Nutrient chapter

Monosodium L-glutamate

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

60 recorded mechanisms · 6 availability situations · 9 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.

MSG is the sodium salt of L-glutamate; the sensory study treats added MSG and NaCl as separate ingredients.
Monosodium L-glutamate → L-Glutamate source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text; background and test samples
experimental_model
Chemical identity and ingredient design in the primary sensory study.
limitations
This is background chemistry, not a measurement of absorption or tissue delivery.
nutrient_topic
Monosodium Glutamate (MSG) collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Monosodium L-glutamate
plain_language
The ingredient contributes both glutamate and sodium.
primary_references
Validation of preferred salt concentration in soup based on a randomized blinded experiment in multiple regions in Japan-influence of umami (L-glutamate) on saltiness and palatability of low-salt solutions. · 2020 · https://pubmed.ncbi.nlm.nih.gov/31996813/ · DOI 10.1038/s41440-020-0397-1
Monosodium Glutamate (MSG): taste, gut sensing, exposure and cross-nutrient mechanisms (2026-09-20) · lines 18–24
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Chemical identity and ingredient design in the primary sensory study. · source_derived_draft · unverified_draft
## monosodium-glutamate-salt-identity The ingredient contributes both glutamate and sodium. MSG is the sodium salt of L-glutamate; the sensory study treats added MSG and NaCl as separate ingredients. Model: Chemical identity and ingredient design in the primary sensory study. Limitations: This is background chemistry, not a measurement of absorption or tissue delivery. Evidence access: Primary full text; background and test samples Validation of preferred salt concentration in soup based on a randomized blinded experiment in multiple regions in Japan-influence of umami (L-glutamate) on saltiness and palatability of low-salt solutions. · 2020 · https://pubmed.ncbi.nlm.nih.gov/31996813/ · DOI 10.1038/s41440-020-0397-1
Complete structured claim and evidence
In eight adults receiving 150 mg/kg MSG in water, adding 1.1 g/kg hydrolyzed corn starch lowered mean peak plasma glutamate from 59.4 to 7.18 micromol/dL.
Partially hydrolyzed corn starch → 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
Human high-dose oral loading, with versus without carbohydrate.
limitations
Small acute study; not a fixed conversion fraction for foods or a brain measurement.
nutrient_topic
Monosodium Glutamate (MSG) collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Monosodium L-glutamate
plain_language
Carbohydrate changed how much glutamate appeared in blood.
primary_references
Effect of carbohydrate on plasma and erythrocyte glutamate levels in humans ingesting large doses of monosodium L-glutamate in water. · 1983 · https://pubmed.ncbi.nlm.nih.gov/6133445/ · DOI 10.1093/ajcn/37.6.961
trigger_kind
biomarker_context Imported condition classification; unverified.
Monosodium Glutamate (MSG): taste, gut sensing, exposure and cross-nutrient mechanisms (2026-09-20) · lines 26–32
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human high-dose oral loading, with versus without carbohydrate. · source_derived_draft · unverified_draft
## monosodium-glutamate-carbohydrate-exposure Carbohydrate changed how much glutamate appeared in blood. In eight adults receiving 150 mg/kg MSG in water, adding 1.1 g/kg hydrolyzed corn starch lowered mean peak plasma glutamate from 59.4 to 7.18 micromol/dL. Model: Human high-dose oral loading, with versus without carbohydrate. Limitations: Small acute study; not a fixed conversion fraction for foods or a brain measurement. Evidence access: Primary abstract Effect of carbohydrate on plasma and erythrocyte glutamate levels in humans ingesting large doses of monosodium L-glutamate in water. · 1983 · https://pubmed.ncbi.nlm.nih.gov/6133445/ · DOI 10.1093/ajcn/37.6.961
Complete structured claim and evidence
Erythrocyte glutamate and aspartate concentrations did not change in either arm of the eight-person MSG/carbohydrate experiment.
Monosodium L-glutamate → Human erythrocyte glutamate/aspartate during MSG loading source_derived_draftungraded
Experimental context and source evidence
availability_state
biomarker_context Imported condition classification; unverified.
evidence_access
Primary abstract
experimental_model
150 mg/kg MSG with or without hydrolyzed corn starch.
limitations
Other cells and later times were not established by this result.
nutrient_topic
Monosodium Glutamate (MSG) collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Monosodium L-glutamate
plain_language
A plasma change did not imply the same change in red cells.
primary_references
Effect of carbohydrate on plasma and erythrocyte glutamate levels in humans ingesting large doses of monosodium L-glutamate in water. · 1983 · https://pubmed.ncbi.nlm.nih.gov/6133445/ · DOI 10.1093/ajcn/37.6.961
trigger_kind
biomarker_context Imported condition classification; unverified.
Monosodium Glutamate (MSG): taste, gut sensing, exposure and cross-nutrient mechanisms (2026-09-20) · lines 34–40
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · 150 mg/kg MSG with or without hydrolyzed corn starch. · source_derived_draft · unverified_draft
## monosodium-glutamate-red-cell-compartment A plasma change did not imply the same change in red cells. Erythrocyte glutamate and aspartate concentrations did not change in either arm of the eight-person MSG/carbohydrate experiment. Model: 150 mg/kg MSG with or without hydrolyzed corn starch. Limitations: Other cells and later times were not established by this result. Evidence access: Primary abstract Effect of carbohydrate on plasma and erythrocyte glutamate levels in humans ingesting large doses of monosodium L-glutamate in water. · 1983 · https://pubmed.ncbi.nlm.nih.gov/6133445/ · DOI 10.1093/ajcn/37.6.961
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
Nine men received 150 mg/kg MSG capsules 30 minutes before a drink; plasma glutamate rose about tenfold without carbohydrate and sixfold with a 75 g carbohydrate drink.
Monosodium L-glutamate → 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
Four-condition human acute supplementation experiment.
limitations
A high-dose loading protocol does not describe customary MSG use.
nutrient_topic
Monosodium Glutamate (MSG) collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Monosodium L-glutamate
plain_language
Timing between amino acid and carbohydrate also matters.
primary_references
Glutamate supplementation is associated with improved glucose metabolism following carbohydrate ingestion in healthy males. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23750536/ · DOI 10.1017/S0007114513001633
trigger_kind
biomarker_context Imported condition classification; unverified.
Monosodium Glutamate (MSG): taste, gut sensing, exposure and cross-nutrient mechanisms (2026-09-20) · lines 50–56
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Four-condition human acute supplementation experiment. · source_derived_draft · unverified_draft
## monosodium-glutamate-staggered-exposure Timing between amino acid and carbohydrate also matters. Nine men received 150 mg/kg MSG capsules 30 minutes before a drink; plasma glutamate rose about tenfold without carbohydrate and sixfold with a 75 g carbohydrate drink. Model: Four-condition human acute supplementation experiment. Limitations: A high-dose loading protocol does not describe customary MSG use. Evidence access: Primary abstract Glutamate supplementation is associated with improved glucose metabolism following carbohydrate ingestion in healthy males. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23750536/ · DOI 10.1017/S0007114513001633
Complete structured claim and evidence
The MSG-plus-carbohydrate condition had lower peak serum glucose than carbohydrate alone, 5.50 versus 7.69 mmol/L.
Monosodium L-glutamate → Human glucose response after staggered MSG/carbohydrate ingestion source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Same nine-person acute study.
limitations
No diabetes-treatment efficacy or durable metabolic benefit was tested.
nutrient_topic
Monosodium Glutamate (MSG) collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Monosodium L-glutamate
plain_language
A measured glucose effect does not by itself reveal the enzyme responsible.
primary_references
Glutamate supplementation is associated with improved glucose metabolism following carbohydrate ingestion in healthy males. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23750536/ · DOI 10.1017/S0007114513001633
Monosodium Glutamate (MSG): taste, gut sensing, exposure and cross-nutrient mechanisms (2026-09-20) · lines 58–64
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Same nine-person acute study. · source_derived_draft · unverified_draft
## monosodium-glutamate-glucose-response A measured glucose effect does not by itself reveal the enzyme responsible. The MSG-plus-carbohydrate condition had lower peak serum glucose than carbohydrate alone, 5.50 versus 7.69 mmol/L. Model: Same nine-person acute study. Limitations: No diabetes-treatment efficacy or durable metabolic benefit was tested. Evidence access: Primary abstract Glutamate supplementation is associated with improved glucose metabolism following carbohydrate ingestion in healthy males. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23750536/ · DOI 10.1017/S0007114513001633
Complete structured claim and evidence
C-peptide-based insulin secretion did not differ on average: four participants increased and five decreased in the MSG-plus-carbohydrate condition.
Monosodium L-glutamate → Human insulin-secretion estimates after staggered MSG source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Same nine men; C-peptide interpretation.
limitations
This does not identify responder genotypes or a direct insulin-receptor target.
nutrient_topic
Monosodium Glutamate (MSG) collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Monosodium L-glutamate
plain_language
The average and individual responses tell different parts of the story.
primary_references
Glutamate supplementation is associated with improved glucose metabolism following carbohydrate ingestion in healthy males. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23750536/ · DOI 10.1017/S0007114513001633
Monosodium Glutamate (MSG): taste, gut sensing, exposure and cross-nutrient mechanisms (2026-09-20) · lines 66–72
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Same nine men; C-peptide interpretation. · source_derived_draft · unverified_draft
## monosodium-glutamate-insulin-heterogeneity The average and individual responses tell different parts of the story. C-peptide-based insulin secretion did not differ on average: four participants increased and five decreased in the MSG-plus-carbohydrate condition. Model: Same nine men; C-peptide interpretation. Limitations: This does not identify responder genotypes or a direct insulin-receptor target. Evidence access: Primary abstract Glutamate supplementation is associated with improved glucose metabolism following carbohydrate ingestion in healthy males. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23750536/ · DOI 10.1017/S0007114513001633
Complete structured claim and evidence
Receptor chimeras, mutagenesis and modeling support glutamate binding near the hinge of the T1R1 Venus-flytrap domain.
