloating in children with congenital sucrase-isomaltase deficiency source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
dose
Yeast sucrase preparation, 6000 IU/mg protein; full strength and 1:10, 1:100, 1:1000 dilutions; >15 kg received 2 mL; lower-weight dose volume missing from accessed abstract
duration
Single-dose breath tests; four 10-day dose periods
evidence_access
Primary abstract/metadata; unrecovered methods explicitly retained.
evidence_scope
literature_reviewed; source-specific curation
experimental_model
28 children aged 5 months to 11 years with congenital sucrase-isomaltase deficiency; randomized double-blind trial
exposure_scope
Drug rescue of human genetic digestive impairment
limitations
Enzyme replacement in diagnosed CSID, not sucrose supplementation for a nutrient deficiency. Exact sucrose challenge amount and lower-weight volume unrecovered. Vomiting did not differ; wheezing occurred in one child with asthma. Not prescribing guidance.
nutrient_topic
Sucrose chapter; direct sucrose observations are distinguished from shared component metabolism. · Sucrose
organism
28 children aged 5 months to 11 years with congenital sucrase-isomaltase deficiency; randomized double-blind trial
plain_language
Higher sacrosidase concentrations reduced gas, cramps and bloating during carbohydrate-containing diets in children with CSID.
primary_references
Sacrosidase therapy for congenital sucrase-isomaltase deficiency. (1999). https://pubmed.ncbi.nlm.nih.gov/9932843/ DOI: 10.1097/00005176-199902000-00008
route
Oral enzyme with sucrose challenge or normal carbohydrate-containing diet
tissue
Intestinal sucrose handling and stool/symptom outcomes
trigger_kind
machinery_impairment Imported condition classification; unverified.
Sucrose: mechanism of action and metabolic impact (2026-09-20) · lines 187–197
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 · 28 children aged 5 months to 11 years with congenital sucrase-isomaltase deficiency; randomized double-blind trial · source_derived_draft · unverified_draft
## sucrose-sacrosidase-symptoms Higher sacrosidase concentrations reduced gas, cramps and bloating during carbohydrate-containing diets in children with CSID. Model/species: 28 children aged 5 months to 11 years with congenital sucrase-isomaltase deficiency; randomized double-blind trial Tissue: Intestinal sucrose handling and stool/symptom outcomes Exposure: Yeast sucrase preparation, 6000 IU/mg protein; full strength and 1:10, 1:100, 1:1000 dilutions; >15 kg received 2 mL; lower-weight dose volume missing from accessed abstract Route: Oral enzyme with sucrose challenge or normal carbohydrate-containing diet Duration: Single-dose breath tests; four 10-day dose periods Exposure scope: Drug rescue of human genetic digestive impairment Limits: Enzyme replacement in diagnosed CSID, not sucrose supplementation for a nutrient deficiency. Exact sucrose challenge amount and lower-weight volume unrecovered. Vomiting did not differ; wheezing occurred in one child with asthma. Not prescribing guidance. Reference: Sacrosidase therapy for congenital sucrase-isomaltase deficiency. (1999). https://pubmed.ncbi.nlm.nih.gov/9932843/ DOI: 10.1097/00005176-199902000-00008 Access: Primary abstract/metadata; unrecovered methods explicitly retained.
Complete structured claim and evidence
Acarbose 200 mg reduced blood-glucose response area by 89% after a 50 g sucrose load in healthy volunteers.
Acarbose → Human blood glucose response to sucrose challenge source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
dose
50 g carbohydrate load; 200 or 50 mg acarbose
duration
Acute tolerance tests; exact sampling duration unrecovered
evidence_access
Primary abstract/metadata; unrecovered methods explicitly retained.
evidence_scope
literature_reviewed; source-specific curation
experimental_model
Healthy human volunteers; sample size unavailable in accessed abstract
exposure_scope
Drug and nutrient interaction
limitations
Acarbose inhibits carbohydrate hydrolysis. The glucose-only comparison does not support direct blockade of glucose transport. Experimental doses are not a dosing recommendation.
nutrient_topic
Sucrose chapter; direct sucrose observations are distinguished from shared component metabolism. · Sucrose
organism
Healthy human volunteers; sample size unavailable in accessed abstract
plain_language
Acarbose 200 mg reduced blood-glucose response area by 89% after a 50 g sucrose load in healthy volunteers.
primary_references
Scope and specificity of acarbose in slowing carbohydrate absorption in man. (1981). https://pubmed.ncbi.nlm.nih.gov/7028548/ DOI: 10.2337/diab.30.11.951
route
Oral carbohydrate and drug
tissue
Carbohydrate tolerance and breath hydrogen
trigger_kind
machinery_impairment Imported condition classification; unverified.
Sucrose: mechanism of action and metabolic impact (2026-09-20) · lines 199–209
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 · Healthy human volunteers; sample size unavailable in accessed abstract · source_derived_draft · unverified_draft
## sucrose-acarbose-glycemia Acarbose 200 mg reduced blood-glucose response area by 89% after a 50 g sucrose load in healthy volunteers. Model/species: Healthy human volunteers; sample size unavailable in accessed abstract Tissue: Carbohydrate tolerance and breath hydrogen Exposure: 50 g carbohydrate load; 200 or 50 mg acarbose Route: Oral carbohydrate and drug Duration: Acute tolerance tests; exact sampling duration unrecovered Exposure scope: Drug and nutrient interaction Limits: Acarbose inhibits carbohydrate hydrolysis. The glucose-only comparison does not support direct blockade of glucose transport. Experimental doses are not a dosing recommendation. Reference: Scope and specificity of acarbose in slowing carbohydrate absorption in man. (1981). https://pubmed.ncbi.nlm.nih.gov/7028548/ DOI: 10.2337/diab.30.11.951 Access: Primary abstract/metadata; unrecovered methods explicitly retained.
Complete structured claim and evidence
Breath hydrogen after 200 mg acarbose with 50 g sucrose indicated nearly complete sucrose malabsorption in the tolerance study.
Acarbose → Human sucrose malabsorption assessed by breath hydrogen source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
dose
50 g carbohydrate load; 200 or 50 mg acarbose
duration
Acute tolerance tests; exact sampling duration unrecovered
evidence_access
Primary abstract/metadata; unrecovered methods explicitly retained.
evidence_scope
literature_reviewed; source-specific curation
experimental_model
Healthy human volunteers; sample size unavailable in accessed abstract
exposure_scope
Drug and nutrient interaction
limitations
Acarbose inhibits carbohydrate hydrolysis. The glucose-only comparison does not support direct blockade of glucose transport. Experimental doses are not a dosing recommendation.
nutrient_topic
Sucrose chapter; direct sucrose observations are distinguished from shared component metabolism. · Sucrose
organism
Healthy human volunteers; sample size unavailable in accessed abstract
plain_language
Breath hydrogen after 200 mg acarbose with 50 g sucrose indicated nearly complete sucrose malabsorption in the tolerance study.
primary_references
Scope and specificity of acarbose in slowing carbohydrate absorption in man. (1981). https://pubmed.ncbi.nlm.nih.gov/7028548/ DOI: 10.2337/diab.30.11.951
route
Oral carbohydrate and drug
tissue
Carbohydrate tolerance and breath hydrogen
trigger_kind
machinery_impairment Imported condition classification; unverified.
Sucrose: mechanism of action and metabolic impact (2026-09-20) · lines 211–221
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 · Healthy human volunteers; sample size unavailable in accessed abstract · source_derived_draft · unverified_draft
## sucrose-acarbose-hydrogen Breath hydrogen after 200 mg acarbose with 50 g sucrose indicated nearly complete sucrose malabsorption in the tolerance study. Model/species: Healthy human volunteers; sample size unavailable in accessed abstract Tissue: Carbohydrate tolerance and breath hydrogen Exposure: 50 g carbohydrate load; 200 or 50 mg acarbose Route: Oral carbohydrate and drug Duration: Acute tolerance tests; exact sampling duration unrecovered Exposure scope: Drug and nutrient interaction Limits: Acarbose inhibits carbohydrate hydrolysis. The glucose-only comparison does not support direct blockade of glucose transport. Experimental doses are not a dosing recommendation. Reference: Scope and specificity of acarbose in slowing carbohydrate absorption in man. (1981). https://pubmed.ncbi.nlm.nih.gov/7028548/ DOI: 10.2337/diab.30.11.951 Access: Primary abstract/metadata; unrecovered methods explicitly retained.
Complete structured claim and evidence
Acarbose 200 mg had no detected effect on the blood-glucose response to a glucose-only load.
Acarbose → Human blood glucose response to glucose challenge source_derived_draftungraded
Experimental context and source evidence
dose
50 g carbohydrate load; 200 or 50 mg acarbose
duration
Acute tolerance tests; exact sampling duration unrecovered
evidence_access
Primary abstract/metadata; unrecovered methods explicitly retained.
evidence_scope
literature_reviewed; source-specific curation
experimental_model
Healthy human volunteers; sample size unavailable in accessed abstract
exposure_scope
Drug and nutrient interaction
limitations
Acarbose inhibits carbohydrate hydrolysis. The glucose-only comparison does not support direct blockade of glucose transport. Experimental doses are not a dosing recommendation.
nutrient_topic
Sucrose chapter; direct sucrose observations are distinguished from shared component metabolism. · Sucrose
organism
Healthy human volunteers; sample size unavailable in accessed abstract
plain_language
Acarbose 200 mg had no detected effect on the blood-glucose response to a glucose-only load.
primary_references
Scope and specificity of acarbose in slowing carbohydrate absorption in man. (1981). https://pubmed.ncbi.nlm.nih.gov/7028548/ DOI: 10.2337/diab.30.11.951
route
Oral carbohydrate and drug
tissue
Carbohydrate tolerance and breath hydrogen
Sucrose: mechanism of action and metabolic impact (2026-09-20) · lines 223–233
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 · Healthy human volunteers; sample size unavailable in accessed abstract · source_derived_draft · unverified_draft
## sucrose-acarbose-glucose-null Acarbose 200 mg had no detected effect on the blood-glucose response to a glucose-only load. Model/species: Healthy human volunteers; sample size unavailable in accessed abstract Tissue: Carbohydrate tolerance and breath hydrogen Exposure: 50 g carbohydrate load; 200 or 50 mg acarbose Route: Oral carbohydrate and drug Duration: Acute tolerance tests; exact sampling duration unrecovered Exposure scope: Drug and nutrient interaction Limits: Acarbose inhibits carbohydrate hydrolysis. The glucose-only comparison does not support direct blockade of glucose transport. Experimental doses are not a dosing recommendation. Reference: Scope and specificity of acarbose in slowing carbohydrate absorption in man. (1981). https://pubmed.ncbi.nlm.nih.gov/7028548/ DOI: 10.2337/diab.30.11.951 Access: Primary abstract/metadata; unrecovered methods explicitly retained.
Complete structured claim and evidence
Acarbose 50 mg still reduced the blood-glucose response to sucrose, without a significant breath-hydrogen increase.
Acarbose → Human blood glucose response to sucrose challenge source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
dose
50 g carbohydrate load; 200 or 50 mg acarbose
duration
Acute tolerance tests; exact sampling duration unrecovered
evidence_access
Primary abstract/metadata; unrecovered methods explicitly retained.
evidence_scope
literature_reviewed; source-specific curation
experimental_model
Healthy human volunteers; sample size unavailable in accessed abstract
exposure_scope
Drug and nutrient interaction
limitations
Acarbose inhibits carbohydrate hydrolysis. The glucose-only comparison does not support direct blockade of glucose transport. Experimental doses are not a dosing recommendation.
nutrient_topic
Sucrose chapter; direct sucrose observations are distinguished from shared component metabolism. · Sucrose
organism
Healthy human volunteers; sample size unavailable in accessed abstract
