Glucagon-like peptide 1 / GLP-1

evidence_span

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experimental_model

Randomised double-blind crossover trial in 33 normal-weight subjects with an unrestricted test meal

exposure

A breakfast containing 4 grams of high molecular weight oat beta-glucan against a control breakfast

limitations

An acute crossover in normal-weight subjects. Fullness and satiety rose without any change in what was actually eaten afterwards.

nutrient_topic

Beta-glucan research collection; topical membership is not evidence of a direct clinical effect, and each preparation is recorded as its own entity with no family link joining any pair. · Beta-glucan

organism

Human

plain_language

People felt fuller and ate the same amount, and the gut hormone usually credited for fullness went down, not up.

primary_references

[bg-p29920323] Effects of oat β-glucan consumption at breakfast on ad libitum eating, appetite, glycemia, insulinemia and GLP-1 concentrations in healthy subjects. (2018). https://pubmed.ncbi.nlm.nih.gov/29920323/ DOI: 10.1016/j.appet.2018.06.019

tissue_or_cell_type

Postprandial circulation and appetite

Beta-glucan: a structural family rather than an agent, what decides whether a bound glucan actually signals, the complement route that a cereal and a yeast preparation share, and the unequal human evidence behind each (2026-09-22) · lines 593–604

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomised double-blind crossover trial in 33 normal-weight subjects with an unrestricted test meal · source_derived_draft · unverified_draft

### bg-satiety-rises-but-glp1-falls Oat beta-glucan increased feelings of fullness and satiety but did not affect energy and amount eaten at the ad libitum test meal, and there was a treatment by time interaction for plasma GLP-1, plasma insulin and blood glucose, with GLP-1 significantly reduced at 90 minutes, blood glucose at 30 minutes and plasma insulin at 30 and 60 minutes following the oat beta-glucan breakfast compared with the control breakfast, so four grams of high molecular weight oat beta-glucan lowers appetite but not ad libitum eating and beneficially modulates postprandial glycaemia, it does however not increase plasma GLP-1 secretion. Condition category: normal nutrient_topic: Beta-glucan research collection; topical membership is not evidence of a direct clinical effect, and each preparation is recorded as its own entity with no family link joining any pair. plain_language: People felt fuller and ate the same amount, and the gut hormone usually credited for fullness went down, not up. organism: Human tissue_or_cell_type: Postprandial circulation and appetite experimental_model: Randomised double-blind crossover trial in 33 normal-weight subjects with an unrestricted test meal limitations: An acute crossover in normal-weight subjects. Fullness and satiety rose without any change in what was actually eaten afterwards. exposure: A breakfast containing 4 grams of high molecular weight oat beta-glucan against a control breakfast evidence_span: {"source_cache": "artifacts/glucan-research/29920323.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8038ec81d42b26e4b4892cd24cd0ce26597ba28ef57296a90062428f6ecbceb4", "start_char": 0, "end_char": 1413, "text_sha256": "8038ec81d42b26e4b4892cd24cd0ce26597ba28ef57296a90062428f6ecbceb4"} [bg-p29920323] Effects of oat β-glucan consumption at breakfast on ad libitum eating, appetite, glycemia, insulinemia and GLP-1 concentrations in healthy subjects. (2018). https://pubmed.ncbi.nlm.nih.gov/29920323/ DOI: 10.1016/j.appet.2018.06.019

evidence_span

{"source_cache": "artifacts/metformin-research/27216492.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c874a5c13e2e709b4b36040f281e2b187e7956b4610decddc35403170c0ed45d", "start_char": 0, "end_char": 3863, "text_sha256": "c874a5c13e2e709b4b36040f281e2b187e7956b4610decddc35403170c0ed45d"}

experimental_model

Two randomised crossover trials of delayed-release metformin targeted to the ileum

exposure

Delayed-release versus immediate-release metformin over 5 to 7 day periods

limitations

The dissociation of effect from plasma exposure is the key observation. Funded by the manufacturer of the delayed-release formulation, which the record retains.