L-Glutamate → Human taste receptor TAS1R1 source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
T1R receptor molecular assays and computational model.
limitations
A supported binding model, not a directly observed ligand-bound structure in this paper.
nutrient_topic
Monosodium Glutamate (MSG) collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Monosodium L-glutamate
plain_language
Glutamate and its enhancer are not assigned the same binding site.
primary_references
Molecular mechanism for the umami taste synergism. · 2008 · https://pubmed.ncbi.nlm.nih.gov/19104071/ · DOI 10.1073/pnas.0810174106
Monosodium Glutamate (MSG): taste, gut sensing, exposure and cross-nutrient mechanisms (2026-09-20) · lines 74–80
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · T1R receptor molecular assays and computational model. · source_derived_draft · unverified_draft
## monosodium-glutamate-umami-binding-model Glutamate and its enhancer are not assigned the same binding site. Receptor chimeras, mutagenesis and modeling support glutamate binding near the hinge of the T1R1 Venus-flytrap domain. Model: T1R receptor molecular assays and computational model. Limitations: A supported binding model, not a directly observed ligand-bound structure in this paper. Evidence access: Primary abstract Molecular mechanism for the umami taste synergism. · 2008 · https://pubmed.ncbi.nlm.nih.gov/19104071/ · DOI 10.1073/pnas.0810174106
Complete structured claim and evidence
The cooperative model places a 5-prime-ribonucleotide at an adjacent opening-side site, stabilizing the closed glutamate-bound receptor conformation.
Inosine 5-prime-monophosphate / IMP → Human taste receptor TAS1R1 source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Same mutagenesis/chimera/model study.
limitations
Do not extrapolate taste synergy to a general systemic metabolic benefit.
nutrient_topic
Monosodium Glutamate (MSG) collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Monosodium L-glutamate
plain_language
IMP can amplify a glutamate signal through a different receptor contact.
primary_references
Molecular mechanism for the umami taste synergism. · 2008 · https://pubmed.ncbi.nlm.nih.gov/19104071/ · DOI 10.1073/pnas.0810174106
Monosodium Glutamate (MSG): taste, gut sensing, exposure and cross-nutrient mechanisms (2026-09-20) · lines 82–88
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Same mutagenesis/chimera/model study. · source_derived_draft · unverified_draft
## monosodium-glutamate-imp-cooperation IMP can amplify a glutamate signal through a different receptor contact. The cooperative model places a 5-prime-ribonucleotide at an adjacent opening-side site, stabilizing the closed glutamate-bound receptor conformation. Model: Same mutagenesis/chimera/model study. Limitations: Do not extrapolate taste synergy to a general systemic metabolic benefit. Evidence access: Primary abstract Molecular mechanism for the umami taste synergism. · 2008 · https://pubmed.ncbi.nlm.nih.gov/19104071/ · DOI 10.1073/pnas.0810174106
Complete structured claim and evidence
Plcb2 knockout abolished tested sweet, amino-acid and bitter responses while sparing sour and salty responses in the reported mouse experiments.
Mouse phospholipase C beta 2 / Plcb2 → Mouse sweet, bitter and umami taste responses source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_access
Primary abstract
experimental_model
Mouse knockout taste behavior and nerve assays.
limitations
Reported assay phenotype; not an MSG deficiency or a universal result at every stimulus concentration.
nutrient_topic
Monosodium Glutamate (MSG) collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Monosodium L-glutamate
plain_language
Recognizing the molecule requires downstream signaling machinery.
primary_references
Coding of sweet, bitter, and umami tastes: different receptor cells sharing similar signaling pathways. · 2003 · https://pubmed.ncbi.nlm.nih.gov/12581520/ · DOI 10.1016/s0092-8674(03)00071-0
trigger_kind
machinery_impairment Imported condition classification; unverified.
Monosodium Glutamate (MSG): taste, gut sensing, exposure and cross-nutrient mechanisms (2026-09-20) · lines 90–96
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse knockout taste behavior and nerve assays. · source_derived_draft · unverified_draft
## monosodium-glutamate-plcb2-loss Recognizing the molecule requires downstream signaling machinery. Plcb2 knockout abolished tested sweet, amino-acid and bitter responses while sparing sour and salty responses in the reported mouse experiments. Model: Mouse knockout taste behavior and nerve assays. Limitations: Reported assay phenotype; not an MSG deficiency or a universal result at every stimulus concentration. Evidence access: Primary abstract Coding of sweet, bitter, and umami tastes: different receptor cells sharing similar signaling pathways. · 2003 · https://pubmed.ncbi.nlm.nih.gov/12581520/ · DOI 10.1016/s0092-8674(03)00071-0
Complete structured claim and evidence
Trpm5 knockout disrupted the same tested taste modalities in the mouse study.
Mouse calcium-activated monovalent cation channel / Trpm5 → Mouse sweet, bitter and umami taste responses source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_access
Primary abstract
experimental_model
Mouse genetic loss-of-function.
limitations
Separate from human TRPM5 and from steviol-glycoside effects in other preparations.
nutrient_topic
Monosodium Glutamate (MSG) collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Monosodium L-glutamate
plain_language
An ion channel is another gate after receptor recognition.
primary_references
Coding of sweet, bitter, and umami tastes: different receptor cells sharing similar signaling pathways. · 2003 · https://pubmed.ncbi.nlm.nih.gov/12581520/ · DOI 10.1016/s0092-8674(03)00071-0
trigger_kind
machinery_impairment Imported condition classification; unverified.
Monosodium Glutamate (MSG): taste, gut sensing, exposure and cross-nutrient mechanisms (2026-09-20) · lines 98–104
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse genetic loss-of-function. · source_derived_draft · unverified_draft
## monosodium-glutamate-trpm5-loss An ion channel is another gate after receptor recognition. Trpm5 knockout disrupted the same tested taste modalities in the mouse study. Model: Mouse genetic loss-of-function. Limitations: Separate from human TRPM5 and from steviol-glycoside effects in other preparations. Evidence access: Primary abstract Coding of sweet, bitter, and umami tastes: different receptor cells sharing similar signaling pathways. · 2003 · https://pubmed.ncbi.nlm.nih.gov/12581520/ · DOI 10.1016/s0092-8674(03)00071-0
Complete structured claim and evidence
Restoring Plcb2 only in bitter-receptor cells rescued bitter responses but not sweet or amino-acid responses.
Mouse phospholipase C beta 2 / Plcb2 → Mouse bitter-cell-specific Plcb2 rescue source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_access
Primary abstract
experimental_model
Transgenic rescue in Plcb2-deficient mice.
limitations
This defines cell-specific routing in the model, not a nutritional intervention.
nutrient_topic
Monosodium Glutamate (MSG) collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Monosodium L-glutamate
plain_language
Putting back machinery in the wrong cell type does not restore every signal.
primary_references
Coding of sweet, bitter, and umami tastes: different receptor cells sharing similar signaling pathways. · 2003 · https://pubmed.ncbi.nlm.nih.gov/12581520/ · DOI 10.1016/s0092-8674(03)00071-0
trigger_kind
machinery_impairment Imported condition classification; unverified.
Monosodium Glutamate (MSG): taste, gut sensing, exposure and cross-nutrient mechanisms (2026-09-20) · lines 106–112
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Transgenic rescue in Plcb2-deficient mice. · source_derived_draft · unverified_draft
## monosodium-glutamate-cell-specific-rescue Putting back machinery in the wrong cell type does not restore every signal. Restoring Plcb2 only in bitter-receptor cells rescued bitter responses but not sweet or amino-acid responses. Model: Transgenic rescue in Plcb2-deficient mice. Limitations: This defines cell-specific routing in the model, not a nutritional intervention. Evidence access: Primary abstract Coding of sweet, bitter, and umami tastes: different receptor cells sharing similar signaling pathways. · 2003 · https://pubmed.ncbi.nlm.nih.gov/12581520/ · DOI 10.1016/s0092-8674(03)00071-0
Complete structured claim and evidence
Calhm1 knockout reduced taste-evoked ATP release without eliminating taste-cell excitability to the stimuli.
Mouse CALHM1 / Calhm1 → Mouse type II taste-cell ATP release source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_access
Primary abstract
experimental_model
Mouse taste-bud knockout physiology.
limitations
The later CALHM3 work refines the channel composition; CALHM1 is not treated as the sole physiological subunit.
nutrient_topic
Monosodium Glutamate (MSG) collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Monosodium L-glutamate
plain_language
A cell can detect a stimulus yet fail to transmit its message.
primary_references
CALHM1 ion channel mediates purinergic neurotransmission of sweet, bitter and umami tastes. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23467090/ · DOI 10.1038/nature11906
trigger_kind
machinery_impairment Imported condition classification; unverified.