plain_language
Acarbose 50 mg still reduced the blood-glucose response to sucrose, without a significant breath-hydrogen increase.
primary_references
Scope and specificity of acarbose in slowing carbohydrate absorption in man. (1981). https://pubmed.ncbi.nlm.nih.gov/7028548/ DOI: 10.2337/diab.30.11.951
route
Oral carbohydrate and drug
tissue
Carbohydrate tolerance and breath hydrogen
trigger_kind
machinery_impairment Imported condition classification; unverified.
Sucrose: mechanism of action and metabolic impact (2026-09-20) · lines 235–245
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 · Healthy human volunteers; sample size unavailable in accessed abstract · source_derived_draft · unverified_draft
## sucrose-acarbose-low-dose Acarbose 50 mg still reduced the blood-glucose response to sucrose, without a significant breath-hydrogen increase. Model/species: Healthy human volunteers; sample size unavailable in accessed abstract Tissue: Carbohydrate tolerance and breath hydrogen Exposure: 50 g carbohydrate load; 200 or 50 mg acarbose Route: Oral carbohydrate and drug Duration: Acute tolerance tests; exact sampling duration unrecovered Exposure scope: Drug and nutrient interaction Limits: Acarbose inhibits carbohydrate hydrolysis. The glucose-only comparison does not support direct blockade of glucose transport. Experimental doses are not a dosing recommendation. Reference: Scope and specificity of acarbose in slowing carbohydrate absorption in man. (1981). https://pubmed.ncbi.nlm.nih.gov/7028548/ DOI: 10.2337/diab.30.11.951 Access: Primary abstract/metadata; unrecovered methods explicitly retained.
Complete structured claim and evidence
Reducing added sucrose from 50 to 5 g lowered the 15-minute active GLP-1 response to the mixed meal.
Sucrose → Plasma GLP-1 response in the specified meal or glucose challenge source_derived_draftungraded
Experimental context and source evidence
dose
50 versus 5 g sucrose; 5 g plus mixed sucralose/acesulfame/aspartame/erythritol to match sweetness
duration
15-minute comparison; sampling to 60 minutes
evidence_access
Primary full-text methods/results and metadata inspected.
evidence_scope
literature_reviewed; source-specific curation
experimental_model
Healthy Japanese men in low-sucrose meal substudy
exposure_scope
Sucrose dose versus matched perceived sweetness
limitations
Methods say n=6 for sweetener substudy, results report n=7; discrepancy preserved. Lower sucrose also lowers calories; this is not a calorie-matched isolated receptor experiment.
nutrient_topic
Sucrose chapter; direct sucrose observations are distinguished from shared component metabolism. · Sucrose
organism
Healthy Japanese men in low-sucrose meal substudy
plain_language
Reducing added sucrose from 50 to 5 g lowered the 15-minute active GLP-1 response to the mixed meal.
primary_references
Glucagon-like peptide-1 secretion by direct stimulation of L cells with luminal sugar vs non-nutritive sweetener. (2012). https://pubmed.ncbi.nlm.nih.gov/24843559/ DOI: 10.1111/j.2040-1124.2011.00163.x
route
Oral mixed meal
tissue
Plasma active GLP-1 after mixed meal
Sucrose: mechanism of action and metabolic impact (2026-09-20) · lines 247–257
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 · Healthy Japanese men in low-sucrose meal substudy · source_derived_draft · unverified_draft
## sucrose-low-sucrose-glp1 Reducing added sucrose from 50 to 5 g lowered the 15-minute active GLP-1 response to the mixed meal. Model/species: Healthy Japanese men in low-sucrose meal substudy Tissue: Plasma active GLP-1 after mixed meal Exposure: 50 versus 5 g sucrose; 5 g plus mixed sucralose/acesulfame/aspartame/erythritol to match sweetness Route: Oral mixed meal Duration: 15-minute comparison; sampling to 60 minutes Exposure scope: Sucrose dose versus matched perceived sweetness Limits: Methods say n=6 for sweetener substudy, results report n=7; discrepancy preserved. Lower sucrose also lowers calories; this is not a calorie-matched isolated receptor experiment. Reference: Glucagon-like peptide-1 secretion by direct stimulation of L cells with luminal sugar vs non-nutritive sweetener. (2012). https://pubmed.ncbi.nlm.nih.gov/24843559/ DOI: 10.1111/j.2040-1124.2011.00163.x Access: Primary full-text methods/results and metadata inspected.
Complete structured claim and evidence
Matching sweetness with nonnutritive sweeteners did not restore the GLP-1 response lost when meal sucrose was reduced.
Sucrose → Plasma GLP-1 response in the specified meal or glucose challenge source_derived_draftungraded
Experimental context and source evidence
dose
50 versus 5 g sucrose; 5 g plus mixed sucralose/acesulfame/aspartame/erythritol to match sweetness
duration
15-minute comparison; sampling to 60 minutes
evidence_access
Primary full-text methods/results and metadata inspected.
evidence_scope
literature_reviewed; source-specific curation
experimental_model
Healthy Japanese men in low-sucrose meal substudy
exposure_scope
Sucrose dose versus matched perceived sweetness
limitations
Methods say n=6 for sweetener substudy, results report n=7; discrepancy preserved. Lower sucrose also lowers calories; this is not a calorie-matched isolated receptor experiment.
nutrient_topic
Sucrose chapter; direct sucrose observations are distinguished from shared component metabolism. · Sucrose
organism
Healthy Japanese men in low-sucrose meal substudy
plain_language
Matching sweetness with nonnutritive sweeteners did not restore the GLP-1 response lost when meal sucrose was reduced.
primary_references
Glucagon-like peptide-1 secretion by direct stimulation of L cells with luminal sugar vs non-nutritive sweetener. (2012). https://pubmed.ncbi.nlm.nih.gov/24843559/ DOI: 10.1111/j.2040-1124.2011.00163.x
route
Oral mixed meal
tissue
Plasma active GLP-1 after mixed meal
Sucrose: mechanism of action and metabolic impact (2026-09-20) · lines 259–269
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 · Healthy Japanese men in low-sucrose meal substudy · source_derived_draft · unverified_draft
## sucrose-sweetness-glp1-null Matching sweetness with nonnutritive sweeteners did not restore the GLP-1 response lost when meal sucrose was reduced. Model/species: Healthy Japanese men in low-sucrose meal substudy Tissue: Plasma active GLP-1 after mixed meal Exposure: 50 versus 5 g sucrose; 5 g plus mixed sucralose/acesulfame/aspartame/erythritol to match sweetness Route: Oral mixed meal Duration: 15-minute comparison; sampling to 60 minutes Exposure scope: Sucrose dose versus matched perceived sweetness Limits: Methods say n=6 for sweetener substudy, results report n=7; discrepancy preserved. Lower sucrose also lowers calories; this is not a calorie-matched isolated receptor experiment. Reference: Glucagon-like peptide-1 secretion by direct stimulation of L cells with luminal sugar vs non-nutritive sweetener. (2012). https://pubmed.ncbi.nlm.nih.gov/24843559/ DOI: 10.1111/j.2040-1124.2011.00163.x Access: Primary full-text methods/results and metadata inspected.
Complete structured claim and evidence
Acarbose pretreatment prolonged active GLP-1 elevation to 60 minutes after the sucrose-containing mixed meal.
Acarbose → Plasma GLP-1 response in the specified meal or glucose challenge source_derived_draftungraded
Experimental context and source evidence
dose
Meal with 50 g added sucrose in 200 mL; with or without 100 mg acarbose before meal
duration
GLP-1 through 60 minutes; ApoB-48 at 120 minutes
evidence_access
Primary full-text methods/results and metadata inspected.
evidence_scope
literature_reviewed; source-specific curation
experimental_model
Healthy Japanese men; 21 total, 12 in acarbose comparison
exposure_scope
Sucrose-containing mixed meal, drug and peptide response
limitations
Mixed meal includes starch, protein and fat. Association does not prove intact sucrose sensing by human L cells or GLP-1 mediation of ApoB-48; proposed paracrine mechanism remains a hypothesis.
nutrient_topic
Sucrose chapter; direct sucrose observations are distinguished from shared component metabolism. · Sucrose
organism
Healthy Japanese men; 21 total, 12 in acarbose comparison
plain_language
Acarbose pretreatment prolonged active GLP-1 elevation to 60 minutes after the sucrose-containing mixed meal.
primary_references
Glucagon-like peptide-1 secretion by direct stimulation of L cells with luminal sugar vs non-nutritive sweetener. (2012). https://pubmed.ncbi.nlm.nih.gov/24843559/ DOI: 10.1111/j.2040-1124.2011.00163.x
route
Oral mixed meal and drug
tissue
Plasma active GLP-1 and ApoB-48 after mixed meal
Sucrose: mechanism of action and metabolic impact (2026-09-20) · lines 271–281
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 · Healthy Japanese men; 21 total, 12 in acarbose comparison · source_derived_draft · unverified_draft
## sucrose-acarbose-glp1 Acarbose pretreatment prolonged active GLP-1 elevation to 60 minutes after the sucrose-containing mixed meal. Model/species: Healthy Japanese men; 21 total, 12 in acarbose comparison Tissue: Plasma active GLP-1 and ApoB-48 after mixed meal Exposure: Meal with 50 g added sucrose in 200 mL; with or without 100 mg acarbose before meal Route: Oral mixed meal and drug Duration: GLP-1 through 60 minutes; ApoB-48 at 120 minutes Exposure scope: Sucrose-containing mixed meal, drug and peptide response Limits: Mixed meal includes starch, protein and fat. Association does not prove intact sucrose sensing by human L cells or GLP-1 mediation of ApoB-48; proposed paracrine mechanism remains a hypothesis. Reference: Glucagon-like peptide-1 secretion by direct stimulation of L cells with luminal sugar vs non-nutritive sweetener. (2012). https://pubmed.ncbi.nlm.nih.gov/24843559/ DOI: 10.1111/j.2040-1124.2011.00163.x Access: Primary full-text methods/results and metadata inspected.
Complete structured claim and evidence
Acarbose pretreatment prevented the 120-minute ApoB-48 increase after the sucrose-containing mixed meal.
Acarbose → Human postprandial circulating apolipoprotein B-48 source_derived_draftungraded
Experimental context and source evidence
dose
Meal with 50 g added sucrose in 200 mL; with or without 100 mg acarbose before meal
duration
GLP-1 through 60 minutes; ApoB-48 at 120 minutes
evidence_access
Primary full-text methods/results and metadata inspected.
evidence_scope
literature_reviewed; source-specific curation
experimental_model
Healthy Japanese men; 21 total, 12 in acarbose comparison
exposure_scope
Sucrose-containing mixed meal, drug and peptide response
limitations
Mixed meal includes starch, protein and fat. Association does not prove intact sucrose sensing by human L cells or GLP-1 mediation of ApoB-48; proposed paracrine mechanism remains a hypothesis.
nutrient_topic
Sucrose chapter; direct sucrose observations are distinguished from shared component metabolism. · Sucrose
organism
Healthy Japanese men; 21 total, 12 in acarbose comparison
plain_language
Acarbose pretreatment prevented the 120-minute ApoB-48 increase after the sucrose-containing mixed meal.
primary_references
Glucagon-like peptide-1 secretion by direct stimulation of L cells with luminal sugar vs non-nutritive sweetener. (2012). https://pubmed.ncbi.nlm.nih.gov/24843559/ DOI: 10.1111/j.2040-1124.2011.00163.x
route
Oral mixed meal and drug
tissue
Plasma active GLP-1 and ApoB-48 after mixed meal
Sucrose: mechanism of action and metabolic impact (2026-09-20) · lines 283–293
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 · Healthy Japanese men; 21 total, 12 in acarbose comparison · source_derived_draft · unverified_draft
## sucrose-acarbose-apob48 Acarbose pretreatment prevented the 120-minute ApoB-48 increase after the sucrose-containing mixed meal. Model/species: Healthy Japanese men; 21 total, 12 in acarbose comparison Tissue: Plasma active GLP-1 and ApoB-48 after mixed meal Exposure: Meal with 50 g added sucrose in 200 mL; with or without 100 mg acarbose before meal Route: Oral mixed meal and drug Duration: GLP-1 through 60 minutes; ApoB-48 at 120 minutes Exposure scope: Sucrose-containing mixed meal, drug and peptide response Limits: Mixed meal includes starch, protein and fat. Association does not prove intact sucrose sensing by human L cells or GLP-1 mediation of ApoB-48; proposed paracrine mechanism remains a hypothesis. Reference: Glucagon-like peptide-1 secretion by direct stimulation of L cells with luminal sugar vs non-nutritive sweetener. (2012). https://pubmed.ncbi.nlm.nih.gov/24843559/ DOI: 10.1111/j.2040-1124.2011.00163.x Access: Primary full-text methods/results and metadata inspected.
Complete structured claim and evidence