nutrient_topic

Metformin research collection; topical membership is not evidence of a direct clinical effect, and pharmacological exposure is not dietary intake. · Metformin

organism

Human

plain_language

Gut hormones rose alongside the glucose effect.

primary_references

[metformin-p27216492] Once-daily delayed-release metformin lowers plasma glucose and enhances fasting and postprandial GLP-1 and PYY: results from two randomised trials. (2016). https://pubmed.ncbi.nlm.nih.gov/27216492/ DOI: 10.1007/s00125-016-3992-6

tissue_or_cell_type

Distal small intestine

Metformin: transport, molecular targets, gut mechanisms and nutrient interactions (2026-09-19) · lines 840–851

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Two randomised crossover trials of delayed-release metformin targeted to the ileum · source_derived_draft · unverified_draft

### metformin-ileal-glp1 Fasting and postprandial GLP-1 rose with all metformin treatments, with day-5 to baseline AUC ratios of 1.6-1.9. Condition category: normal nutrient_topic: Metformin research collection; topical membership is not evidence of a direct clinical effect, and pharmacological exposure is not dietary intake. plain_language: Gut hormones rose alongside the glucose effect. organism: Human tissue_or_cell_type: Distal small intestine experimental_model: Two randomised crossover trials of delayed-release metformin targeted to the ileum limitations: The dissociation of effect from plasma exposure is the key observation. Funded by the manufacturer of the delayed-release formulation, which the record retains. exposure: Delayed-release versus immediate-release metformin over 5 to 7 day periods evidence_span: {"source_cache": "artifacts/metformin-research/27216492.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c874a5c13e2e709b4b36040f281e2b187e7956b4610decddc35403170c0ed45d", "start_char": 0, "end_char": 3863, "text_sha256": "c874a5c13e2e709b4b36040f281e2b187e7956b4610decddc35403170c0ed45d"} [metformin-p27216492] Once-daily delayed-release metformin lowers plasma glucose and enhances fasting and postprandial GLP-1 and PYY: results from two randomised trials. (2016). https://pubmed.ncbi.nlm.nih.gov/27216492/ DOI: 10.1007/s00125-016-3992-6

evidence_access

Primary abstract

experimental_model

Mouse STC-1 cells, live-cell signaling and pharmacologic experiments.

limitations

Exposure details beyond the accessed abstract are unresolved; this is not direct human gut evidence.

nutrient_topic

L-Phenylalanine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Phenylalanine

plain_language

A gut-cell model used a receptor-to-calcium pathway to release a hormone.

primary_references

Identification of a regulatory pathway of L-phenylalanine-induced GLP-1 secretion in the enteroendocrine L cells. · 2022 · https://pubmed.ncbi.nlm.nih.gov/34953208/ · DOI 10.1016/j.bbrc.2021.12.043

L-Phenylalanine: transport, protein synthesis, cofactor recycling and cross-nutrient mechanisms (2026-09-19) · lines 310–316

AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse STC-1 cells, live-cell signaling and pharmacologic experiments. · source_derived_draft · unverified_draft

## l-phenylalanine-stc-gpr142 A gut-cell model used a receptor-to-calcium pathway to release a hormone. In STC-1 enteroendocrine cells, phenylalanine stimulated a GPR142/Gq-linked calcium response contributing to GLP-1 release. Model: Mouse STC-1 cells, live-cell signaling and pharmacologic experiments. Limitations: Exposure details beyond the accessed abstract are unresolved; this is not direct human gut evidence. Evidence access: Primary abstract Identification of a regulatory pathway of L-phenylalanine-induced GLP-1 secretion in the enteroendocrine L cells. · 2022 · https://pubmed.ncbi.nlm.nih.gov/34953208/ · DOI 10.1016/j.bbrc.2021.12.043

evidence_access

Primary abstract

experimental_model

Mouse STC-1 cell transport, membrane-potential and secretion assays.

limitations

The accessed abstract does not identify a specific transporter isoform; B0AT1 is not assigned by inference.

nutrient_topic

L-Phenylalanine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Phenylalanine

plain_language

Amino-acid transport can supply an electrical signal as well as a nutrient.