Monosodium Glutamate (MSG): taste, gut sensing, exposure and cross-nutrient mechanisms (2026-09-20) · lines 114–120
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse taste-bud knockout physiology. · source_derived_draft · unverified_draft
## monosodium-glutamate-calhm1-release A cell can detect a stimulus yet fail to transmit its message. Calhm1 knockout reduced taste-evoked ATP release without eliminating taste-cell excitability to the stimuli. Model: Mouse taste-bud knockout physiology. Limitations: The later CALHM3 work refines the channel composition; CALHM1 is not treated as the sole physiological subunit. Evidence access: Primary abstract CALHM1 ion channel mediates purinergic neurotransmission of sweet, bitter and umami tastes. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23467090/ · DOI 10.1038/nature11906
Complete structured claim and evidence
CALHM3 coassembly with CALHM1 conferred rapid voltage-dependent ATP-release-channel gating; the study connected this complex to type II taste-cell physiology.
Mouse CALHM3 / Calhm3 → Mouse CALHM1 / Calhm1 source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Heterologous channel experiments and mouse taste-cell physiology.
limitations
Functional coassembly is recorded without treating the historical proposed stoichiometry as a universal structural assignment.
nutrient_topic
Monosodium Glutamate (MSG) collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Monosodium L-glutamate
plain_language
Two separately stored subunits form the output channel.
primary_references
CALHM3 Is Essential for Rapid Ion Channel-Mediated Purinergic Neurotransmission of GPCR-Mediated Tastes. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29681531/ · DOI 10.1016/j.neuron.2018.03.043
Monosodium Glutamate (MSG): taste, gut sensing, exposure and cross-nutrient mechanisms (2026-09-20) · lines 122–128
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Heterologous channel experiments and mouse taste-cell physiology. · source_derived_draft · unverified_draft
## monosodium-glutamate-calhm3-channel Two separately stored subunits form the output channel. CALHM3 coassembly with CALHM1 conferred rapid voltage-dependent ATP-release-channel gating; the study connected this complex to type II taste-cell physiology. Model: Heterologous channel experiments and mouse taste-cell physiology. Limitations: Functional coassembly is recorded without treating the historical proposed stoichiometry as a universal structural assignment. Evidence access: Primary abstract CALHM3 Is Essential for Rapid Ion Channel-Mediated Purinergic Neurotransmission of GPCR-Mediated Tastes. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29681531/ · DOI 10.1016/j.neuron.2018.03.043
Complete structured claim and evidence
Calhm3 deletion abolished taste-evoked ATP release and disrupted GPCR-mediated taste perception in mice.
Mouse CALHM3 / Calhm3 → Mouse type II taste-cell ATP release source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_access
Primary abstract
experimental_model
Mouse knockout experiments.
limitations
Shares investigators with the CALHM1 study; no human deficiency threshold follows.
nutrient_topic
Monosodium Glutamate (MSG) collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Monosodium L-glutamate
plain_language
Intact upstream sensing cannot compensate for a missing release channel.
primary_references
CALHM3 Is Essential for Rapid Ion Channel-Mediated Purinergic Neurotransmission of GPCR-Mediated Tastes. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29681531/ · DOI 10.1016/j.neuron.2018.03.043
trigger_kind
machinery_impairment Imported condition classification; unverified.
Monosodium Glutamate (MSG): taste, gut sensing, exposure and cross-nutrient mechanisms (2026-09-20) · lines 130–136
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse knockout experiments. · source_derived_draft · unverified_draft
## monosodium-glutamate-calhm3-loss Intact upstream sensing cannot compensate for a missing release channel. Calhm3 deletion abolished taste-evoked ATP release and disrupted GPCR-mediated taste perception in mice. Model: Mouse knockout experiments. Limitations: Shares investigators with the CALHM1 study; no human deficiency threshold follows. Evidence access: Primary abstract CALHM3 Is Essential for Rapid Ion Channel-Mediated Purinergic Neurotransmission of GPCR-Mediated Tastes. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29681531/ · DOI 10.1016/j.neuron.2018.03.043
Complete structured claim and evidence
Tas1r3-null mice retained diminished behavioral and nerve responses to umami compounds.
Mouse taste receptor T1R3 / Tas1r3 → Mouse residual umami response without T1R3 source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_access
Primary abstract
experimental_model
Mouse receptor knockout.
limitations
This result does not identify one exclusive alternative receptor or negate human T1R1/T1R3 activation.
nutrient_topic
Monosodium Glutamate (MSG) collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Monosodium L-glutamate
plain_language
The main receptor is not necessarily the only detectable route.
primary_references
Detection of sweet and umami taste in the absence of taste receptor T1r3. · 2003 · https://pubmed.ncbi.nlm.nih.gov/12869700/ · DOI 10.1126/science.1087155
trigger_kind
machinery_impairment Imported condition classification; unverified.
Monosodium Glutamate (MSG): taste, gut sensing, exposure and cross-nutrient mechanisms (2026-09-20) · lines 138–144
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse receptor knockout. · source_derived_draft · unverified_draft
## monosodium-glutamate-residual-umami The main receptor is not necessarily the only detectable route. Tas1r3-null mice retained diminished behavioral and nerve responses to umami compounds. Model: Mouse receptor knockout. Limitations: This result does not identify one exclusive alternative receptor or negate human T1R1/T1R3 activation. Evidence access: Primary abstract Detection of sweet and umami taste in the absence of taste receptor T1r3. · 2003 · https://pubmed.ncbi.nlm.nih.gov/12869700/ · DOI 10.1126/science.1087155
Complete structured claim and evidence
Glutamate taste with a consonant savory odor produced supralinear fMRI responses in medial orbitofrontal and pregenual cingulate regions, related to flavor pleasantness.
Consonant savory odor in human taste experiments → Human cortical response to glutamate taste with savory odor source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Human sensory ratings and fMRI.
limitations
BOLD activation is not evidence that ingested glutamate crossed the blood-brain barrier.
nutrient_topic
Monosodium Glutamate (MSG) collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Monosodium L-glutamate
plain_language
Smell changes the perceived flavor through sensory convergence.
primary_references
Umami: a delicious flavor formed by convergence of taste and olfactory pathways in the human brain. · 2007 · https://pubmed.ncbi.nlm.nih.gov/17432971/ · DOI 10.1111/j.1460-9568.2007.05445.x
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AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human sensory ratings and fMRI. · source_derived_draft · unverified_draft
## monosodium-glutamate-odor-convergence Smell changes the perceived flavor through sensory convergence. Glutamate taste with a consonant savory odor produced supralinear fMRI responses in medial orbitofrontal and pregenual cingulate regions, related to flavor pleasantness. Model: Human sensory ratings and fMRI. Limitations: BOLD activation is not evidence that ingested glutamate crossed the blood-brain barrier. Evidence access: Primary abstract Umami: a delicious flavor formed by convergence of taste and olfactory pathways in the human brain. · 2007 · https://pubmed.ncbi.nlm.nih.gov/17432971/ · DOI 10.1111/j.1460-9568.2007.05445.x
Complete structured claim and evidence
Serotonin depletion blocked glutamate-evoked gastric vagal firing in rats.
Serotonin → Rat gastric vagal afferent activity source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_access
Primary abstract
experimental_model
Rat gastric nutrient-sensing experiment.
limitations
Does not establish dietary tryptophan depletion from MSG or a human clinical syndrome.
nutrient_topic
Monosodium Glutamate (MSG) collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Monosodium L-glutamate
plain_language
A locally available mediator was required in the tested pathway.
primary_references
Luminal amino acid sensing in the rat gastric mucosa. · 2006 · https://pubmed.ncbi.nlm.nih.gov/16809638/ · DOI 10.1152/ajpgi.00587.2005
trigger_kind
machinery_impairment Imported condition classification; unverified.
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AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Rat gastric nutrient-sensing experiment. · source_derived_draft · unverified_draft
## monosodium-glutamate-serotonin-gate A locally available mediator was required in the tested pathway. Serotonin depletion blocked glutamate-evoked gastric vagal firing in rats. Model: Rat gastric nutrient-sensing experiment. Limitations: Does not establish dietary tryptophan depletion from MSG or a human clinical syndrome. Evidence access: Primary abstract Luminal amino acid sensing in the rat gastric mucosa. · 2006 · https://pubmed.ncbi.nlm.nih.gov/16809638/ · DOI 10.1152/ajpgi.00587.2005
Complete structured claim and evidence
Blocking 5-HT3 receptors prevented the rat gastric vagal response to luminal glutamate.
Rat gastric 5-HT3 receptor activity, subunit composition unresolved → Rat gastric vagal afferent activity source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_access
Primary abstract
experimental_model
Rat pharmacological blockade.
limitations
Subunits and an exclusive linear pathway are not established by the accessed abstract.
nutrient_topic
Monosodium Glutamate (MSG) collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Monosodium L-glutamate
plain_language
A serotonin receptor relays part of the gut signal.
primary_references
Luminal amino acid sensing in the rat gastric mucosa. · 2006 · https://pubmed.ncbi.nlm.nih.gov/16809638/ · DOI 10.1152/ajpgi.00587.2005
trigger_kind
machinery_impairment Imported condition classification; unverified.
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AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Rat pharmacological blockade. · source_derived_draft · unverified_draft
## monosodium-glutamate-5ht3-gate A serotonin receptor relays part of the gut signal. Blocking 5-HT3 receptors prevented the rat gastric vagal response to luminal glutamate. Model: Rat pharmacological blockade. Limitations: Subunits and an exclusive linear pathway are not established by the accessed abstract. Evidence access: Primary abstract Luminal amino acid sensing in the rat gastric mucosa. · 2006 · https://pubmed.ncbi.nlm.nih.gov/16809638/ · DOI 10.1152/ajpgi.00587.2005
Complete structured claim and evidence
NOS inhibition blocked glutamate-evoked vagal firing; an NO donor mimicked firing and its response was blocked by 5-HT3 antagonism.