Liver glycogen did not significantly decline during three hours of cycling with sucrose ingestion; preservation did not differ from glucose.
Sucrose → Human hepatic glycogen during prolonged cycling source_derived_draftungraded
Experimental context and source evidence
dose
Sucrose or glucose 1.7 g/min, 102 g/hour, during cycling at 50% peak power
duration
3 hours
evidence_access
Primary abstract/metadata; unrecovered methods explicitly retained.
evidence_scope
literature_reviewed; source-specific curation
experimental_model
14 trained cyclists in crossover; four completed additional water reference trial
exposure_scope
Exercise fuel, not sedentary beverage exposure
limitations
Water reference had four participants, not all 14. Whole-body utilization is not isolated exogenous sucrose oxidation. No demonstrated sucrose advantage for liver glycogen preservation. NCT02110836; Sugar Nutrition UK sponsor listed in trial record.
nutrient_topic
Sucrose chapter; direct sucrose observations are distinguished from shared component metabolism. · Sucrose
organism
14 trained cyclists in crossover; four completed additional water reference trial
plain_language
Liver glycogen did not significantly decline during three hours of cycling with sucrose ingestion; preservation did not differ from glucose.
primary_references
Ingestion of glucose or sucrose prevents liver but not muscle glycogen depletion during prolonged endurance-type exercise in trained cyclists. (2015). https://pubmed.ncbi.nlm.nih.gov/26487008/ DOI: 10.1152/ajpendo.00376.2015
route
Oral carbohydrate during exercise
tissue
Liver and muscle glycogen by carbon-13 MRS; expired-gas substrate use
Sucrose: mechanism of action and metabolic impact (2026-09-20) · lines 295–305
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 · 14 trained cyclists in crossover; four completed additional water reference trial · source_derived_draft · unverified_draft
## sucrose-exercise-liver Liver glycogen did not significantly decline during three hours of cycling with sucrose ingestion; preservation did not differ from glucose. Model/species: 14 trained cyclists in crossover; four completed additional water reference trial Tissue: Liver and muscle glycogen by carbon-13 MRS; expired-gas substrate use Exposure: Sucrose or glucose 1.7 g/min, 102 g/hour, during cycling at 50% peak power Route: Oral carbohydrate during exercise Duration: 3 hours Exposure scope: Exercise fuel, not sedentary beverage exposure Limits: Water reference had four participants, not all 14. Whole-body utilization is not isolated exogenous sucrose oxidation. No demonstrated sucrose advantage for liver glycogen preservation. NCT02110836; Sugar Nutrition UK sponsor listed in trial record. Reference: Ingestion of glucose or sucrose prevents liver but not muscle glycogen depletion during prolonged endurance-type exercise in trained cyclists. (2015). https://pubmed.ncbi.nlm.nih.gov/26487008/ DOI: 10.1152/ajpendo.00376.2015 Access: Primary abstract/metadata; unrecovered methods explicitly retained.
Complete structured claim and evidence
Muscle glycogen declined during prolonged cycling despite sucrose ingestion, as it did with glucose ingestion.
Sucrose → Human exercise muscle glycogen utilization source_derived_draftungraded
Experimental context and source evidence
dose
Sucrose or glucose 1.7 g/min, 102 g/hour, during cycling at 50% peak power
duration
3 hours
evidence_access
Primary abstract/metadata; unrecovered methods explicitly retained.
evidence_scope
literature_reviewed; source-specific curation
experimental_model
14 trained cyclists in crossover; four completed additional water reference trial
exposure_scope
Exercise fuel, not sedentary beverage exposure
limitations
Water reference had four participants, not all 14. Whole-body utilization is not isolated exogenous sucrose oxidation. No demonstrated sucrose advantage for liver glycogen preservation. NCT02110836; Sugar Nutrition UK sponsor listed in trial record.
nutrient_topic
Sucrose chapter; direct sucrose observations are distinguished from shared component metabolism. · Sucrose
organism
14 trained cyclists in crossover; four completed additional water reference trial
plain_language
Muscle glycogen declined during prolonged cycling despite sucrose ingestion, as it did with glucose ingestion.
primary_references
Ingestion of glucose or sucrose prevents liver but not muscle glycogen depletion during prolonged endurance-type exercise in trained cyclists. (2015). https://pubmed.ncbi.nlm.nih.gov/26487008/ DOI: 10.1152/ajpendo.00376.2015
route
Oral carbohydrate during exercise
tissue
Liver and muscle glycogen by carbon-13 MRS; expired-gas substrate use
Sucrose: mechanism of action and metabolic impact (2026-09-20) · lines 307–317
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 · 14 trained cyclists in crossover; four completed additional water reference trial · source_derived_draft · unverified_draft
## sucrose-exercise-muscle Muscle glycogen declined during prolonged cycling despite sucrose ingestion, as it did with glucose ingestion. Model/species: 14 trained cyclists in crossover; four completed additional water reference trial Tissue: Liver and muscle glycogen by carbon-13 MRS; expired-gas substrate use Exposure: Sucrose or glucose 1.7 g/min, 102 g/hour, during cycling at 50% peak power Route: Oral carbohydrate during exercise Duration: 3 hours Exposure scope: Exercise fuel, not sedentary beverage exposure Limits: Water reference had four participants, not all 14. Whole-body utilization is not isolated exogenous sucrose oxidation. No demonstrated sucrose advantage for liver glycogen preservation. NCT02110836; Sugar Nutrition UK sponsor listed in trial record. Reference: Ingestion of glucose or sucrose prevents liver but not muscle glycogen depletion during prolonged endurance-type exercise in trained cyclists. (2015). https://pubmed.ncbi.nlm.nih.gov/26487008/ DOI: 10.1152/ajpendo.00376.2015 Access: Primary abstract/metadata; unrecovered methods explicitly retained.
Complete structured claim and evidence
Whole-body carbohydrate utilization during cycling was greater with sucrose than glucose, 2.03 versus 1.66 g/min.
Sucrose → Human whole-body carbohydrate utilization during exercise source_derived_draftungraded
Experimental context and source evidence
dose
Sucrose or glucose 1.7 g/min, 102 g/hour, during cycling at 50% peak power
duration
3 hours
evidence_access
Primary abstract/metadata; unrecovered methods explicitly retained.
evidence_scope
literature_reviewed; source-specific curation
experimental_model
14 trained cyclists in crossover; four completed additional water reference trial
exposure_scope
Exercise fuel, not sedentary beverage exposure
limitations
Water reference had four participants, not all 14. Whole-body utilization is not isolated exogenous sucrose oxidation. No demonstrated sucrose advantage for liver glycogen preservation. NCT02110836; Sugar Nutrition UK sponsor listed in trial record.
nutrient_topic
Sucrose chapter; direct sucrose observations are distinguished from shared component metabolism. · Sucrose
organism
14 trained cyclists in crossover; four completed additional water reference trial
plain_language
Whole-body carbohydrate utilization during cycling was greater with sucrose than glucose, 2.03 versus 1.66 g/min.
primary_references
Ingestion of glucose or sucrose prevents liver but not muscle glycogen depletion during prolonged endurance-type exercise in trained cyclists. (2015). https://pubmed.ncbi.nlm.nih.gov/26487008/ DOI: 10.1152/ajpendo.00376.2015
route
Oral carbohydrate during exercise
tissue
Liver and muscle glycogen by carbon-13 MRS; expired-gas substrate use
Sucrose: mechanism of action and metabolic impact (2026-09-20) · lines 319–329
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 · 14 trained cyclists in crossover; four completed additional water reference trial · source_derived_draft · unverified_draft
## sucrose-exercise-utilization Whole-body carbohydrate utilization during cycling was greater with sucrose than glucose, 2.03 versus 1.66 g/min. Model/species: 14 trained cyclists in crossover; four completed additional water reference trial Tissue: Liver and muscle glycogen by carbon-13 MRS; expired-gas substrate use Exposure: Sucrose or glucose 1.7 g/min, 102 g/hour, during cycling at 50% peak power Route: Oral carbohydrate during exercise Duration: 3 hours Exposure scope: Exercise fuel, not sedentary beverage exposure Limits: Water reference had four participants, not all 14. Whole-body utilization is not isolated exogenous sucrose oxidation. No demonstrated sucrose advantage for liver glycogen preservation. NCT02110836; Sugar Nutrition UK sponsor listed in trial record. Reference: Ingestion of glucose or sucrose prevents liver but not muscle glycogen depletion during prolonged endurance-type exercise in trained cyclists. (2015). https://pubmed.ncbi.nlm.nih.gov/26487008/ DOI: 10.1152/ajpendo.00376.2015 Access: Primary abstract/metadata; unrecovered methods explicitly retained.
Complete structured claim and evidence
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
Sucrose beverages reduced Matsuda insulin sensitivity compared with aspartame in the matched-group intervention.
Sucrose → Human Matsuda insulin sensitivity index 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 reduced Matsuda insulin sensitivity compared with aspartame in the matched-group intervention.
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 343–353
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-matsuda Sucrose beverages reduced Matsuda insulin sensitivity compared with aspartame in the matched-group intervention. 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
Sucrose beverages increased postprandial triglycerides compared with aspartame after the intervention.
Sucrose → Human postprandial triglyceride response 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 postprandial triglycerides compared with aspartame after the intervention.
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 355–365
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-triglycerides Sucrose beverages increased postprandial triglycerides compared with aspartame after the intervention. 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
Sucrose beverages increased fasting LDL cholesterol compared with aspartame.
Sucrose → Human plasma LDL cholesterol 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 fasting LDL cholesterol compared with 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 367–377
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-ldl Sucrose beverages increased fasting LDL cholesterol compared with 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
Sucrose beverages increased 24-hour plasma urate exposure compared with aspartame.
Sucrose → Human plasma urate concentration 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 24-hour plasma urate exposure compared with 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 379–389
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-urate Sucrose beverages increased 24-hour plasma urate exposure compared with 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
None of ten healthy volunteers showed breath-hydrogen malabsorption after the tested 50, 75 or 100 g sucrose loads.
Sucrose → Human sucrose malabsorption assessed by breath hydrogen source_derived_draftungraded
Experimental context and source evidence
dose
Sucrose 50, 75 or 100 g; comparison with fructose alone
duration
Breath sampling over 3-4 hours
evidence_access
Primary abstract/metadata; unrecovered methods explicitly retained.
evidence_scope
literature_reviewed; source-specific curation
experimental_model
Ten healthy adult volunteers
exposure_scope
Human sucrose absorption
limitations
No detected breath-hydrogen malabsorption in a small healthy cohort is not proof that every person tolerates every dose; CSID is a distinct condition.
nutrient_topic
Sucrose chapter; direct sucrose observations are distinguished from shared component metabolism. · Sucrose