primary_references

Identification of a regulatory pathway of L-phenylalanine-induced GLP-1 secretion in the enteroendocrine L cells. · 2022 · https://pubmed.ncbi.nlm.nih.gov/34953208/ · DOI 10.1016/j.bbrc.2021.12.043

L-Phenylalanine: transport, protein synthesis, cofactor recycling and cross-nutrient mechanisms (2026-09-19) · lines 318–324

AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse STC-1 cell transport, membrane-potential and secretion assays. · source_derived_draft · unverified_draft

## l-phenylalanine-stc-sodium Amino-acid transport can supply an electrical signal as well as a nutrient. Sodium-dependent phenylalanine uptake contributed to depolarization and GLP-1 secretion in STC-1 cells. Model: Mouse STC-1 cell transport, membrane-potential and secretion assays. Limitations: The accessed abstract does not identify a specific transporter isoform; B0AT1 is not assigned by inference. Evidence access: Primary abstract Identification of a regulatory pathway of L-phenylalanine-induced GLP-1 secretion in the enteroendocrine L cells. · 2022 · https://pubmed.ncbi.nlm.nih.gov/34953208/ · DOI 10.1016/j.bbrc.2021.12.043

evidence_access

Primary abstract

experimental_model

Human HuTu-80 cells, with separate mouse STC-1 experiments.

limitations

The accessed abstract does not provide the tested concentration range; no oral human GLP-1 response is asserted.

nutrient_topic

Stevia collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Stevia

plain_language

An intestinal cell sensor can connect exposure to hormone release.

primary_references

Rebaudioside A from Stevia rebaudiana stimulates GLP-1 release by enteroendocrine cells via bitter taste signalling pathways. · 2023 · https://pubmed.ncbi.nlm.nih.gov/37431625/ · DOI 10.1039/d3fo00818e

Stevia: glycoside metabolism, taste, ion channels and cross-nutrient mechanisms (2026-09-19) · lines 258–264

AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human HuTu-80 cells, with separate mouse STC-1 experiments. · source_derived_draft · unverified_draft

## stevia-gut-glp1 An intestinal cell sensor can connect exposure to hormone release. Rebaudioside A concentration-dependently stimulated GLP-1 release in human HuTu-80 enteroendocrine cells. Model: Human HuTu-80 cells, with separate mouse STC-1 experiments. Limitations: The accessed abstract does not provide the tested concentration range; no oral human GLP-1 response is asserted. Evidence access: Primary abstract Rebaudioside A from Stevia rebaudiana stimulates GLP-1 release by enteroendocrine cells via bitter taste signalling pathways. · 2023 · https://pubmed.ncbi.nlm.nih.gov/37431625/ · DOI 10.1039/d3fo00818e

evidence_access

Primary abstract

experimental_model

Human cell-line pharmacology; sweet-signaling inhibition did not explain the response.

limitations

Pharmacological inhibition does not establish exclusive receptor involvement or in vivo necessity.

nutrient_topic

Stevia collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Stevia

plain_language

A bitter receptor participates in a gut-hormone response.

primary_references

Rebaudioside A from Stevia rebaudiana stimulates GLP-1 release by enteroendocrine cells via bitter taste signalling pathways. · 2023 · https://pubmed.ncbi.nlm.nih.gov/37431625/ · DOI 10.1039/d3fo00818e

Stevia: glycoside metabolism, taste, ion channels and cross-nutrient mechanisms (2026-09-19) · lines 266–272

AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human cell-line pharmacology; sweet-signaling inhibition did not explain the response. · source_derived_draft · unverified_draft

## stevia-gut-tas2r4 A bitter receptor participates in a gut-hormone response. Inhibitor experiments in human HuTu-80 cells supported TAS2R4 involvement in rebaudioside-A-evoked GLP-1 release. Model: Human cell-line pharmacology; sweet-signaling inhibition did not explain the response. Limitations: Pharmacological inhibition does not establish exclusive receptor involvement or in vivo necessity. Evidence access: Primary abstract Rebaudioside A from Stevia rebaudiana stimulates GLP-1 release by enteroendocrine cells via bitter taste signalling pathways. · 2023 · https://pubmed.ncbi.nlm.nih.gov/37431625/ · DOI 10.1039/d3fo00818e

evidence_access

Primary abstract

experimental_model

Human enteroendocrine cell-line signaling experiments.