Rat gastric nitric-oxide synthase activity, isoform unresolved → Rat gastric vagal afferent activity source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_access
Primary abstract
experimental_model
Rat mucosal pharmacology.
limitations
Supports pathway ordering; not direct proof of each cell source or a human MSG–arginine interaction.
nutrient_topic
Monosodium Glutamate (MSG) collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Monosodium L-glutamate
plain_language
Nitric oxide and serotonin signaling interact upstream of the nerve response.
primary_references
Luminal amino acid sensing in the rat gastric mucosa. · 2006 · https://pubmed.ncbi.nlm.nih.gov/16809638/ · DOI 10.1152/ajpgi.00587.2005
trigger_kind
machinery_impairment Imported condition classification; unverified.
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AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Rat mucosal pharmacology. · source_derived_draft · unverified_draft
## monosodium-glutamate-nos-gate Nitric oxide and serotonin signaling interact upstream of the nerve response. NOS inhibition blocked glutamate-evoked vagal firing; an NO donor mimicked firing and its response was blocked by 5-HT3 antagonism. Model: Rat mucosal pharmacology. Limitations: Supports pathway ordering; not direct proof of each cell source or a human MSG–arginine interaction. Evidence access: Primary abstract Luminal amino acid sensing in the rat gastric mucosa. · 2006 · https://pubmed.ncbi.nlm.nih.gov/16809638/ · DOI 10.1152/ajpgi.00587.2005
Complete structured claim and evidence
Luminal L-glutamate increased epithelial pH in rat duodenum.
L-Glutamate → Rat duodenal epithelial intracellular pH source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Anesthetized-rat perfusion, 0.1–10 mM.
limitations
Local preparation; not blood alkalinization.
nutrient_topic
Monosodium Glutamate (MSG) collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Monosodium L-glutamate
plain_language
A luminal amino acid changed cellular acid-base handling.
primary_references
Luminal L-glutamate enhances duodenal mucosal defense mechanisms via multiple glutamate receptors in rats. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19643955/ · DOI 10.1152/ajpgi.90605.2008
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AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Anesthetized-rat perfusion, 0.1–10 mM. · source_derived_draft · unverified_draft
## monosodium-glutamate-duodenal-ph A luminal amino acid changed cellular acid-base handling. Luminal L-glutamate increased epithelial pH in rat duodenum. Model: Anesthetized-rat perfusion, 0.1–10 mM. Limitations: Local preparation; not blood alkalinization. Evidence access: Primary abstract Luminal L-glutamate enhances duodenal mucosal defense mechanisms via multiple glutamate receptors in rats. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19643955/ · DOI 10.1152/ajpgi.90605.2008
Complete structured claim and evidence
Glutamate increased rat duodenal mucus thickness without increasing measured blood flow.
L-Glutamate → Rat duodenal mucus gel thickness source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Same rat perfusion study.
limitations
Not clinical ulcer prevention.
nutrient_topic
Monosodium Glutamate (MSG) collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Monosodium L-glutamate
plain_language
Barrier and vascular endpoints differed.
primary_references
Luminal L-glutamate enhances duodenal mucosal defense mechanisms via multiple glutamate receptors in rats. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19643955/ · DOI 10.1152/ajpgi.90605.2008
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AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Same rat perfusion study. · source_derived_draft · unverified_draft
## monosodium-glutamate-duodenal-mucus Barrier and vascular endpoints differed. Glutamate increased rat duodenal mucus thickness without increasing measured blood flow. Model: Same rat perfusion study. Limitations: Not clinical ulcer prevention. Evidence access: Primary abstract Luminal L-glutamate enhances duodenal mucosal defense mechanisms via multiple glutamate receptors in rats. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19643955/ · DOI 10.1152/ajpgi.90605.2008
Complete structured claim and evidence
mGluR4 agonists mimicked and an antagonist inhibited glutamate-associated pH and mucus responses.
Rat metabotropic glutamate receptor 4 / Grm4 → Rat duodenal epithelial intracellular pH source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Rat duodenum pharmacology.
limitations
Not a genetic demonstration of exclusive receptor mediation.
nutrient_topic
Monosodium Glutamate (MSG) collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Monosodium L-glutamate
plain_language
Receptor probes help locate a step.
primary_references
Luminal L-glutamate enhances duodenal mucosal defense mechanisms via multiple glutamate receptors in rats. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19643955/ · DOI 10.1152/ajpgi.90605.2008
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AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Rat duodenum pharmacology. · source_derived_draft · unverified_draft
## monosodium-glutamate-duodenal-grm4 Receptor probes help locate a step. mGluR4 agonists mimicked and an antagonist inhibited glutamate-associated pH and mucus responses. Model: Rat duodenum pharmacology. Limitations: Not a genetic demonstration of exclusive receptor mediation. Evidence access: Primary abstract Luminal L-glutamate enhances duodenal mucosal defense mechanisms via multiple glutamate receptors in rats. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19643955/ · DOI 10.1152/ajpgi.90605.2008
Complete structured claim and evidence
Glutamate plus IMP enhanced bicarbonate secretion in rat duodenum.
Inosine 5-prime-monophosphate / IMP → Rat duodenal bicarbonate secretion source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Rat perfusion; IMP 0.1 mM.
limitations
T1R involvement was inferred; not proved by receptor deletion.
nutrient_topic
Monosodium Glutamate (MSG) collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Monosodium L-glutamate
plain_language
The two-compound interaction also reached a gut endpoint.
primary_references
Luminal L-glutamate enhances duodenal mucosal defense mechanisms via multiple glutamate receptors in rats. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19643955/ · DOI 10.1152/ajpgi.90605.2008
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AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Rat perfusion; IMP 0.1 mM. · source_derived_draft · unverified_draft
## monosodium-glutamate-duodenal-imp The two-compound interaction also reached a gut endpoint. Glutamate plus IMP enhanced bicarbonate secretion in rat duodenum. Model: Rat perfusion; IMP 0.1 mM. Limitations: T1R involvement was inferred; not proved by receptor deletion. Evidence access: Primary abstract Luminal L-glutamate enhances duodenal mucosal defense mechanisms via multiple glutamate receptors in rats. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19643955/ · DOI 10.1152/ajpgi.90605.2008
Complete structured claim and evidence
Indomethacin or capsaicin pretreatment reduced glutamate-associated mucus and pH responses.
Indomethacin → Rat duodenal mucus gel thickness source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_access
Primary abstract
experimental_model
Rat pharmacological perturbations.
limitations
No human food–drug interaction magnitude was tested.
nutrient_topic
Monosodium Glutamate (MSG) collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Monosodium L-glutamate
plain_language
Mediator synthesis and afferent function constrain the response.
primary_references
Luminal L-glutamate enhances duodenal mucosal defense mechanisms via multiple glutamate receptors in rats. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19643955/ · DOI 10.1152/ajpgi.90605.2008
trigger_kind
machinery_impairment Imported condition classification; unverified.
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AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Rat pharmacological perturbations. · source_derived_draft · unverified_draft
## monosodium-glutamate-duodenal-cox-gate Mediator synthesis and afferent function constrain the response. Indomethacin or capsaicin pretreatment reduced glutamate-associated mucus and pH responses. Model: Rat pharmacological perturbations. Limitations: No human food–drug interaction magnitude was tested. Evidence access: Primary abstract Luminal L-glutamate enhances duodenal mucosal defense mechanisms via multiple glutamate receptors in rats. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19643955/ · DOI 10.1152/ajpgi.90605.2008
Complete structured claim and evidence
MSG shortened the estimated half-emptying time of a protein-rich liquid meal in ten healthy men.
Monosodium L-glutamate → Human protein-rich liquid-meal emptying with MSG source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
13C-acetate breath-test study; 0.5% MSG.
limitations
Indirect emptying estimate; the study does not establish receptor mediation or treatment of gastroparesis.
nutrient_topic
Monosodium Glutamate (MSG) collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Monosodium L-glutamate
plain_language
A local digestive response depends on the accompanying food.
primary_references
Monosodium L-glutamate added to a high-energy, high-protein liquid diet promotes gastric emptying. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19056566/ · DOI 10.3945/ajcn.2008.26180
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AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · 13C-acetate breath-test study; 0.5% MSG. · source_derived_draft · unverified_draft
## monosodium-glutamate-protein-emptying A local digestive response depends on the accompanying food. MSG shortened the estimated half-emptying time of a protein-rich liquid meal in ten healthy men. Model: 13C-acetate breath-test study; 0.5% MSG. Limitations: Indirect emptying estimate; the study does not establish receptor mediation or treatment of gastroparesis. Evidence access: Primary abstract Monosodium L-glutamate added to a high-energy, high-protein liquid diet promotes gastric emptying. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19056566/ · DOI 10.3945/ajcn.2008.26180
Complete structured claim and evidence
The same study found no significant MSG effect for carbohydrate-rich liquid or water meals in nine men.