organism
Ten healthy adult volunteers
plain_language
None of ten healthy volunteers showed breath-hydrogen malabsorption after the tested 50, 75 or 100 g sucrose loads.
primary_references
Absorption capacity of fructose in healthy adults. Comparison with sucrose and its constituent monosaccharides. (1986). https://pubmed.ncbi.nlm.nih.gov/3781328/ DOI: 10.1136/gut.27.10.1161
route
Oral sugar solutions
tissue
Hydrogen breath tests
Sucrose: mechanism of action and metabolic impact (2026-09-20) · lines 391–401
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 · Ten healthy adult volunteers · source_derived_draft · unverified_draft
## sucrose-absorption None of ten healthy volunteers showed breath-hydrogen malabsorption after the tested 50, 75 or 100 g sucrose loads. Model/species: Ten healthy adult volunteers Tissue: Hydrogen breath tests Exposure: Sucrose 50, 75 or 100 g; comparison with fructose alone Route: Oral sugar solutions Duration: Breath sampling over 3-4 hours Exposure scope: Human sucrose absorption Limits: No detected breath-hydrogen malabsorption in a small healthy cohort is not proof that every person tolerates every dose; CSID is a distinct condition. Reference: Absorption capacity of fructose in healthy adults. Comparison with sucrose and its constituent monosaccharides. (1986). https://pubmed.ncbi.nlm.nih.gov/3781328/ DOI: 10.1136/gut.27.10.1161 Access: Primary abstract/metadata; unrecovered methods explicitly retained.
Complete structured claim and evidence
Sucrose-supported multispecies cultures formed a glucan matrix and structured microcolonies; glucose cultures did not form that matrix under the tested conditions.
Sucrose → Streptococcus mutans extracellular glucan matrix formation source_derived_draftungraded
Experimental context and source evidence
dose
Sucrose versus glucose growth conditions; gtfB or gtfB/gtfC deletion
duration
Biofilm maturation series; exact dose and duration not recovered from accessed abstract
evidence_access
Primary abstract/metadata; unrecovered methods explicitly retained.
evidence_scope
literature_reviewed; source-specific curation
experimental_model
Streptococcus mutans with Streptococcus oralis and Actinomyces naeslundii; gtf mutants
exposure_scope
Sucrose-dependent oral bacterial machinery
limitations
Bacterial matrix formation and mutant phenotypes; not a clinical caries incidence trial. GtfB and GtfC have different contributions. Only primary abstract and metadata used.
nutrient_topic
Sucrose chapter; direct sucrose observations are distinguished from shared component metabolism. · Sucrose
organism
Streptococcus mutans with Streptococcus oralis and Actinomyces naeslundii; gtf mutants
plain_language
Sucrose-supported multispecies cultures formed a glucan matrix and structured microcolonies; glucose cultures did not form that matrix under the tested conditions.
primary_references
Exopolysaccharides produced by Streptococcus mutans glucosyltransferases modulate the establishment of microcolonies within multispecies biofilms. (2010). https://pubmed.ncbi.nlm.nih.gov/20233920/ DOI: 10.1128/JB.01649-09
route
In vitro bacterial culture
tissue
Biofilm on saliva-coated hydroxyapatite
Sucrose: mechanism of action and metabolic impact (2026-09-20) · lines 403–413
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 · Streptococcus mutans with Streptococcus oralis and Actinomyces naeslundii; gtf mutants · source_derived_draft · unverified_draft
## sucrose-biofilm-matrix Sucrose-supported multispecies cultures formed a glucan matrix and structured microcolonies; glucose cultures did not form that matrix under the tested conditions. Model/species: Streptococcus mutans with Streptococcus oralis and Actinomyces naeslundii; gtf mutants Tissue: Biofilm on saliva-coated hydroxyapatite Exposure: Sucrose versus glucose growth conditions; gtfB or gtfB/gtfC deletion Route: In vitro bacterial culture Duration: Biofilm maturation series; exact dose and duration not recovered from accessed abstract Exposure scope: Sucrose-dependent oral bacterial machinery Limits: Bacterial matrix formation and mutant phenotypes; not a clinical caries incidence trial. GtfB and GtfC have different contributions. Only primary abstract and metadata used. Reference: Exopolysaccharides produced by Streptococcus mutans glucosyltransferases modulate the establishment of microcolonies within multispecies biofilms. (2010). https://pubmed.ncbi.nlm.nih.gov/20233920/ DOI: 10.1128/JB.01649-09 Access: Primary abstract/metadata; unrecovered methods explicitly retained.
Complete structured claim and evidence
Deleting gtfB markedly disrupted S. mutans microcolony formation on saliva-coated hydroxyapatite.
Streptococcus mutans glucosyltransferase B / GtfB → Streptococcus mutans biofilm microcolony formation source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
dose
Sucrose versus glucose growth conditions; gtfB or gtfB/gtfC deletion
duration
Biofilm maturation series; exact dose and duration not recovered from accessed abstract
evidence_access
Primary abstract/metadata; unrecovered methods explicitly retained.
evidence_scope
literature_reviewed; source-specific curation
experimental_model
Streptococcus mutans with Streptococcus oralis and Actinomyces naeslundii; gtf mutants
exposure_scope
Sucrose-dependent oral bacterial machinery
limitations
Bacterial matrix formation and mutant phenotypes; not a clinical caries incidence trial. GtfB and GtfC have different contributions. Only primary abstract and metadata used.
nutrient_topic
Sucrose chapter; direct sucrose observations are distinguished from shared component metabolism. · Sucrose
organism
Streptococcus mutans with Streptococcus oralis and Actinomyces naeslundii; gtf mutants
plain_language
Deleting gtfB markedly disrupted S. mutans microcolony formation on saliva-coated hydroxyapatite.
primary_references
Exopolysaccharides produced by Streptococcus mutans glucosyltransferases modulate the establishment of microcolonies within multispecies biofilms. (2010). https://pubmed.ncbi.nlm.nih.gov/20233920/ DOI: 10.1128/JB.01649-09
route
In vitro bacterial culture
tissue
Biofilm on saliva-coated hydroxyapatite
trigger_kind
machinery_impairment Imported condition classification; unverified.
Sucrose: mechanism of action and metabolic impact (2026-09-20) · lines 415–425
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 · Streptococcus mutans with Streptococcus oralis and Actinomyces naeslundii; gtf mutants · source_derived_draft · unverified_draft
## sucrose-gtfb-deletion Deleting gtfB markedly disrupted S. mutans microcolony formation on saliva-coated hydroxyapatite. Model/species: Streptococcus mutans with Streptococcus oralis and Actinomyces naeslundii; gtf mutants Tissue: Biofilm on saliva-coated hydroxyapatite Exposure: Sucrose versus glucose growth conditions; gtfB or gtfB/gtfC deletion Route: In vitro bacterial culture Duration: Biofilm maturation series; exact dose and duration not recovered from accessed abstract Exposure scope: Sucrose-dependent oral bacterial machinery Limits: Bacterial matrix formation and mutant phenotypes; not a clinical caries incidence trial. GtfB and GtfC have different contributions. Only primary abstract and metadata used. Reference: Exopolysaccharides produced by Streptococcus mutans glucosyltransferases modulate the establishment of microcolonies within multispecies biofilms. (2010). https://pubmed.ncbi.nlm.nih.gov/20233920/ DOI: 10.1128/JB.01649-09 Access: Primary abstract/metadata; unrecovered methods explicitly retained.
Complete structured claim and evidence
Deleting both gtfB and gtfC produced the greatest reduction in the S. mutans extracellular matrix among the tested mutants.
Streptococcus mutans glucosyltransferase B / GtfB → Streptococcus mutans extracellular glucan matrix formation source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
dose
Sucrose versus glucose growth conditions; gtfB or gtfB/gtfC deletion
duration
Biofilm maturation series; exact dose and duration not recovered from accessed abstract
evidence_access
Primary abstract/metadata; unrecovered methods explicitly retained.
evidence_scope
literature_reviewed; source-specific curation
experimental_model
Streptococcus mutans with Streptococcus oralis and Actinomyces naeslundii; gtf mutants
exposure_scope
Sucrose-dependent oral bacterial machinery
limitations
Bacterial matrix formation and mutant phenotypes; not a clinical caries incidence trial. GtfB and GtfC have different contributions. Only primary abstract and metadata used.
nutrient_topic
Sucrose chapter; direct sucrose observations are distinguished from shared component metabolism. · Sucrose
organism
Streptococcus mutans with Streptococcus oralis and Actinomyces naeslundii; gtf mutants
plain_language
Deleting both gtfB and gtfC produced the greatest reduction in the S. mutans extracellular matrix among the tested mutants.
primary_references
Exopolysaccharides produced by Streptococcus mutans glucosyltransferases modulate the establishment of microcolonies within multispecies biofilms. (2010). https://pubmed.ncbi.nlm.nih.gov/20233920/ DOI: 10.1128/JB.01649-09
route
In vitro bacterial culture
tissue
Biofilm on saliva-coated hydroxyapatite
trigger_kind
machinery_impairment Imported condition classification; unverified.
Sucrose: mechanism of action and metabolic impact (2026-09-20) · lines 427–437
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 · Streptococcus mutans with Streptococcus oralis and Actinomyces naeslundii; gtf mutants · source_derived_draft · unverified_draft
## sucrose-gtfbc-deletion Deleting both gtfB and gtfC produced the greatest reduction in the S. mutans extracellular matrix among the tested mutants. Model/species: Streptococcus mutans with Streptococcus oralis and Actinomyces naeslundii; gtf mutants Tissue: Biofilm on saliva-coated hydroxyapatite Exposure: Sucrose versus glucose growth conditions; gtfB or gtfB/gtfC deletion Route: In vitro bacterial culture Duration: Biofilm maturation series; exact dose and duration not recovered from accessed abstract Exposure scope: Sucrose-dependent oral bacterial machinery Limits: Bacterial matrix formation and mutant phenotypes; not a clinical caries incidence trial. GtfB and GtfC have different contributions. Only primary abstract and metadata used. Reference: Exopolysaccharides produced by Streptococcus mutans glucosyltransferases modulate the establishment of microcolonies within multispecies biofilms. (2010). https://pubmed.ncbi.nlm.nih.gov/20233920/ DOI: 10.1128/JB.01649-09 Access: Primary abstract/metadata; unrecovered methods explicitly retained.
Complete structured claim and evidence
Repeated sucrose exposure lowered calcium concentration in whole in-situ dental biofilm relative to water.
Sucrose → Calcium concentration in human in-situ whole dental biofilm source_derived_draftungraded
Experimental context and source evidence
dose
Sucrose or glucose+fructose solution 8 times/day versus water; concentration and sample size unrecovered
duration
14 days; 24-hour carbohydrate withdrawal follow-up
evidence_access
Primary abstract/metadata; unrecovered methods explicitly retained.
evidence_scope
literature_reviewed; source-specific curation
experimental_model
Human volunteers wearing enamel blocks in palatal appliances
exposure_scope
Sucrose and local mineral availability
limitations
Local biofilm calcium, phosphate and fluoride pools are not systemic nutrient status. Whole-biofilm and fluid results differ; no dietary calcium-deficiency inference.
nutrient_topic
Sucrose chapter; direct sucrose observations are distinguished from shared component metabolism. · Sucrose
organism
Human volunteers wearing enamel blocks in palatal appliances
plain_language
Repeated sucrose exposure lowered calcium concentration in whole in-situ dental biofilm relative to water.
primary_references
Ca, Pi, and F in the fluid of biofilm formed under sucrose. (2006). https://pubmed.ncbi.nlm.nih.gov/16931867/ DOI: 10.1177/154405910608500911
route
Repeated local oral exposure
tissue
Whole dental biofilm versus its fluid compartment
Sucrose: mechanism of action and metabolic impact (2026-09-20) · lines 439–449
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 · Human volunteers wearing enamel blocks in palatal appliances · source_derived_draft · unverified_draft