limitations

The species-specific human protein node is distinct from mouse Trpm5 and the incompletely resolved expression construct.

nutrient_topic

Stevia collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Stevia

plain_language

Taste-associated ion-channel machinery is shared with intestinal signaling.

primary_references

Rebaudioside A from Stevia rebaudiana stimulates GLP-1 release by enteroendocrine cells via bitter taste signalling pathways. · 2023 · https://pubmed.ncbi.nlm.nih.gov/37431625/ · DOI 10.1039/d3fo00818e

Stevia: glycoside metabolism, taste, ion channels and cross-nutrient mechanisms (2026-09-19) · lines 274–280

AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human enteroendocrine cell-line signaling experiments. · source_derived_draft · unverified_draft

## stevia-gut-trpm5 Taste-associated ion-channel machinery is shared with intestinal signaling. The human HuTu-80 experiments also supported TRPM5 involvement in rebaudioside-A-evoked GLP-1 release. Model: Human enteroendocrine cell-line signaling experiments. Limitations: The species-specific human protein node is distinct from mouse Trpm5 and the incompletely resolved expression construct. Evidence access: Primary abstract Rebaudioside A from Stevia rebaudiana stimulates GLP-1 release by enteroendocrine cells via bitter taste signalling pathways. · 2023 · https://pubmed.ncbi.nlm.nih.gov/37431625/ · DOI 10.1039/d3fo00818e

evidence_access

Primary abstract

experimental_model

Acute paired crossover; four-hour blood sampling.

limitations

Small study and gram-level dose; not evidence of long-term disease treatment or of equivalence to rebaudioside A.

nutrient_topic

Stevia collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Stevia

plain_language

A small human meal trial found a glycemic effect but did not confirm every proposed hormonal route.

primary_references

Antihyperglycemic effects of stevioside in type 2 diabetic subjects. · 2004 · https://pubmed.ncbi.nlm.nih.gov/14681845/ · DOI 10.1016/j.metabol.2003.07.013

Stevia: glycoside metabolism, taste, ion channels and cross-nutrient mechanisms (2026-09-19) · lines 362–368

AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Acute paired crossover; four-hour blood sampling. · source_derived_draft · unverified_draft

## stevia-meal-trial A small human meal trial found a glycemic effect but did not confirm every proposed hormonal route. In a 12-person type-2-diabetes crossover trial, adding 1 g stevioside to a meal reduced glucose incremental AUC by 18% versus maize starch, without a significant change in insulin or GLP-1 AUC. Model: Acute paired crossover; four-hour blood sampling. Limitations: Small study and gram-level dose; not evidence of long-term disease treatment or of equivalence to rebaudioside A. Evidence access: Primary abstract Antihyperglycemic effects of stevioside in type 2 diabetic subjects. · 2004 · https://pubmed.ncbi.nlm.nih.gov/14681845/ · DOI 10.1016/j.metabol.2003.07.013

evidence_span

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experimental_model

Transgenic monomeric red fluorescent protein reporter mice with FACS purification and quantitative PCR

exposure

Cell-type resolved expression of FFAR2 and FFAR3 reporters, with receptor-specific synthetic agonists on colonic crypt cultures

limitations

Reporter expression is not the same as receptor protein. The FFAR2 result here is weaker in enteroendocrine cells than the rat immunohistochemistry in this collection reports.

nutrient_topic

Acetic acid research collection; topical membership is not evidence of a direct clinical effect, and the ingested acid is recorded separately from the circulating acetate anion. · Acetic acid

organism

Mouse

plain_language

The FFAR3 reporter marks nearly every hormone-making cell of the gut, and the gut nerves as well.