Monosodium L-glutamate → Human carbohydrate/water meal emptying with MSG source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Within-study meal comparisons.
limitations
Not a contradiction caused by different chemical identities.
nutrient_topic
Monosodium Glutamate (MSG) collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Monosodium L-glutamate
plain_language
The positive protein-meal result did not generalize to all liquids.
primary_references
Monosodium L-glutamate added to a high-energy, high-protein liquid diet promotes gastric emptying. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19056566/ · DOI 10.3945/ajcn.2008.26180
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AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Within-study meal comparisons. · source_derived_draft · unverified_draft
## monosodium-glutamate-carbohydrate-emptying-null The positive protein-meal result did not generalize to all liquids. The same study found no significant MSG effect for carbohydrate-rich liquid or water meals in nine men. Model: Within-study meal comparisons. Limitations: Not a contradiction caused by different chemical identities. Evidence access: Primary abstract Monosodium L-glutamate added to a high-energy, high-protein liquid diet promotes gastric emptying. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19056566/ · DOI 10.3945/ajcn.2008.26180
Complete structured claim and evidence
In ten men, 60-minute gastric residual volume did not differ significantly between mixed liquid meals with and without 0.5% MSG, P=0.45.
Monosodium L-glutamate → Human gastric residual volume in MSG MRI study source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text; results
experimental_model
200 kcal/200 mL meal; serial MRI.
limitations
Different meal and measurement from the breath-test study.
nutrient_topic
Monosodium Glutamate (MSG) collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Monosodium L-glutamate
plain_language
The whole-cohort test must stay visible.
primary_references
Gastric emptying and duodenal motility upon intake of a liquid meal with monosodium glutamate in healthy subjects. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24744869/ · DOI 10.1002/phy2.187
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AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · 200 kcal/200 mL meal; serial MRI. · source_derived_draft · unverified_draft
## monosodium-glutamate-mri-whole-cohort The whole-cohort test must stay visible. In ten men, 60-minute gastric residual volume did not differ significantly between mixed liquid meals with and without 0.5% MSG, P=0.45. Model: 200 kcal/200 mL meal; serial MRI. Limitations: Different meal and measurement from the breath-test study. Evidence access: Primary full text; results Gastric emptying and duodenal motility upon intake of a liquid meal with monosodium glutamate in healthy subjects. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24744869/ · DOI 10.1002/phy2.187
Complete structured claim and evidence
Eight participants had faster emptying with MSG; two slowed. Duodenal wall-motion analysis in four of the eight showed increased motility.
Monosodium L-glutamate → Selected responders in human MSG MRI study source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text; results and disclosures
experimental_model
Same ten-person MRI experiment; subgroup analyses.
limitations
Responder selection and small analyzable subset limit inference. Paper reports umami-research funding and software-company author affiliations.
nutrient_topic
Monosodium Glutamate (MSG) collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Monosodium L-glutamate
plain_language
A selected subgroup can suggest a mechanism without establishing a population effect.
primary_references
Gastric emptying and duodenal motility upon intake of a liquid meal with monosodium glutamate in healthy subjects. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24744869/ · DOI 10.1002/phy2.187
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AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Same ten-person MRI experiment; subgroup analyses. · source_derived_draft · unverified_draft
## monosodium-glutamate-mri-responder-analysis A selected subgroup can suggest a mechanism without establishing a population effect. Eight participants had faster emptying with MSG; two slowed. Duodenal wall-motion analysis in four of the eight showed increased motility. Model: Same ten-person MRI experiment; subgroup analyses. Limitations: Responder selection and small analyzable subset limit inference. Paper reports umami-research funding and software-company author affiliations. Evidence access: Primary full text; results and disclosures Gastric emptying and duodenal motility upon intake of a liquid meal with monosodium glutamate in healthy subjects. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24744869/ · DOI 10.1002/phy2.187
Complete structured claim and evidence
In 584 participants, adding 0.3% MSG improved palatability ratings at tested 0.3%, 0.6% and 0.9% NaCl concentrations.
Monosodium L-glutamate → Human low-salt solution palatability with MSG source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
Randomized blinded tasting across nineteen Japanese regions.
limitations
MSG itself adds sodium; net reduction requires NaCl replacement. No long-term sodium intake or blood-pressure effect was measured. Three authors were Ajinomoto employees.
nutrient_topic
Monosodium Glutamate (MSG) collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Monosodium L-glutamate
plain_language
Flavor enhancement may help a lower-salt recipe remain acceptable.
primary_references
Validation of preferred salt concentration in soup based on a randomized blinded experiment in multiple regions in Japan-influence of umami (L-glutamate) on saltiness and palatability of low-salt solutions. · 2020 · https://pubmed.ncbi.nlm.nih.gov/31996813/ · DOI 10.1038/s41440-020-0397-1
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AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Randomized blinded tasting across nineteen Japanese regions. · source_derived_draft · unverified_draft
## monosodium-glutamate-sodium-substitution Flavor enhancement may help a lower-salt recipe remain acceptable. In 584 participants, adding 0.3% MSG improved palatability ratings at tested 0.3%, 0.6% and 0.9% NaCl concentrations. Model: Randomized blinded tasting across nineteen Japanese regions. Limitations: MSG itself adds sodium; net reduction requires NaCl replacement. No long-term sodium intake or blood-pressure effect was measured. Three authors were Ajinomoto employees. Evidence access: Primary full text Validation of preferred salt concentration in soup based on a randomized blinded experiment in multiple regions in Japan-influence of umami (L-glutamate) on saltiness and palatability of low-salt solutions. · 2020 · https://pubmed.ncbi.nlm.nih.gov/31996813/ · DOI 10.1038/s41440-020-0397-1
Complete structured claim and evidence
In 130 self-reported MSG-reactive volunteers given 5 g without food, 50 responded to MSG only, 17 to placebo only and 19 to both.
Monosodium L-glutamate → Human symptoms during blinded MSG challenge source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Multicenter blinded crossover; positive response required at least two listed symptoms within two hours.
limitations
Self-selected group and acute bolus; molecular cause was not identified.
nutrient_topic
Monosodium Glutamate (MSG) collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Monosodium L-glutamate
plain_language
The initial challenge showed more symptoms after MSG than placebo.
primary_references
Multicenter, double-blind, placebo-controlled, multiple-challenge evaluation of reported reactions to monosodium glutamate. · 2000 · https://pubmed.ncbi.nlm.nih.gov/11080723/ · DOI 10.1067/mai.2000.110794
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AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Multicenter blinded crossover; positive response required at least two listed symptoms within two hours. · source_derived_draft · unverified_draft
## monosodium-glutamate-initial-symptoms The initial challenge showed more symptoms after MSG than placebo. In 130 self-reported MSG-reactive volunteers given 5 g without food, 50 responded to MSG only, 17 to placebo only and 19 to both. Model: Multicenter blinded crossover; positive response required at least two listed symptoms within two hours. Limitations: Self-selected group and acute bolus; molecular cause was not identified. Evidence access: Primary abstract Multicenter, double-blind, placebo-controlled, multiple-challenge evaluation of reported reactions to monosodium glutamate. · 2000 · https://pubmed.ncbi.nlm.nih.gov/11080723/ · DOI 10.1067/mai.2000.110794
Complete structured claim and evidence
Repeated challenges did not establish consistent individual symptom patterns; the two final participants each reacted to only one of three MSG-with-food challenges.
Monosodium L-glutamate → Human symptoms during blinded MSG challenge source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Sequential retesting in the same study.
limitations
Only two people reached the food protocol, so it is not a large general test of all meals.
nutrient_topic
Monosodium Glutamate (MSG) collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Monosodium L-glutamate
plain_language
An initial response and a reproducible sensitivity are different findings.
primary_references
Multicenter, double-blind, placebo-controlled, multiple-challenge evaluation of reported reactions to monosodium glutamate. · 2000 · https://pubmed.ncbi.nlm.nih.gov/11080723/ · DOI 10.1067/mai.2000.110794
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AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Sequential retesting in the same study. · source_derived_draft · unverified_draft
## monosodium-glutamate-retest-inconsistency An initial response and a reproducible sensitivity are different findings. Repeated challenges did not establish consistent individual symptom patterns; the two final participants each reacted to only one of three MSG-with-food challenges. Model: Sequential retesting in the same study. Limitations: Only two people reached the food protocol, so it is not a large general test of all meals. Evidence access: Primary abstract Multicenter, double-blind, placebo-controlled, multiple-challenge evaluation of reported reactions to monosodium glutamate. · 2000 · https://pubmed.ncbi.nlm.nih.gov/11080723/ · DOI 10.1067/mai.2000.110794
Complete structured claim and evidence
A blinded crossover in twelve adults reporting MSG-associated asthma found no definite immediate or late asthmatic reaction to 1 g or 5 g MSG versus lactose placebo.