## sucrose-biofilm-calcium Repeated sucrose exposure lowered calcium concentration in whole in-situ dental biofilm relative to water. Model/species: Human volunteers wearing enamel blocks in palatal appliances Tissue: Whole dental biofilm versus its fluid compartment Exposure: Sucrose or glucose+fructose solution 8 times/day versus water; concentration and sample size unrecovered Route: Repeated local oral exposure Duration: 14 days; 24-hour carbohydrate withdrawal follow-up Exposure scope: Sucrose and local mineral availability Limits: Local biofilm calcium, phosphate and fluoride pools are not systemic nutrient status. Whole-biofilm and fluid results differ; no dietary calcium-deficiency inference. Reference: Ca, Pi, and F in the fluid of biofilm formed under sucrose. (2006). https://pubmed.ncbi.nlm.nih.gov/16931867/ DOI: 10.1177/154405910608500911 Access: Primary abstract/metadata; unrecovered methods explicitly retained.
Complete structured claim and evidence
Sucrose exposure did not lower calcium in the biofilm fluid compartment, including after the cariogenic challenge.
Sucrose → Calcium concentration in fluid from human in-situ dental biofilm source_derived_draftungraded
Experimental context and source evidence
dose
Sucrose or glucose+fructose solution 8 times/day versus water; concentration and sample size unrecovered
duration
14 days; 24-hour carbohydrate withdrawal follow-up
evidence_access
Primary abstract/metadata; unrecovered methods explicitly retained.
evidence_scope
literature_reviewed; source-specific curation
experimental_model
Human volunteers wearing enamel blocks in palatal appliances
exposure_scope
Sucrose and local mineral availability
limitations
Local biofilm calcium, phosphate and fluoride pools are not systemic nutrient status. Whole-biofilm and fluid results differ; no dietary calcium-deficiency inference.
nutrient_topic
Sucrose chapter; direct sucrose observations are distinguished from shared component metabolism. · Sucrose
organism
Human volunteers wearing enamel blocks in palatal appliances
plain_language
Sucrose exposure did not lower calcium in the biofilm fluid compartment, including after the cariogenic challenge.
primary_references
Ca, Pi, and F in the fluid of biofilm formed under sucrose. (2006). https://pubmed.ncbi.nlm.nih.gov/16931867/ DOI: 10.1177/154405910608500911
route
Repeated local oral exposure
tissue
Whole dental biofilm versus its fluid compartment
Sucrose: mechanism of action and metabolic impact (2026-09-20) · lines 451–461
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 · Human volunteers wearing enamel blocks in palatal appliances · source_derived_draft · unverified_draft
## sucrose-biofilm-fluid-calcium-null Sucrose exposure did not lower calcium in the biofilm fluid compartment, including after the cariogenic challenge. Model/species: Human volunteers wearing enamel blocks in palatal appliances Tissue: Whole dental biofilm versus its fluid compartment Exposure: Sucrose or glucose+fructose solution 8 times/day versus water; concentration and sample size unrecovered Route: Repeated local oral exposure Duration: 14 days; 24-hour carbohydrate withdrawal follow-up Exposure scope: Sucrose and local mineral availability Limits: Local biofilm calcium, phosphate and fluoride pools are not systemic nutrient status. Whole-biofilm and fluid results differ; no dietary calcium-deficiency inference. Reference: Ca, Pi, and F in the fluid of biofilm formed under sucrose. (2006). https://pubmed.ncbi.nlm.nih.gov/16931867/ DOI: 10.1177/154405910608500911 Access: Primary abstract/metadata; unrecovered methods explicitly retained.
Complete structured claim and evidence
Increasing fluoride from 0.50 to 0.75 ppm reduced enamel mineral loss during repeated sucrose exposure in the artificial-mouth model.
Fluoride ion → Mineral loss from human enamel in artificial-mouth biofilm experiments source_derived_draftungraded
Experimental context and source evidence
dose
3% or 5% sucrose for 30 minutes three times/day; 0.50 or 0.75 ppm fluoride for 22.5 hours/day
duration
5 days; separate 3-versus-9-day biofilm comparison
evidence_access
Primary full-text methods/results and metadata inspected.
evidence_scope
literature_reviewed; source-specific curation
experimental_model
Human enamel slabs with mixed streptococcal/lactobacillus biofilms in artificial mouth
exposure_scope
Sucrose, bacterial biofilm and fluoride interaction
limitations
Artificial-mouth lesion endpoint, not systemic fluoride or clinical prevention estimate. 3 versus 5% sucrose did not differ under this protocol; this does not establish general dose independence.
nutrient_topic
Sucrose chapter; direct sucrose observations are distinguished from shared component metabolism. · Sucrose
organism
Human enamel slabs with mixed streptococcal/lactobacillus biofilms in artificial mouth
plain_language
Increasing fluoride from 0.50 to 0.75 ppm reduced enamel mineral loss during repeated sucrose exposure in the artificial-mouth model.
primary_references
Enamel Carious Lesion Development in Response to Sucrose and Fluoride Concentrations and to Time of Biofilm Formation: An Artificial-Mouth Study. (2014). https://pubmed.ncbi.nlm.nih.gov/25664342/ DOI: 10.1155/2014/348032
route
In vitro repeated local exposure
tissue
Enamel lesion depth and integrated mineral loss
Sucrose: mechanism of action and metabolic impact (2026-09-20) · lines 463–473
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 · Human enamel slabs with mixed streptococcal/lactobacillus biofilms in artificial mouth · source_derived_draft · unverified_draft
## sucrose-fluoride-mineral Increasing fluoride from 0.50 to 0.75 ppm reduced enamel mineral loss during repeated sucrose exposure in the artificial-mouth model. Model/species: Human enamel slabs with mixed streptococcal/lactobacillus biofilms in artificial mouth Tissue: Enamel lesion depth and integrated mineral loss Exposure: 3% or 5% sucrose for 30 minutes three times/day; 0.50 or 0.75 ppm fluoride for 22.5 hours/day Route: In vitro repeated local exposure Duration: 5 days; separate 3-versus-9-day biofilm comparison Exposure scope: Sucrose, bacterial biofilm and fluoride interaction Limits: Artificial-mouth lesion endpoint, not systemic fluoride or clinical prevention estimate. 3 versus 5% sucrose did not differ under this protocol; this does not establish general dose independence. Reference: Enamel Carious Lesion Development in Response to Sucrose and Fluoride Concentrations and to Time of Biofilm Formation: An Artificial-Mouth Study. (2014). https://pubmed.ncbi.nlm.nih.gov/25664342/ DOI: 10.1155/2014/348032 Access: Primary full-text methods/results and metadata inspected.
Complete structured claim and evidence
Oral sucrose lowered the composite PIPP score after heel lance compared with water in the neonatal randomized trial.
Sucrose → Human neonatal heel-lance Premature Infant Pain Profile score source_derived_draftungraded
Experimental context and source evidence
dose
0.5 mL of 24% sucrose versus 0.5 mL sterile water
duration
2 minutes before lance; acute responses
evidence_access
Primary full-text methods/results and metadata inspected.
evidence_scope
literature_reviewed; source-specific curation
experimental_model
59 newborn infants randomized; 44 included in primary EEG analysis
exposure_scope
Neonatal sensory and nociceptive endpoints
limitations
Twenty sucrose and 24 water infants in primary EEG analysis. Different pain-related readouts are not interchangeable. Null EEG/reflex results are not universal clinical guidance; no opioid receptor mechanism was tested.
nutrient_topic
Sucrose chapter; direct sucrose observations are distinguished from shared component metabolism. · Sucrose
organism
59 newborn infants randomized; 44 included in primary EEG analysis
plain_language
Oral sucrose lowered the composite PIPP score after heel lance compared with water in the neonatal randomized trial.
primary_references
Oral sucrose as an analgesic drug for procedural pain in newborn infants: a randomised controlled trial. (2010). https://pubmed.ncbi.nlm.nih.gov/20817247/ DOI: 10.1016/S0140-6736(10)61303-7
route
Oral solution before clinically required heel lance
tissue
Heel-lance behavioral score, EEG and spinal reflex
Sucrose: mechanism of action and metabolic impact (2026-09-20) · lines 475–485
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 · 59 newborn infants randomized; 44 included in primary EEG analysis · source_derived_draft · unverified_draft
## sucrose-neonatal-pipp Oral sucrose lowered the composite PIPP score after heel lance compared with water in the neonatal randomized trial. Model/species: 59 newborn infants randomized; 44 included in primary EEG analysis Tissue: Heel-lance behavioral score, EEG and spinal reflex Exposure: 0.5 mL of 24% sucrose versus 0.5 mL sterile water Route: Oral solution before clinically required heel lance Duration: 2 minutes before lance; acute responses Exposure scope: Neonatal sensory and nociceptive endpoints Limits: Twenty sucrose and 24 water infants in primary EEG analysis. Different pain-related readouts are not interchangeable. Null EEG/reflex results are not universal clinical guidance; no opioid receptor mechanism was tested. Reference: Oral sucrose as an analgesic drug for procedural pain in newborn infants: a randomised controlled trial. (2010). https://pubmed.ncbi.nlm.nih.gov/20817247/ DOI: 10.1016/S0140-6736(10)61303-7 Access: Primary full-text methods/results and metadata inspected.
Complete structured claim and evidence
Oral sucrose did not significantly reduce heel-lance nociceptive EEG activity compared with water.
Sucrose → Human neonatal heel-lance nociceptive EEG activity source_derived_draftungraded
Experimental context and source evidence
dose
0.5 mL of 24% sucrose versus 0.5 mL sterile water
duration
2 minutes before lance; acute responses
evidence_access
Primary full-text methods/results and metadata inspected.
evidence_scope
literature_reviewed; source-specific curation
experimental_model
59 newborn infants randomized; 44 included in primary EEG analysis
exposure_scope
Neonatal sensory and nociceptive endpoints
limitations
Twenty sucrose and 24 water infants in primary EEG analysis. Different pain-related readouts are not interchangeable. Null EEG/reflex results are not universal clinical guidance; no opioid receptor mechanism was tested.
nutrient_topic
Sucrose chapter; direct sucrose observations are distinguished from shared component metabolism. · Sucrose
organism
59 newborn infants randomized; 44 included in primary EEG analysis
plain_language
Oral sucrose did not significantly reduce heel-lance nociceptive EEG activity compared with water.
primary_references
Oral sucrose as an analgesic drug for procedural pain in newborn infants: a randomised controlled trial. (2010). https://pubmed.ncbi.nlm.nih.gov/20817247/ DOI: 10.1016/S0140-6736(10)61303-7
route
Oral solution before clinically required heel lance
tissue
Heel-lance behavioral score, EEG and spinal reflex
Sucrose: mechanism of action and metabolic impact (2026-09-20) · lines 487–497
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 · 59 newborn infants randomized; 44 included in primary EEG analysis · source_derived_draft · unverified_draft
## sucrose-neonatal-eeg-null Oral sucrose did not significantly reduce heel-lance nociceptive EEG activity compared with water. Model/species: 59 newborn infants randomized; 44 included in primary EEG analysis Tissue: Heel-lance behavioral score, EEG and spinal reflex Exposure: 0.5 mL of 24% sucrose versus 0.5 mL sterile water Route: Oral solution before clinically required heel lance Duration: 2 minutes before lance; acute responses Exposure scope: Neonatal sensory and nociceptive endpoints Limits: Twenty sucrose and 24 water infants in primary EEG analysis. Different pain-related readouts are not interchangeable. Null EEG/reflex results are not universal clinical guidance; no opioid receptor mechanism was tested. Reference: Oral sucrose as an analgesic drug for procedural pain in newborn infants: a randomised controlled trial. (2010). https://pubmed.ncbi.nlm.nih.gov/20817247/ DOI: 10.1016/S0140-6736(10)61303-7 Access: Primary full-text methods/results and metadata inspected.
Complete structured claim and evidence