primary_references

[acetate-p23885020] GPR41/FFAR3 and GPR43/FFAR2 as cosensors for short-chain fatty acids in enteroendocrine cells vs FFAR3 in enteric neurons and FFAR2 in enteric leukocytes. (2013). https://pubmed.ncbi.nlm.nih.gov/23885020/ DOI: 10.1210/en.2013-1142

tissue_or_cell_type

Whole gastrointestinal tract

Acetic acid: the ingested acid, the receptors acetate binds, the acetyl-CoA it becomes, and the acetyl groups that reach histones (2026-09-21) · lines 290–301

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Transgenic monomeric red fluorescent protein reporter mice with FACS purification and quantitative PCR · source_derived_draft · unverified_draft

### acetate-ffar3-on-l-cells The FFAR3 reporter was strongly expressed in all cholecystokinin, glucose-dependent insulinotropic peptide and secretin cells of the proximal small intestine, in all GLP-1, peptide YY and neurotensin cells of the distal small intestine, and in the large population of peptide YY and GLP-1 cells throughout the colon and rectum, and also in the neuronal cells of the submucosal and myenteric ganglia. Condition category: normal nutrient_topic: Acetic acid research collection; topical membership is not evidence of a direct clinical effect, and the ingested acid is recorded separately from the circulating acetate anion. plain_language: The FFAR3 reporter marks nearly every hormone-making cell of the gut, and the gut nerves as well. organism: Mouse tissue_or_cell_type: Whole gastrointestinal tract experimental_model: Transgenic monomeric red fluorescent protein reporter mice with FACS purification and quantitative PCR limitations: Reporter expression is not the same as receptor protein. The FFAR2 result here is weaker in enteroendocrine cells than the rat immunohistochemistry in this collection reports. exposure: Cell-type resolved expression of FFAR2 and FFAR3 reporters, with receptor-specific synthetic agonists on colonic crypt cultures evidence_span: {"source_cache": "artifacts/acetate-research/23885020.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "b834455e11c2b8fa3c4c19c5d01375815e46c3b0f8e25eb184f0eaa6a51c749e", "start_char": 0, "end_char": 2144, "text_sha256": "b834455e11c2b8fa3c4c19c5d01375815e46c3b0f8e25eb184f0eaa6a51c749e"} [acetate-p23885020] GPR41/FFAR3 and GPR43/FFAR2 as cosensors for short-chain fatty acids in enteroendocrine cells vs FFAR3 in enteric neurons and FFAR2 in enteric leukocytes. (2013). https://pubmed.ncbi.nlm.nih.gov/23885020/ DOI: 10.1210/en.2013-1142

evidence_span

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experimental_model

Wistar rats, C57BL6 mice and FFA2 knockout mice, with colonic crypt cultures and portal vein sampling

exposure

Propionate applied to colonic crypt cultures and infused into the colon, with FFA2 deletion as the test of mediation

limitations

Establishes the receptor-to-hormone step in rodents using propionate rather than acetate. The knockout is the strength of the design.

nutrient_topic

Acetic acid research collection; topical membership is not evidence of a direct clinical effect, and the ingested acid is recorded separately from the circulating acetate anion. · Acetic acid

organism

Rat and mouse

plain_language

In rodents the receptor is what releases the two gut hormones; delete it and the response goes.

primary_references

[acetate-p25109781] The short chain fatty acid propionate stimulates GLP-1 and PYY secretion via free fatty acid receptor 2 in rodents. (2015). https://pubmed.ncbi.nlm.nih.gov/25109781/ DOI: 10.1038/ijo.2014.153

tissue_or_cell_type

Colon

Acetic acid: the ingested acid, the receptors acetate binds, the acetyl-CoA it becomes, and the acetyl groups that reach histones (2026-09-21) · lines 316–327

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Wistar rats, C57BL6 mice and FFA2 knockout mice, with colonic crypt cultures and portal vein sampling · source_derived_draft · unverified_draft