Monosodium L-glutamate → Human asthma response during controlled MSG challenge source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Fasted capsule challenges with three control days and spirometry.
limitations
Small study; does not establish universal absence of reactions or identify an immune mechanism.
nutrient_topic
Monosodium Glutamate (MSG) collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Monosodium L-glutamate
plain_language
Time-matched baseline variation changed interpretation of a lung-function fall.
primary_references
The effects of monosodium glutamate in adults with asthma who perceive themselves to be monosodium glutamate-intolerant. · 1998 · https://pubmed.ncbi.nlm.nih.gov/9648703/ · DOI 10.1016/s0091-6749(98)70305-7
Monosodium Glutamate (MSG): taste, gut sensing, exposure and cross-nutrient mechanisms (2026-09-20) · lines 274–280
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Fasted capsule challenges with three control days and spirometry. · source_derived_draft · unverified_draft
## monosodium-glutamate-asthma-challenge Time-matched baseline variation changed interpretation of a lung-function fall. A blinded crossover in twelve adults reporting MSG-associated asthma found no definite immediate or late asthmatic reaction to 1 g or 5 g MSG versus lactose placebo. Model: Fasted capsule challenges with three control days and spirometry. Limitations: Small study; does not establish universal absence of reactions or identify an immune mechanism. Evidence access: Primary abstract The effects of monosodium glutamate in adults with asthma who perceive themselves to be monosodium glutamate-intolerant. · 1998 · https://pubmed.ncbi.nlm.nih.gov/9648703/ · DOI 10.1016/s0091-6749(98)70305-7
Complete structured claim and evidence
In postabsorptive healthy adults, tracer comparisons estimated 96 ± 1% first-pass splanchnic extraction of enterally delivered glutamate.
Human first-pass splanchnic glutamate handling → L-Glutamate source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Human crossover intravenous/nasogastric tracer infusion, 3.5 hours per route in each seven-hour study.
limitations
Splanchnic means gut plus liver region; the percentage is protocol-specific, not a fixed value for every meal or dose.
nutrient_topic
L-Glutamate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Glutamate
plain_language
Much of an enteral tracer was handled before reaching the general circulation.
primary_references
Oxidation of glutamic acid by the splanchnic bed in humans. · 1995 · https://pubmed.ncbi.nlm.nih.gov/7653544/ · DOI 10.1152/ajpendo.1995.269.2.E269
L-Glutamate / L-glutamic acid: carbon and nitrogen allocation, signaling and cross-nutrient mechanisms (2026-09-19) · lines 18–24
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human crossover intravenous/nasogastric tracer infusion, 3.5 hours per route in each seven-hour study. · source_derived_draft · unverified_draft
## glutamate-first-pass Much of an enteral tracer was handled before reaching the general circulation. In postabsorptive healthy adults, tracer comparisons estimated 96 ± 1% first-pass splanchnic extraction of enterally delivered glutamate. Model: Human crossover intravenous/nasogastric tracer infusion, 3.5 hours per route in each seven-hour study. Limitations: Splanchnic means gut plus liver region; the percentage is protocol-specific, not a fixed value for every meal or dose. Evidence access: Primary abstract Oxidation of glutamic acid by the splanchnic bed in humans. · 1995 · https://pubmed.ncbi.nlm.nih.gov/7653544/ · DOI 10.1152/ajpendo.1995.269.2.E269
Complete structured claim and evidence
About 78 ± 3% of enterally delivered carbon-labeled glutamate tracer was recovered as exhaled CO2 in the study.
Human first-pass splanchnic glutamate handling → L-Glutamate source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Human [1,2-13C2]glutamate tracer and breath CO2 measurements.
limitations
Whole-body breath recovery does not identify the cell type oxidizing each molecule.
nutrient_topic
L-Glutamate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Glutamate
plain_language
Glutamate carbon was used as fuel, not merely redistributed as amino nitrogen.
primary_references
Oxidation of glutamic acid by the splanchnic bed in humans. · 1995 · https://pubmed.ncbi.nlm.nih.gov/7653544/ · DOI 10.1152/ajpendo.1995.269.2.E269
L-Glutamate / L-glutamic acid: carbon and nitrogen allocation, signaling and cross-nutrient mechanisms (2026-09-19) · lines 26–32
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human [1,2-13C2]glutamate tracer and breath CO2 measurements. · source_derived_draft · unverified_draft
## glutamate-first-pass-oxidation Glutamate carbon was used as fuel, not merely redistributed as amino nitrogen. About 78 ± 3% of enterally delivered carbon-labeled glutamate tracer was recovered as exhaled CO2 in the study. Model: Human [1,2-13C2]glutamate tracer and breath CO2 measurements. Limitations: Whole-body breath recovery does not identify the cell type oxidizing each molecule. Evidence access: Primary abstract Oxidation of glutamic acid by the splanchnic bed in humans. · 1995 · https://pubmed.ncbi.nlm.nih.gov/7653544/ · DOI 10.1152/ajpendo.1995.269.2.E269
Complete structured claim and evidence
After six fasted adults ingested 100 mg nitrogen-labeled L-glutamic acid, most recovered circulating amino-acid label appeared in alanine and glutamine, with no significant amino-acid concentration changes during 150 minutes.
L-Glutamate → Human arterial alanine/glutamine nitrogen labeling source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Human oral 15N tracer, arterialized blood sampling for 150 minutes.
limitations
Small tracer experiment; it does not establish supplement efficacy or a universal conversion fraction.
nutrient_topic
L-Glutamate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Glutamate
plain_language
The incoming amino nitrogen could leave the gut region in different molecules.
primary_references
Measurement of the transfer of the nitrogen moiety of intestinal lumen glutamic acid in man after oral ingestion of l-[15N]glutamic acid. · 1988 · https://pubmed.ncbi.nlm.nih.gov/2908193/ · DOI 10.1042/cs0750499
L-Glutamate / L-glutamic acid: carbon and nitrogen allocation, signaling and cross-nutrient mechanisms (2026-09-19) · lines 34–40
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human oral 15N tracer, arterialized blood sampling for 150 minutes. · source_derived_draft · unverified_draft
## glutamate-dietary-nitrogen The incoming amino nitrogen could leave the gut region in different molecules. After six fasted adults ingested 100 mg nitrogen-labeled L-glutamic acid, most recovered circulating amino-acid label appeared in alanine and glutamine, with no significant amino-acid concentration changes during 150 minutes. Model: Human oral 15N tracer, arterialized blood sampling for 150 minutes. Limitations: Small tracer experiment; it does not establish supplement efficacy or a universal conversion fraction. Evidence access: Primary abstract Measurement of the transfer of the nitrogen moiety of intestinal lumen glutamic acid in man after oral ingestion of l-[15N]glutamic acid. · 1988 · https://pubmed.ncbi.nlm.nih.gov/2908193/ · DOI 10.1042/cs0750499
Complete structured claim and evidence
Coexpressed human T1R1/T1R3 responded to L-glutamate in receptor assays.
L-Glutamate → Human umami receptor TAS1R1/TAS1R3 source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Heterologous expression of human taste receptors.
limitations
Taste-receptor activation does not establish a brain neurotransmitter effect.
nutrient_topic
L-Glutamate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Glutamate
plain_language
Two receptor proteins recognize the umami signal.
primary_references
Human receptors for sweet and umami taste. · 2002 · https://pubmed.ncbi.nlm.nih.gov/11917125/ · DOI 10.1073/pnas.072090199
L-Glutamate / L-glutamic acid: carbon and nitrogen allocation, signaling and cross-nutrient mechanisms (2026-09-19) · lines 42–48
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Heterologous expression of human taste receptors. · source_derived_draft · unverified_draft
## glutamate-umami-receptor Two receptor proteins recognize the umami signal. Coexpressed human T1R1/T1R3 responded to L-glutamate in receptor assays. Model: Heterologous expression of human taste receptors. Limitations: Taste-receptor activation does not establish a brain neurotransmitter effect. Evidence access: Primary abstract Human receptors for sweet and umami taste. · 2002 · https://pubmed.ncbi.nlm.nih.gov/11917125/ · DOI 10.1073/pnas.072090199
Complete structured claim and evidence
5-prime-ribonucleotides enhanced the human T1R1/T1R3 response to L-glutamate.
Inosine 5-prime-monophosphate / IMP → Human umami receptor TAS1R1/TAS1R3 source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Human receptor coexpression and ligand-response assays.
limitations
A measured receptor interaction, not a general metabolic or clinical synergy.
nutrient_topic
L-Glutamate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Glutamate
plain_language
A nucleotide can enhance the response to an amino acid at a receptor.
primary_references
Human receptors for sweet and umami taste. · 2002 · https://pubmed.ncbi.nlm.nih.gov/11917125/ · DOI 10.1073/pnas.072090199
L-Glutamate / L-glutamic acid: carbon and nitrogen allocation, signaling and cross-nutrient mechanisms (2026-09-19) · lines 50–56
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human receptor coexpression and ligand-response assays. · source_derived_draft · unverified_draft
## glutamate-umami-nucleotide A nucleotide can enhance the response to an amino acid at a receptor. 5-prime-ribonucleotides enhanced the human T1R1/T1R3 response to L-glutamate. Model: Human receptor coexpression and ligand-response assays. Limitations: A measured receptor interaction, not a general metabolic or clinical synergy. Evidence access: Primary abstract Human receptors for sweet and umami taste. · 2002 · https://pubmed.ncbi.nlm.nih.gov/11917125/ · DOI 10.1073/pnas.072090199
Complete structured claim and evidence
Human/mouse receptor chimeras and point mutants mapped acidic-amino-acid selectivity to the T1R1 ligand-binding region and identified other residues that broadened mouse-type responses.