Oral sucrose did not significantly reduce the spinal withdrawal reflex after heel lance compared with water.
Sucrose → Human neonatal heel-lance spinal withdrawal reflex source_derived_draftungraded
Experimental context and source evidence
dose
0.5 mL of 24% sucrose versus 0.5 mL sterile water
duration
2 minutes before lance; acute responses
evidence_access
Primary full-text methods/results and metadata inspected.
evidence_scope
literature_reviewed; source-specific curation
experimental_model
59 newborn infants randomized; 44 included in primary EEG analysis
exposure_scope
Neonatal sensory and nociceptive endpoints
limitations
Twenty sucrose and 24 water infants in primary EEG analysis. Different pain-related readouts are not interchangeable. Null EEG/reflex results are not universal clinical guidance; no opioid receptor mechanism was tested.
nutrient_topic
Sucrose chapter; direct sucrose observations are distinguished from shared component metabolism. · Sucrose
organism
59 newborn infants randomized; 44 included in primary EEG analysis
plain_language
Oral sucrose did not significantly reduce the spinal withdrawal reflex after heel lance compared with water.
primary_references
Oral sucrose as an analgesic drug for procedural pain in newborn infants: a randomised controlled trial. (2010). https://pubmed.ncbi.nlm.nih.gov/20817247/ DOI: 10.1016/S0140-6736(10)61303-7
route
Oral solution before clinically required heel lance
tissue
Heel-lance behavioral score, EEG and spinal reflex
Sucrose: mechanism of action and metabolic impact (2026-09-20) · lines 499–509
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 · 59 newborn infants randomized; 44 included in primary EEG analysis · source_derived_draft · unverified_draft
## sucrose-neonatal-reflex-null Oral sucrose did not significantly reduce the spinal withdrawal reflex after heel lance compared with water. Model/species: 59 newborn infants randomized; 44 included in primary EEG analysis Tissue: Heel-lance behavioral score, EEG and spinal reflex Exposure: 0.5 mL of 24% sucrose versus 0.5 mL sterile water Route: Oral solution before clinically required heel lance Duration: 2 minutes before lance; acute responses Exposure scope: Neonatal sensory and nociceptive endpoints Limits: Twenty sucrose and 24 water infants in primary EEG analysis. Different pain-related readouts are not interchangeable. Null EEG/reflex results are not universal clinical guidance; no opioid receptor mechanism was tested. Reference: Oral sucrose as an analgesic drug for procedural pain in newborn infants: a randomised controlled trial. (2010). https://pubmed.ncbi.nlm.nih.gov/20817247/ DOI: 10.1016/S0140-6736(10)61303-7 Access: Primary full-text methods/results and metadata inspected.
Complete structured claim and evidence
Normal intestinal SGLT1 couples glucose entry to the inward sodium electrochemical gradient.
Human sodium/glucose cotransporter SGLT1 / SLC5A1 → D-glucose source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/sodium-research/2008213.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ba4e32dc5111895acfe9e109cf57a7e07bc3c4e07e82ad3b4f7715cfaf10af74", "start_char": 0, "end_char": 1357, "text_sha256": "ba4e32dc5111895acfe9e109cf57a7e07bc3c4e07e82ad3b4f7715cfaf10af74"}
experimental_model
Family segregation and Xenopus oocyte transport assay
exposure
Disease-associated SGLT1 missense variant versus normal transporter
limitations
A genetic transporter defect is not sodium dietary deficiency; the sugar-malabsorption phenotype must not be presented as a reason to add salt.
nutrient_topic
Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
organism
Human SGLT1 expressed in frog oocytes
plain_language
A sodium gradient helps intestinal cells take up glucose.
primary_references
[sodium-p2008213] Glucose/galactose malabsorption caused by a defect in the Na+/glucose cotransporter. (1991). https://pubmed.ncbi.nlm.nih.gov/2008213/ DOI: 10.1038/350354a0
tissue_or_cell_type
Intestinal brush border
transport_effect
raises Couples glucose entry to the inward sodium electrochemical gradient.
transport_pool
the enterocyte interior Couples glucose entry to the inward sodium electrochemical gradient.
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 291–302
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Family segregation and Xenopus oocyte transport assay · source_derived_draft · unverified_draft
### sodium-sglt1-gradient Normal intestinal SGLT1 couples glucose entry to the inward sodium electrochemical gradient. Condition category: normal nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A sodium gradient helps intestinal cells take up glucose. organism: Human SGLT1 expressed in frog oocytes tissue_or_cell_type: Intestinal brush border experimental_model: Family segregation and Xenopus oocyte transport assay limitations: A genetic transporter defect is not sodium dietary deficiency; the sugar-malabsorption phenotype must not be presented as a reason to add salt. exposure: Disease-associated SGLT1 missense variant versus normal transporter evidence_span: {"source_cache": "artifacts/sodium-research/2008213.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ba4e32dc5111895acfe9e109cf57a7e07bc3c4e07e82ad3b4f7715cfaf10af74", "start_char": 0, "end_char": 1357, "text_sha256": "ba4e32dc5111895acfe9e109cf57a7e07bc3c4e07e82ad3b4f7715cfaf10af74"} [sodium-p2008213] Glucose/galactose malabsorption caused by a defect in the Na+/glucose cotransporter. (1991). https://pubmed.ncbi.nlm.nih.gov/2008213/ DOI: 10.1038/350354a0
Complete structured claim and evidence
Expressed human GLUT5 selectively transported fructose, with a reported Km near 6 mM.
Human fructose transporter GLUT5 / SLC2A5 → Fructose source_derived_draftungraded
Experimental context and source evidence
dose
Fructose kinetic series; reported Km about 6 mM
duration
Assay interval unavailable in abstract
evidence_access
Primary abstract/metadata; unrecovered methods explicitly retained.
evidence_scope
literature_reviewed; source-specific curation
experimental_model
Human GLUT5 expressed in Xenopus oocytes
exposure_scope
Isolated fructose / human protein
limitations
Human protein in an amphibian expression system; not a measured human intake threshold.
nutrient_topic
HFCS chapter: actual formulation studies, component biochemistry and interventions are explicitly distinguished. · High-Fructose Corn Syrup / HFCS
organism
Human GLUT5 expressed in Xenopus oocytes
plain_language
Expressed human GLUT5 selectively transported fructose, with a reported Km near 6 mM.
primary_references
Fructose transporter in human spermatozoa and small intestine is GLUT5. (1992). https://pubmed.ncbi.nlm.nih.gov/1634504/
route
In vitro substrate addition
tissue
Recombinant transport assay
transport_effect
raises Fructose uptake measured in the expressing cell with a reported Km near 6 mM.
transport_pool
the expressing cell Fructose uptake measured in the expressing cell with a reported Km near 6 mM.
High-Fructose Corn Syrup: mechanism of action and metabolic impact (2026-09-20) · lines 65–75
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 · Human GLUT5 expressed in Xenopus oocytes · source_derived_draft · unverified_draft
## hfcs-glut5 Expressed human GLUT5 selectively transported fructose, with a reported Km near 6 mM. Model/species: Human GLUT5 expressed in Xenopus oocytes Tissue: Recombinant transport assay Exposure: Fructose kinetic series; reported Km about 6 mM Route: In vitro substrate addition Duration: Assay interval unavailable in abstract Exposure scope: Isolated fructose / human protein Limits: Human protein in an amphibian expression system; not a measured human intake threshold. Reference: Fructose transporter in human spermatozoa and small intestine is GLUT5. (1992). https://pubmed.ncbi.nlm.nih.gov/1634504/ Access: Primary abstract/metadata; unrecovered methods explicitly retained.
Complete structured claim and evidence
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
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
Deleting intestinal Khk-C increased fructose spillover and hepatic lipogenesis during sucrose feeding in mice.
Mouse ketohexokinase C isoform / Khk-C → Mouse hepatic de novo lipogenesis source_derived_draftungraded
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
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
HFCS and sucrose produced similar 24-hour insulin profiles with isocaloric meals.
HFCS-55 → Human endocrine responses to HFCS versus sucrose source_derived_draftungraded
Experimental context and source evidence
dose
HFCS or sucrose beverages with 3 isocaloric meals; exact sugar allocation not recovered from primary abstract
duration
24-hour profiles
evidence_access
Primary abstract/metadata; unrecovered methods explicitly retained.
evidence_scope
literature_reviewed; source-specific curation
experimental_model
34 adults in crossover meal study; 8 men also received pure monosaccharides
exposure_scope
Direct HFCS versus sucrose
limitations
Short feeding study; eight-man fructose/glucose comparison is a subset and does not establish long-term equivalence or appetite control.
nutrient_topic
HFCS chapter: actual formulation studies, component biochemistry and interventions are explicitly distinguished. · High-Fructose Corn Syrup / HFCS
organism
34 adults in crossover meal study; 8 men also received pure monosaccharides
plain_language
HFCS and sucrose produced similar 24-hour insulin profiles with isocaloric meals.
primary_references
Twenty-four-hour endocrine and metabolic profiles following consumption of high-fructose corn syrup-, sucrose-, fructose-, and glucose-sweetened beverages with meals. (2008). https://pubmed.ncbi.nlm.nih.gov/18469239/ DOI: 10.1093/ajcn/87.5.1194
route
Oral beverages with meals
tissue
24-hour endocrine and triglyceride profiles
High-Fructose Corn Syrup: mechanism of action and metabolic impact (2026-09-20) · lines 353–363
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 · 34 adults in crossover meal study; 8 men also received pure monosaccharides · source_derived_draft · unverified_draft
## hfcs-acute-insulin HFCS and sucrose produced similar 24-hour insulin profiles with isocaloric meals. Model/species: 34 adults in crossover meal study; 8 men also received pure monosaccharides Tissue: 24-hour endocrine and triglyceride profiles Exposure: HFCS or sucrose beverages with 3 isocaloric meals; exact sugar allocation not recovered from primary abstract Route: Oral beverages with meals Duration: 24-hour profiles Exposure scope: Direct HFCS versus sucrose Limits: Short feeding study; eight-man fructose/glucose comparison is a subset and does not establish long-term equivalence or appetite control. Reference: Twenty-four-hour endocrine and metabolic profiles following consumption of high-fructose corn syrup-, sucrose-, fructose-, and glucose-sweetened beverages with meals. (2008). https://pubmed.ncbi.nlm.nih.gov/18469239/ DOI: 10.1093/ajcn/87.5.1194 Access: Primary abstract/metadata; unrecovered methods explicitly retained.
Complete structured claim and evidence
HFCS and sucrose produced similar 24-hour circulating leptin profiles in the crossover study.
HFCS-55 → LEP source_derived_draftungraded
Experimental context and source evidence
dose
HFCS or sucrose beverages with 3 isocaloric meals; exact sugar allocation not recovered from primary abstract
duration
24-hour profiles
evidence_access
Primary abstract/metadata; unrecovered methods explicitly retained.
evidence_scope
literature_reviewed; source-specific curation
experimental_model
34 adults in crossover meal study; 8 men also received pure monosaccharides
exposure_scope
Direct HFCS versus sucrose
limitations
Short feeding study; eight-man fructose/glucose comparison is a subset and does not establish long-term equivalence or appetite control.
nutrient_topic
HFCS chapter: actual formulation studies, component biochemistry and interventions are explicitly distinguished. · High-Fructose Corn Syrup / HFCS
organism
34 adults in crossover meal study; 8 men also received pure monosaccharides
plain_language
HFCS and sucrose produced similar 24-hour circulating leptin profiles in the crossover study.
primary_references