### acetate-scfa-glp1-rodent Propionate stimulated secretion of both peptide YY and GLP-1 from wild-type murine colonic crypt cultures and this effect was significantly attenuated in cultures from FFA2 knockout mice, while intra-colonic infusion of propionate elevated both hormones in portal vein plasma in rats and mice but did not significantly stimulate their release in FFA2 knockout mice. Condition category: normal nutrient_topic: Acetic acid research collection; topical membership is not evidence of a direct clinical effect, and the ingested acid is recorded separately from the circulating acetate anion. plain_language: In rodents the receptor is what releases the two gut hormones; delete it and the response goes. organism: Rat and mouse tissue_or_cell_type: Colon experimental_model: Wistar rats, C57BL6 mice and FFA2 knockout mice, with colonic crypt cultures and portal vein sampling limitations: Establishes the receptor-to-hormone step in rodents using propionate rather than acetate. The knockout is the strength of the design. exposure: Propionate applied to colonic crypt cultures and infused into the colon, with FFA2 deletion as the test of mediation evidence_span: {"source_cache": "artifacts/acetate-research/25109781.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c3c934644f9308be7b2c26f969858debd0d1dbf19bee7e307e529d392fe135d6", "start_char": 0, "end_char": 1621, "text_sha256": "c3c934644f9308be7b2c26f969858debd0d1dbf19bee7e307e529d392fe135d6"} [acetate-p25109781] The short chain fatty acid propionate stimulates GLP-1 and PYY secretion via free fatty acid receptor 2 in rodents. (2015). https://pubmed.ncbi.nlm.nih.gov/25109781/ DOI: 10.1038/ijo.2014.153

dose

Fructose concentration series, EC50 0.155 mM; blocker experiment 10 mM fructose plus 340 micromolar diazoxide

duration

2 h

evidence_access

Primary full-text methods/results and metadata inspected.

evidence_scope

literature_reviewed; source-specific curation

experimental_model

Mouse GLUTag enteroendocrine cell line

exposure_scope

Isolated fructose / drug-peptide assay

limitations

Pharmacological channel control in a cell line does not establish a human drug-food interaction or a reason to consume fructose therapeutically.

nutrient_topic

HFCS chapter: actual formulation studies, component biochemistry and interventions are explicitly distinguished. · High-Fructose Corn Syrup / HFCS

organism

Mouse GLUTag enteroendocrine cell line

plain_language

Fructose stimulated GLP-1 secretion in mouse GLUTag cells with a reported EC50 of 0.155 mM.

primary_references

Fructose stimulates GLP-1 but not GIP secretion in mice, rats, and humans. (2014). https://pubmed.ncbi.nlm.nih.gov/24525020/ DOI: 10.1152/ajpgi.00372.2013

route

In vitro sugar and drug exposure

tissue

GLP-1 secretion assay

High-Fructose Corn Syrup: mechanism of action and metabolic impact (2026-09-20) · lines 473–483

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 · Mouse GLUTag enteroendocrine cell line · source_derived_draft · unverified_draft

## hfcs-cell-glp1 Fructose stimulated GLP-1 secretion in mouse GLUTag cells with a reported EC50 of 0.155 mM. Model/species: Mouse GLUTag enteroendocrine cell line Tissue: GLP-1 secretion assay Exposure: Fructose concentration series, EC50 0.155 mM; blocker experiment 10 mM fructose plus 340 micromolar diazoxide Route: In vitro sugar and drug exposure Duration: 2 h Exposure scope: Isolated fructose / drug-peptide assay Limits: Pharmacological channel control in a cell line does not establish a human drug-food interaction or a reason to consume fructose therapeutically. Reference: Fructose stimulates GLP-1 but not GIP secretion in mice, rats, and humans. (2014). https://pubmed.ncbi.nlm.nih.gov/24525020/ DOI: 10.1152/ajpgi.00372.2013 Access: Primary full-text methods/results and metadata inspected.

availability_state

machinery_impairment Imported condition classification; unverified.

dose

Fructose concentration series, EC50 0.155 mM; blocker experiment 10 mM fructose plus 340 micromolar diazoxide

duration

2 h

evidence_access

Primary full-text methods/results and metadata inspected.