Human taste receptor TAS1R1 → Human umami receptor TAS1R1/TAS1R3 source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
Human/mouse receptor chimeras and mutagenesis.
limitations
Sequence-dependent selectivity is not evidence that all mammalian umami receptors behave identically.
nutrient_topic
L-Glutamate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Glutamate
plain_language
The species of the receptor changes what the same ligand experiment means.
primary_references
Two distinct determinants of ligand specificity in T1R1/T1R3 (the umami taste receptor). · 2013 · https://pubmed.ncbi.nlm.nih.gov/24214976/ · DOI 10.1074/jbc.M113.494443
L-Glutamate / L-glutamic acid: carbon and nitrogen allocation, signaling and cross-nutrient mechanisms (2026-09-19) · lines 58–64
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human/mouse receptor chimeras and mutagenesis. · source_derived_draft · unverified_draft
## glutamate-umami-species The species of the receptor changes what the same ligand experiment means. Human/mouse receptor chimeras and point mutants mapped acidic-amino-acid selectivity to the T1R1 ligand-binding region and identified other residues that broadened mouse-type responses. Model: Human/mouse receptor chimeras and mutagenesis. Limitations: Sequence-dependent selectivity is not evidence that all mammalian umami receptors behave identically. Evidence access: Primary full text Two distinct determinants of ligand specificity in T1R1/T1R3 (the umami taste receptor). · 2013 · https://pubmed.ncbi.nlm.nih.gov/24214976/ · DOI 10.1074/jbc.M113.494443
Complete structured claim and evidence
Intragastric 150 mM MSG increased gastric vagal afferent discharge in anesthetized rats.
Monosodium L-glutamate → Rat gastric vagal afferent activity source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
Anesthetized rats; 2 mL intragastric infusion at 1 mL/min, nerve discharge assessed after infusion.
limitations
MSG was the exposure; human food intake and subjective effects were not tested.
nutrient_topic
L-Glutamate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Glutamate
plain_language
Glutamate in the stomach can signal through nerves without first acting at a brain glutamate receptor.
primary_references
Effects of intragastric infusion of inosine monophosphate and L: -glutamate on vagal gastric afferent activity and subsequent autonomic reflexes. · 2011 · https://pubmed.ncbi.nlm.nih.gov/21132420/ · DOI 10.1007/s12576-010-0121-z
L-Glutamate / L-glutamic acid: carbon and nitrogen allocation, signaling and cross-nutrient mechanisms (2026-09-19) · lines 66–72
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Anesthetized rats; 2 mL intragastric infusion at 1 mL/min, nerve discharge assessed after infusion. · source_derived_draft · unverified_draft
## glutamate-gastric-vagal Glutamate in the stomach can signal through nerves without first acting at a brain glutamate receptor. Intragastric 150 mM MSG increased gastric vagal afferent discharge in anesthetized rats. Model: Anesthetized rats; 2 mL intragastric infusion at 1 mL/min, nerve discharge assessed after infusion. Limitations: MSG was the exposure; human food intake and subjective effects were not tested. Evidence access: Primary full text Effects of intragastric infusion of inosine monophosphate and L: -glutamate on vagal gastric afferent activity and subsequent autonomic reflexes. · 2011 · https://pubmed.ncbi.nlm.nih.gov/21132420/ · DOI 10.1007/s12576-010-0121-z
Complete structured claim and evidence
MSG-evoked celiac vagal and adrenal splanchnic efferent responses were abolished by gastric vagotomy in rats.
Rat gastric vagal afferent activity → Rat gastric glutamate-evoked autonomic reflex source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
Anesthetized-rat intragastric infusion with gastric-branch vagotomy.
limitations
Nerve discharge is not direct measurement of a human hormonal or health benefit.
nutrient_topic
L-Glutamate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Glutamate
plain_language
Cutting the sensory route interrupted the downstream reflex.
primary_references
Effects of intragastric infusion of inosine monophosphate and L: -glutamate on vagal gastric afferent activity and subsequent autonomic reflexes. · 2011 · https://pubmed.ncbi.nlm.nih.gov/21132420/ · DOI 10.1007/s12576-010-0121-z
L-Glutamate / L-glutamic acid: carbon and nitrogen allocation, signaling and cross-nutrient mechanisms (2026-09-19) · lines 74–80
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Anesthetized-rat intragastric infusion with gastric-branch vagotomy. · source_derived_draft · unverified_draft
## glutamate-gastric-reflex Cutting the sensory route interrupted the downstream reflex. MSG-evoked celiac vagal and adrenal splanchnic efferent responses were abolished by gastric vagotomy in rats. Model: Anesthetized-rat intragastric infusion with gastric-branch vagotomy. Limitations: Nerve discharge is not direct measurement of a human hormonal or health benefit. Evidence access: Primary full text Effects of intragastric infusion of inosine monophosphate and L: -glutamate on vagal gastric afferent activity and subsequent autonomic reflexes. · 2011 · https://pubmed.ncbi.nlm.nih.gov/21132420/ · DOI 10.1007/s12576-010-0121-z
Complete structured claim and evidence
Current reversal measurements supported uptake of one glutamate anion with three sodium ions and one proton, coupled to outward movement of one potassium ion.
Mammalian glial glutamate transporter GLT-1 in the CHO assay → L-Glutamate source_derived_draftungraded
Experimental context and source evidence
evidence_span
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experimental_model
Whole-cell current reversal measurements
exposure
Ion substitution, intracellular sodium/glutamate and extracellular potassium
limitations
Stoichiometry inferred from reversal potentials; the predicted ischemic extracellular glutamate concentration is not an in-vivo result.
nutrient_topic
Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
organism
Mammalian GLT-1 expressed in Chinese hamster ovary cells
plain_language
Glutamate clearance uses sodium, potassium and proton gradients together.
primary_references
[sodium-p9822723] Stoichiometry of the glial glutamate transporter GLT-1 expressed inducibly in a Chinese hamster ovary cell line selected for low endogenous Na+-dependent glutamate uptake. (1998). https://pubmed.ncbi.nlm.nih.gov/9822723/ DOI: 10.1523/jneurosci.18-23-09620.1998
tissue_or_cell_type
Plasma membrane
transport_effect
raises Uptake of one glutamate anion with three sodium ions and one proton.
transport_pool
the expressing cell Uptake of one glutamate anion with three sodium ions and one proton.
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 369–380
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Whole-cell current reversal measurements · source_derived_draft · unverified_draft
### sodium-glt1-stoichiometry Current reversal measurements supported uptake of one glutamate anion with three sodium ions and one proton, coupled to outward movement of one potassium ion. Condition category: normal nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Glutamate clearance uses sodium, potassium and proton gradients together. organism: Mammalian GLT-1 expressed in Chinese hamster ovary cells tissue_or_cell_type: Plasma membrane experimental_model: Whole-cell current reversal measurements limitations: Stoichiometry inferred from reversal potentials; the predicted ischemic extracellular glutamate concentration is not an in-vivo result. exposure: Ion substitution, intracellular sodium/glutamate and extracellular potassium evidence_span: {"source_cache": "artifacts/sodium-research/9822723.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7612750fb1528dcd6212222b248bc74a2ec7a3813f50cbe5cf8ccdadbe448064", "start_char": 0, "end_char": 1740, "text_sha256": "7612750fb1528dcd6212222b248bc74a2ec7a3813f50cbe5cf8ccdadbe448064"} [sodium-p9822723] Stoichiometry of the glial glutamate transporter GLT-1 expressed inducibly in a Chinese hamster ovary cell line selected for low endogenous Na+-dependent glutamate uptake. (1998). https://pubmed.ncbi.nlm.nih.gov/9822723/ DOI: 10.1523/jneurosci.18-23-09620.1998
Complete structured claim and evidence
Bovine brain-capillary membrane preparations contained EAAT1/2/3 on the abluminal side and showed voltage- and potassium-dependent glutamate uptake.
Bovine blood-brain-barrier EAAT1/EAAT2/EAAT3 transporter panel → L-Glutamate source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Bovine capillary RNA, membrane protein analysis and transport kinetics; aggregate apparent Km 14 micromolar at −61 mV.
limitations
The panel is not a physical three-protein complex; transport assays do not measure whole human brain exposure after food intake.
nutrient_topic
L-Glutamate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Glutamate
plain_language
The brain-facing barrier membrane participates in removing extracellular glutamate.
primary_references
Na(+)-dependent glutamate transporters (EAAT1, EAAT2, and EAAT3) of the blood-brain barrier. A mechanism for glutamate removal. · 1999 · https://pubmed.ncbi.nlm.nih.gov/10542215/ · DOI 10.1074/jbc.274.45.31891
L-Glutamate / L-glutamic acid: carbon and nitrogen allocation, signaling and cross-nutrient mechanisms (2026-09-19) · lines 106–112
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Bovine capillary RNA, membrane protein analysis and transport kinetics; aggregate apparent Km 14 micromolar at −61 mV. · source_derived_draft · unverified_draft
## glutamate-bbb-clearance The brain-facing barrier membrane participates in removing extracellular glutamate. Bovine brain-capillary membrane preparations contained EAAT1/2/3 on the abluminal side and showed voltage- and potassium-dependent glutamate uptake. Model: Bovine capillary RNA, membrane protein analysis and transport kinetics; aggregate apparent Km 14 micromolar at −61 mV. Limitations: The panel is not a physical three-protein complex; transport assays do not measure whole human brain exposure after food intake. Evidence access: Primary abstract Na(+)-dependent glutamate transporters (EAAT1, EAAT2, and EAAT3) of the blood-brain barrier. A mechanism for glutamate removal. · 1999 · https://pubmed.ncbi.nlm.nih.gov/10542215/ · DOI 10.1074/jbc.274.45.31891
Complete structured claim and evidence
Glutamate-cysteine ligase joins glutamate and cysteine to form gamma-glutamylcysteine in the first glutathione-synthesis step.