Twenty-four-hour endocrine and metabolic profiles following consumption of high-fructose corn syrup-, sucrose-, fructose-, and glucose-sweetened beverages with meals. (2008). https://pubmed.ncbi.nlm.nih.gov/18469239/ DOI: 10.1093/ajcn/87.5.1194
route
Oral beverages with meals
tissue
24-hour endocrine and triglyceride profiles
High-Fructose Corn Syrup: mechanism of action and metabolic impact (2026-09-20) · lines 365–375
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 · 34 adults in crossover meal study; 8 men also received pure monosaccharides · source_derived_draft · unverified_draft
## hfcs-acute-leptin HFCS and sucrose produced similar 24-hour circulating leptin profiles in the crossover study. Model/species: 34 adults in crossover meal study; 8 men also received pure monosaccharides Tissue: 24-hour endocrine and triglyceride profiles Exposure: HFCS or sucrose beverages with 3 isocaloric meals; exact sugar allocation not recovered from primary abstract Route: Oral beverages with meals Duration: 24-hour profiles Exposure scope: Direct HFCS versus sucrose Limits: Short feeding study; eight-man fructose/glucose comparison is a subset and does not establish long-term equivalence or appetite control. Reference: Twenty-four-hour endocrine and metabolic profiles following consumption of high-fructose corn syrup-, sucrose-, fructose-, and glucose-sweetened beverages with meals. (2008). https://pubmed.ncbi.nlm.nih.gov/18469239/ DOI: 10.1093/ajcn/87.5.1194 Access: Primary abstract/metadata; unrecovered methods explicitly retained.
Complete structured claim and evidence
In the eight-man subset, HFCS and sucrose produced postprandial triglyceride responses comparable to pure fructose.
HFCS-55 → Human postprandial triglyceride response source_derived_draftungraded
Experimental context and source evidence
dose
HFCS or sucrose beverages with 3 isocaloric meals; exact sugar allocation not recovered from primary abstract
duration
24-hour profiles
evidence_access
Primary abstract/metadata; unrecovered methods explicitly retained.
evidence_scope
literature_reviewed; source-specific curation
experimental_model
34 adults in crossover meal study; 8 men also received pure monosaccharides
exposure_scope
Direct HFCS versus sucrose
limitations
Short feeding study; eight-man fructose/glucose comparison is a subset and does not establish long-term equivalence or appetite control.
nutrient_topic
HFCS chapter: actual formulation studies, component biochemistry and interventions are explicitly distinguished. · High-Fructose Corn Syrup / HFCS
organism
34 adults in crossover meal study; 8 men also received pure monosaccharides
plain_language
In the eight-man subset, HFCS and sucrose produced postprandial triglyceride responses comparable to pure fructose.
primary_references
Twenty-four-hour endocrine and metabolic profiles following consumption of high-fructose corn syrup-, sucrose-, fructose-, and glucose-sweetened beverages with meals. (2008). https://pubmed.ncbi.nlm.nih.gov/18469239/ DOI: 10.1093/ajcn/87.5.1194
route
Oral beverages with meals
tissue
24-hour endocrine and triglyceride profiles
High-Fructose Corn Syrup: mechanism of action and metabolic impact (2026-09-20) · lines 377–387
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 · 34 adults in crossover meal study; 8 men also received pure monosaccharides · source_derived_draft · unverified_draft
## hfcs-acute-tg In the eight-man subset, HFCS and sucrose produced postprandial triglyceride responses comparable to pure fructose. Model/species: 34 adults in crossover meal study; 8 men also received pure monosaccharides Tissue: 24-hour endocrine and triglyceride profiles Exposure: HFCS or sucrose beverages with 3 isocaloric meals; exact sugar allocation not recovered from primary abstract Route: Oral beverages with meals Duration: 24-hour profiles Exposure scope: Direct HFCS versus sucrose Limits: Short feeding study; eight-man fructose/glucose comparison is a subset and does not establish long-term equivalence or appetite control. Reference: Twenty-four-hour endocrine and metabolic profiles following consumption of high-fructose corn syrup-, sucrose-, fructose-, and glucose-sweetened beverages with meals. (2008). https://pubmed.ncbi.nlm.nih.gov/18469239/ DOI: 10.1093/ajcn/87.5.1194 Access: Primary abstract/metadata; unrecovered methods explicitly retained.
Complete structured claim and evidence
Sucrose beverages also increased basal hepatic fractional fatty-acid synthesis/secretion; glucose did not in the same trial.
Sucrose → Human basal hepatic fractional fatty-acid synthesis/secretion source_derived_draftungraded
Experimental context and source evidence
dose
Fructose, sucrose or glucose 80 g/day versus sweetened-beverage abstinence
duration
7 weeks
evidence_access
Primary abstract/metadata; unrecovered methods explicitly retained.
evidence_scope
literature_reviewed; source-specific curation
experimental_model
94 healthy men completing randomized beverage intervention
exposure_scope
Component sugars and sucrose
limitations
Total reported energy intake was similar across groups; this was not a metabolic-ward clamp. Fractional fatty-acid synthesis is distinct from total liver fat and VLDL-TG output. No HFCS arm.
nutrient_topic
HFCS chapter: actual formulation studies, component biochemistry and interventions are explicitly distinguished. · High-Fructose Corn Syrup / HFCS
organism
94 healthy men completing randomized beverage intervention
plain_language
Sucrose beverages also increased basal hepatic fractional fatty-acid synthesis/secretion; glucose did not in the same trial.
primary_references
Fructose- and sucrose- but not glucose-sweetened beverages promote hepatic de novo lipogenesis: A randomized controlled trial. (2021). https://pubmed.ncbi.nlm.nih.gov/33684506/ DOI: 10.1016/j.jhep.2021.02.027
route
Oral beverages in addition to usual diet
tissue
Stable-isotope hepatic lipid synthesis
High-Fructose Corn Syrup: mechanism of action and metabolic impact (2026-09-20) · lines 401–411
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 · 94 healthy men completing randomized beverage intervention · source_derived_draft · unverified_draft
## hfcs-sucrose-dnl Sucrose beverages also increased basal hepatic fractional fatty-acid synthesis/secretion; glucose did not in the same trial. Model/species: 94 healthy men completing randomized beverage intervention Tissue: Stable-isotope hepatic lipid synthesis Exposure: Fructose, sucrose or glucose 80 g/day versus sweetened-beverage abstinence Route: Oral beverages in addition to usual diet Duration: 7 weeks Exposure scope: Component sugars and sucrose Limits: Total reported energy intake was similar across groups; this was not a metabolic-ward clamp. Fractional fatty-acid synthesis is distinct from total liver fat and VLDL-TG output. No HFCS arm. Reference: Fructose- and sucrose- but not glucose-sweetened beverages promote hepatic de novo lipogenesis: A randomized controlled trial. (2021). https://pubmed.ncbi.nlm.nih.gov/33684506/ DOI: 10.1016/j.jhep.2021.02.027 Access: Primary abstract/metadata; unrecovered methods explicitly retained.
Complete structured claim and evidence
In six adults, 0.5 g/kg sucrose with consommé containing 50 mg/kg MSG reduced peak plasma glutamate from 18.1 to 5.48 micromol/dL and reduced exposure area.
Sucrose → Plasma glutamate concentration source_derived_draftungraded
Experimental context and source evidence
availability_state
biomarker_context Imported condition classification; unverified.
evidence_access
Primary abstract
experimental_model
Randomized crossover; three women and three men.
limitations
Same research group as the starch study; small acute experiment, not independent mechanistic replication.
nutrient_topic
Monosodium Glutamate (MSG) collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Monosodium L-glutamate
plain_language
A second carbohydrate changed the response at a different MSG dose.
primary_references
Effect of sucrose ingestion on plasma glutamate concentrations in humans administered monosodium L-glutamate. · 1986 · https://pubmed.ncbi.nlm.nih.gov/2870635/ · DOI 10.1093/ajcn/43.4.510
trigger_kind
biomarker_context Imported condition classification; unverified.
Monosodium Glutamate (MSG): taste, gut sensing, exposure and cross-nutrient mechanisms (2026-09-20) · lines 42–48
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Randomized crossover; three women and three men. · source_derived_draft · unverified_draft
## monosodium-glutamate-sucrose-exposure A second carbohydrate changed the response at a different MSG dose. In six adults, 0.5 g/kg sucrose with consommé containing 50 mg/kg MSG reduced peak plasma glutamate from 18.1 to 5.48 micromol/dL and reduced exposure area. Model: Randomized crossover; three women and three men. Limitations: Same research group as the starch study; small acute experiment, not independent mechanistic replication. Evidence access: Primary abstract Effect of sucrose ingestion on plasma glutamate concentrations in humans administered monosodium L-glutamate. · 1986 · https://pubmed.ncbi.nlm.nih.gov/2870635/ · DOI 10.1093/ajcn/43.4.510
Complete structured claim and evidence
Adding gamma-nonalactone increased rated sweetness of 5% sucrose solution by a reported 23.0% at the optimal tested concentration.
Gamma-nonalactone → Human perceived sweetness of sucrose solution source_derived_draftungraded
Experimental context and source evidence
dose
Gamma-nonalactone concentration series; optimal sweetness reported at 10 mg/kg solution; propylene glycol used at 0.1-0.2% for poorly soluble compounds
duration
Acute sensory sessions; at least 2 min between samples
evidence_access
Primary full-text methods/results inspected; PubMed metadata where indexed.
evidence_scope
literature_reviewed; model-specific source-derived curation
experimental_model
Ten trained human sensory evaluators; five men and five women, mean age 24 years
limitations
Small trained panel and matrix-specific perception, not a glycemic or dietary-intake trial. Docking and molecular dynamics do not prove T1R2/T1R3 activation or binding.
nutrient_topic
Gamma-nonalactone flavor-compound chapter; nutrient and drug interactions retain their experimental settings. · Gamma-nonalactone
organism
Ten trained human sensory evaluators; five men and five women, mean age 24 years
plain_language
Adding gamma-nonalactone increased rated sweetness of 5% sucrose solution by a reported 23.0% at the optimal tested concentration.
primary_references
Sweetness enhancement and mechanism by sweet aroma compounds in the sucrose solution using sensory, electronic tongue, molecular docking, and molecular dynamics simulation. (2026). https://pubmed.ncbi.nlm.nih.gov/41884462/ DOI: 10.1016/j.fochx.2026.103753
route
Oral tasting followed by expectoration
tissue
Sweetness ratings in 5% sucrose solution
Gamma-nonalactone: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 235–244
Original AI-assisted curation of eight primary studies. Study-specific citations, negative findings and limitations retained. Not publisher full text. · supports · Ten trained human sensory evaluators; five men and five women, mean age 24 years · source_derived_draft · unverified_draft
## gamma-nonalactone-sucrose-sweetness Adding gamma-nonalactone increased rated sweetness of 5% sucrose solution by a reported 23.0% at the optimal tested concentration. Model/species: Ten trained human sensory evaluators; five men and five women, mean age 24 years Tissue: Sweetness ratings in 5% sucrose solution Exposure: Gamma-nonalactone concentration series; optimal sweetness reported at 10 mg/kg solution; propylene glycol used at 0.1-0.2% for poorly soluble compounds Route: Oral tasting followed by expectoration Duration: Acute sensory sessions; at least 2 min between samples Limits: Small trained panel and matrix-specific perception, not a glycemic or dietary-intake trial. Docking and molecular dynamics do not prove T1R2/T1R3 activation or binding. Primary reference: Sweetness enhancement and mechanism by sweet aroma compounds in the sucrose solution using sensory, electronic tongue, molecular docking, and molecular dynamics simulation. (2026). https://pubmed.ncbi.nlm.nih.gov/41884462/ DOI: 10.1016/j.fochx.2026.103753 Access: Primary full-text methods/results inspected; PubMed metadata where indexed.
Complete structured claim and evidence