evidence_scope

literature_reviewed; source-specific curation

experimental_model

Mouse GLUTag enteroendocrine cell line

exposure_scope

Isolated fructose / drug-peptide assay

limitations

Pharmacological channel control in a cell line does not establish a human drug-food interaction or a reason to consume fructose therapeutically.

nutrient_topic

HFCS chapter: actual formulation studies, component biochemistry and interventions are explicitly distinguished. · High-Fructose Corn Syrup / HFCS

organism

Mouse GLUTag enteroendocrine cell line

plain_language

Diazoxide at 340 micromolar abolished fructose-stimulated GLP-1 secretion in GLUTag cells.

primary_references

Fructose stimulates GLP-1 but not GIP secretion in mice, rats, and humans. (2014). https://pubmed.ncbi.nlm.nih.gov/24525020/ DOI: 10.1152/ajpgi.00372.2013

route

In vitro sugar and drug exposure

tissue

GLP-1 secretion assay

trigger_kind

machinery_impairment Imported condition classification; unverified.

High-Fructose Corn Syrup: mechanism of action and metabolic impact (2026-09-20) · lines 485–495

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 · Mouse GLUTag enteroendocrine cell line · source_derived_draft · unverified_draft

## hfcs-diazoxide Diazoxide at 340 micromolar abolished fructose-stimulated GLP-1 secretion in GLUTag cells. Model/species: Mouse GLUTag enteroendocrine cell line Tissue: GLP-1 secretion assay Exposure: Fructose concentration series, EC50 0.155 mM; blocker experiment 10 mM fructose plus 340 micromolar diazoxide Route: In vitro sugar and drug exposure Duration: 2 h Exposure scope: Isolated fructose / drug-peptide assay Limits: Pharmacological channel control in a cell line does not establish a human drug-food interaction or a reason to consume fructose therapeutically. Reference: Fructose stimulates GLP-1 but not GIP secretion in mice, rats, and humans. (2014). https://pubmed.ncbi.nlm.nih.gov/24525020/ DOI: 10.1152/ajpgi.00372.2013 Access: Primary full-text methods/results and metadata inspected.

dose

75 g fructose or glucose in 300 mL water after overnight fast

duration

120 min

evidence_access

Primary full-text methods/results and metadata inspected.

evidence_scope

literature_reviewed; source-specific curation

experimental_model

Nine healthy adults, paired single-blinded challenges

exposure_scope

Isolated fructose / peptide response

limitations

Pure fructose stimulated some hormones less than glucose, but was not hormonally inert; not an HFCS meal or chronic satiety study.

nutrient_topic

HFCS chapter: actual formulation studies, component biochemistry and interventions are explicitly distinguished. · High-Fructose Corn Syrup / HFCS

organism

Nine healthy adults, paired single-blinded challenges

plain_language

Oral fructose stimulated GLP-1 release in healthy adults, less strongly than isocaloric glucose.

primary_references

Fructose stimulates GLP-1 but not GIP secretion in mice, rats, and humans. (2014). https://pubmed.ncbi.nlm.nih.gov/24525020/ DOI: 10.1152/ajpgi.00372.2013

route

Oral solution

tissue

Plasma gut-hormone response

High-Fructose Corn Syrup: mechanism of action and metabolic impact (2026-09-20) · lines 449–459

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 · Nine healthy adults, paired single-blinded challenges · source_derived_draft · unverified_draft

## hfcs-human-glp1 Oral fructose stimulated GLP-1 release in healthy adults, less strongly than isocaloric glucose. Model/species: Nine healthy adults, paired single-blinded challenges Tissue: Plasma gut-hormone response Exposure: 75 g fructose or glucose in 300 mL water after overnight fast Route: Oral solution Duration: 120 min Exposure scope: Isolated fructose / peptide response Limits: Pure fructose stimulated some hormones less than glucose, but was not hormonally inert; not an HFCS meal or chronic satiety study. Reference: Fructose stimulates GLP-1 but not GIP secretion in mice, rats, and humans. (2014). https://pubmed.ncbi.nlm.nih.gov/24525020/ DOI: 10.1152/ajpgi.00372.2013 Access: Primary full-text methods/results and metadata inspected.

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.

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.

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.

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.