Availability and dependencies

Each situation shows the normal role first, then what the sources report under a specific condition. A shortfall in the diet, a fault in the machinery, and a low blood reading are kept separate because they are not the same thing.

Sacrosidase replacement improves sucrose handling in congenital enzyme deficiency

Condition: machinery_impairment · Congenital sucrase-isomaltase deficiency

Normal role: Sucrase hydrolysis makes sucrose-derived monosaccharides available for absorption.

Recorded consequence: Replacement lowers sucrose breath hydrogen, stool frequency and gastrointestinal symptoms.

Scope: Randomized pediatric enzyme-replacement study

Pharmacological inhibition slows sucrose digestion

Condition: machinery_impairment · Oral acarbose inhibition of carbohydrate hydrolases

Normal role: Sucrose hydrolysis precedes absorption of glucose and fructose.

Recorded consequence: Sucrose glycemic response falls; high experimental dose increases breath hydrogen.

Scope: 200 or 50 mg acarbose with 50 g carbohydrate challenges

Bacterial glucosyltransferase deletion disrupts sucrose-dependent biofilm structure

Condition: machinery_impairment · gtfB deletion or combined gtfB/gtfC deletion

Normal role: Gtf-mediated sucrose utilization builds extracellular glucans.

Recorded consequence: Microcolony formation and matrix abundance are reduced.

Scope: In vitro oral bacterial genetics

The sources

Every document behind this chapter is preserved word for word. Open one to read it in full with its recorded conflicts marked in place.

Gamma-nonalactone: mechanisms, molecular forms and cross-actor connections (2026-09-20)Original AI-assisted curation of eight primary studies. Study-specific citations, negative findings and limitations retained. Not publisher full text. · unverified_draftRead preserved source
High-Fructose Corn Syrup: mechanism of action and metabolic impact (2026-09-20)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. · unverified_draftRead preserved source
Monosodium Glutamate (MSG): taste, gut sensing, exposure and cross-nutrient mechanisms (2026-09-20)AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · unverified_draftRead preserved source
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17)AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · unverified_draftRead preserved source
Sucrose: mechanism of action and metabolic impact (2026-09-20)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. · unverified_draftRead preserved source

Recorded disagreements

Where two sources say different things, both are kept and the difference is explained. You can discuss a disagreement or propose a mechanism that might account for it.

Open questions in this collection

Questions the curators could not answer from the sources in front of them, kept here with the reason each one is still open. These are gaps in this collection, not findings or proof that no one has studied them.

Chapters are assembled from supplied drafts and curated literature summaries. Statements remain unverified against the primary studies, and the ledger is not medical advice.

Evidence, AI assistance and curation standards

Sucrose

The mechanisms

Human sucrase-isomaltase hydrolyzes sucrose, releasing its glucose moiety.

Cleavage of sucrose by human sucrase-isomaltase also releases fructose.

Adding 0.7 mM glucose partially inhibited sucrose hydrolysis in the human intestinal brush-border enzyme preparation.

Sucrose elicited a calcium response in cells coexpressing human TAS1R2 and TAS1R3, but not either subunit alone.

Lactisole inhibited the sucrose-evoked response of expressed human TAS1R2/TAS1R3.

Coapplied MSG attenuated the sucrose-evoked calcium response in cells expressing human TAS1R2/TAS1R3.

Coapplied Glu-Glu attenuated the sucrose-evoked calcium response in cells expressing human TAS1R2/TAS1R3.

Coapplied Glu-Asp attenuated the sucrose-evoked calcium response in cells expressing human TAS1R2/TAS1R3.

Adding 60 ppm lactisole to the sucrose drink increased subsequent breakfast energy intake by 12.9 +/- 5.8% in the male crossover study.

Adding lactisole to sucrose lowered the plasma serotonin change at 30 minutes relative to sucrose alone.

Adding lactisole to sucrose did not significantly change postprandial plasma CCK.

Adding lactisole to sucrose did not significantly change postprandial plasma ghrelin.

Sacrosidase, with or without milk, reduced breath hydrogen after sucrose compared with placebo in children with CSID.

Higher sacrosidase concentrations reduced stool frequency relative to lower concentrations during carbohydrate-containing diets in children with CSID.

Higher sacrosidase concentrations reduced gas, cramps and bloating during carbohydrate-containing diets in children with CSID.

Acarbose 200 mg reduced blood-glucose response area by 89% after a 50 g sucrose load in healthy volunteers.

Breath hydrogen after 200 mg acarbose with 50 g sucrose indicated nearly complete sucrose malabsorption in the tolerance study.

Acarbose 200 mg had no detected effect on the blood-glucose response to a glucose-only load.

Acarbose 50 mg still reduced the blood-glucose response to sucrose, without a significant breath-hydrogen increase.

Reducing added sucrose from 50 to 5 g lowered the 15-minute active GLP-1 response to the mixed meal.

Matching sweetness with nonnutritive sweeteners did not restore the GLP-1 response lost when meal sucrose was reduced.

Acarbose pretreatment prolonged active GLP-1 elevation to 60 minutes after the sucrose-containing mixed meal.

Acarbose pretreatment prevented the 120-minute ApoB-48 increase after the sucrose-containing mixed meal.

Liver glycogen did not significantly decline during three hours of cycling with sucrose ingestion; preservation did not differ from glucose.

Muscle glycogen declined during prolonged cycling despite sucrose ingestion, as it did with glucose ingestion.

Whole-body carbohydrate utilization during cycling was greater with sucrose than glucose, 2.03 versus 1.66 g/min.

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

Sucrose beverages reduced Matsuda insulin sensitivity compared with aspartame in the matched-group intervention.

Sucrose beverages increased postprandial triglycerides compared with aspartame after the intervention.

Sucrose beverages increased fasting LDL cholesterol compared with aspartame.

Sucrose beverages increased 24-hour plasma urate exposure compared with aspartame.

None of ten healthy volunteers showed breath-hydrogen malabsorption after the tested 50, 75 or 100 g sucrose loads.

Sucrose-supported multispecies cultures formed a glucan matrix and structured microcolonies; glucose cultures did not form that matrix under the tested conditions.

Deleting gtfB markedly disrupted S. mutans microcolony formation on saliva-coated hydroxyapatite.

Deleting both gtfB and gtfC produced the greatest reduction in the S. mutans extracellular matrix among the tested mutants.

Repeated sucrose exposure lowered calcium concentration in whole in-situ dental biofilm relative to water.

Sucrose exposure did not lower calcium in the biofilm fluid compartment, including after the cariogenic challenge.

Increasing fluoride from 0.50 to 0.75 ppm reduced enamel mineral loss during repeated sucrose exposure in the artificial-mouth model.

Oral sucrose lowered the composite PIPP score after heel lance compared with water in the neonatal randomized trial.

Oral sucrose did not significantly reduce heel-lance nociceptive EEG activity compared with water.

Oral sucrose did not significantly reduce the spinal withdrawal reflex after heel lance compared with water.

Normal intestinal SGLT1 couples glucose entry to the inward sodium electrochemical gradient.

Expressed human GLUT5 selectively transported fructose, with a reported Km near 6 mM.

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

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

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

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

HFCS and sucrose produced similar 24-hour insulin profiles with isocaloric meals.

HFCS and sucrose produced similar 24-hour circulating leptin profiles in the crossover study.

In the eight-man subset, HFCS and sucrose produced postprandial triglyceride responses comparable to pure fructose.

Sucrose beverages also increased basal hepatic fractional fatty-acid synthesis/secretion; glucose did not in the same trial.

In six adults, 0.5 g/kg sucrose with consommé containing 50 mg/kg MSG reduced peak plasma glutamate from 18.1 to 5.48 micromol/dL and reduced exposure area.

Adding gamma-nonalactone increased rated sweetness of 5% sucrose solution by a reported 23.0% at the optimal tested concentration.

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