Human glutamate-cysteine ligase catalytic subunit / GCLC → Gamma-glutamylcysteine source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/sulforaphane-research/30581542.fulltext.txt", "locator": "Primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "77cf6674cf9b9bc140a228588a53c937966fd3a67397c1c4970221c5cc58a0b1", "start_char": 762, "end_char": 1092, "text_sha256": "927fa13b085700c20b578ecabc7c8c17a66ea4600b90809e3061d12bcaea3849"}
experimental_model
Human enzyme mutagenesis, kinetics and molecular dynamics
exposure
S-loop variants; established biosynthetic reactions described in the introduction
limitations
Reaction descriptions are background chemistry in a primary enzyme paper, not evidence that sulforaphane corrects inherited GSS deficiency.
nutrient_topic
Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. · Sulforaphane / SFN, stereochemistry specified per study
organism
Human GSS
plain_language
The induced machinery still needs its amino-acid building blocks.
primary_references
[sulforaphane-p30581542] Genetic Mutations in the S-loop of Human Glutathione Synthetase: Links Between Substrate Binding, Active Site Structure and Allostery. (2019). https://pubmed.ncbi.nlm.nih.gov/30581542/ DOI: 10.1016/j.csbj.2018.11.008
tissue_or_cell_type
Glutathione synthesis and substrate binding
Sulforaphane: formation, electrophile sensing and nutrient connections (2026-09-17) · lines 840–851
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human enzyme mutagenesis, kinetics and molecular dynamics · source_derived_draft · unverified_draft
### sulforaphane-gcl-first-step Glutamate-cysteine ligase joins glutamate and cysteine to form gamma-glutamylcysteine in the first glutathione-synthesis step. Condition category: normal nutrient_topic: Sulforaphane research collection; topical membership is not evidence of a direct dietary effect. plain_language: The induced machinery still needs its amino-acid building blocks. organism: Human GSS tissue_or_cell_type: Glutathione synthesis and substrate binding experimental_model: Human enzyme mutagenesis, kinetics and molecular dynamics limitations: Reaction descriptions are background chemistry in a primary enzyme paper, not evidence that sulforaphane corrects inherited GSS deficiency. exposure: S-loop variants; established biosynthetic reactions described in the introduction evidence_span: {"source_cache": "artifacts/sulforaphane-research/30581542.fulltext.txt", "locator": "Primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "77cf6674cf9b9bc140a228588a53c937966fd3a67397c1c4970221c5cc58a0b1", "start_char": 762, "end_char": 1092, "text_sha256": "927fa13b085700c20b578ecabc7c8c17a66ea4600b90809e3061d12bcaea3849"} [sulforaphane-p30581542] Genetic Mutations in the S-loop of Human Glutathione Synthetase: Links Between Substrate Binding, Active Site Structure and Allostery. (2019). https://pubmed.ncbi.nlm.nih.gov/30581542/ DOI: 10.1016/j.csbj.2018.11.008
Complete structured claim and evidence
Added extracellular glutamate inhibited cystine uptake in N18-RE-105 neuronal hybrid cells, and toxicity tracked that inhibition.
L-Glutamate → Cystine uptake in N18-RE-105 neuronal hybrid cells source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Neuroblastoma/primary-retina hybrid-cell culture; transport and toxicity assays.
limitations
The early paper does not genetically resolve SLC7A11; it is not an oral glutamate exposure study.
nutrient_topic
L-Glutamate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Glutamate
plain_language
The same molecule used to build an antioxidant can obstruct another required ingredient when outside these cells.
primary_references
Glutamate toxicity in a neuronal cell line involves inhibition of cystine transport leading to oxidative stress. · 1989 · https://pubmed.ncbi.nlm.nih.gov/2576375/ · DOI 10.1016/0896-6273(89)90043-3
L-Glutamate / L-glutamic acid: carbon and nitrogen allocation, signaling and cross-nutrient mechanisms (2026-09-19) · lines 330–336
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Neuroblastoma/primary-retina hybrid-cell culture; transport and toxicity assays. · source_derived_draft · unverified_draft
## glutamate-extracellular-cystine-block The same molecule used to build an antioxidant can obstruct another required ingredient when outside these cells. Added extracellular glutamate inhibited cystine uptake in N18-RE-105 neuronal hybrid cells, and toxicity tracked that inhibition. Model: Neuroblastoma/primary-retina hybrid-cell culture; transport and toxicity assays. Limitations: The early paper does not genetically resolve SLC7A11; it is not an oral glutamate exposure study. Evidence access: Primary abstract Glutamate toxicity in a neuronal cell line involves inhibition of cystine transport leading to oxidative stress. · 1989 · https://pubmed.ncbi.nlm.nih.gov/2576375/ · DOI 10.1016/0896-6273(89)90043-3
Complete structured claim and evidence
PLP-bound human GAD67 catalyzes glutamate decarboxylation to GABA.
Human glutamate decarboxylase 67 / GAD1 → Gamma-aminobutyric acid source_derived_draftungraded
Experimental context and source evidence
experimental_model
Recombinant human GAD isoforms; crystallography and enzyme kinetics
exposure
Glutamate turnover in recombinant enzyme assays.
limitations
Recombinant chemistry does not establish a human supplementation response.
nutrient_topic
Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B6
organism
Homo sapiens
plain_language
Activated B6 helps this enzyme make GABA.
primary_references
[fenalti-2007-gad] GABA production by glutamic acid decarboxylase is regulated by a dynamic catalytic loop (2007). https://doi.org/10.1038/nsmb1228 DOI: 10.1038/nsmb1228
tissue_or_cell_type
Purified recombinant protein; no intact tissue
Vitamin B6: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 949–959
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant human GAD isoforms; crystallography and enzyme kinetics · source_derived_draft · unverified_draft
### b6-neuro-gad1-gaba PLP-bound human GAD67 catalyzes glutamate decarboxylation to GABA. Condition category: normal nutrient_topic: Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Activated B6 helps this enzyme make GABA. organism: Homo sapiens tissue_or_cell_type: Purified recombinant protein; no intact tissue experimental_model: Recombinant human GAD isoforms; crystallography and enzyme kinetics limitations: Recombinant chemistry does not establish a human supplementation response. exposure: Glutamate turnover in recombinant enzyme assays. [fenalti-2007-gad] GABA production by glutamic acid decarboxylase is regulated by a dynamic catalytic loop (2007). https://doi.org/10.1038/nsmb1228 DOI: 10.1038/nsmb1228
Complete structured claim and evidence
Human GPT catalyzes reversible amino transfer between alanine and 2-oxoglutarate, producing pyruvate and glutamate.
Human cytosolic alanine aminotransferase / GPT → L-Alanine source_derived_draftungraded
Experimental context and source evidence
experimental_model
Purified human cytosolic GOT1 and GPT; coupled kinetic assays
exposure
Kinetic assays at pH 7.4 and 37 C
limitations
Purified-enzyme evidence does not define dietary requirements or cellular PLP thresholds.
nutrient_topic
Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B6
organism
Homo sapiens
plain_language
B6-dependent alanine transamination links nitrogen transfer to pyruvate metabolism.
primary_references
[b6-transaminases-2022] Using Steady-State Kinetics to Quantitate Substrate Selectivity and Specificity: A Case Study with Two Human Transaminases. (2022). https://pmc.ncbi.nlm.nih.gov/articles/PMC8875635/ DOI: 10.3390/molecules27041398
tissue_or_cell_type
Purified recombinant protein; no intact tissue
Vitamin B6: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 753–763
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Purified human cytosolic GOT1 and GPT; coupled kinetic assays · source_derived_draft · unverified_draft
### b6-met-gpt-reaction Human GPT catalyzes reversible amino transfer between alanine and 2-oxoglutarate, producing pyruvate and glutamate. Condition category: normal nutrient_topic: Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. plain_language: B6-dependent alanine transamination links nitrogen transfer to pyruvate metabolism. organism: Homo sapiens tissue_or_cell_type: Purified recombinant protein; no intact tissue experimental_model: Purified human cytosolic GOT1 and GPT; coupled kinetic assays limitations: Purified-enzyme evidence does not define dietary requirements or cellular PLP thresholds. exposure: Kinetic assays at pH 7.4 and 37 C [b6-transaminases-2022] Using Steady-State Kinetics to Quantitate Substrate Selectivity and Specificity: A Case Study with Two Human Transaminases. (2022). https://pmc.ncbi.nlm.nih.gov/articles/PMC8875635/ DOI: 10.3390/molecules27041398
Complete structured claim and evidence
Human GOT1 catalyzes reversible amino transfer between aspartate and 2-oxoglutarate, producing oxaloacetate and glutamate.
Human cytosolic aspartate aminotransferase / GOT1 → L-Aspartate source_derived_draftungraded
Experimental context and source evidence
experimental_model
Purified human cytosolic GOT1 and GPT; coupled kinetic assays
exposure
Kinetic assays at pH 7.4 and 37 C
limitations
Purified-enzyme evidence does not define dietary requirements or cellular PLP thresholds.
nutrient_topic
Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B6
organism
Homo sapiens
plain_language
This B6-dependent enzyme links amino-acid and carbon metabolism.
primary_references
[b6-transaminases-2022] Using Steady-State Kinetics to Quantitate Substrate Selectivity and Specificity: A Case Study with Two Human Transaminases. (2022). https://pmc.ncbi.nlm.nih.gov/articles/PMC8875635/ DOI: 10.3390/molecules27041398
tissue_or_cell_type
Purified recombinant protein; no intact tissue
Vitamin B6: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 741–751
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Purified human cytosolic GOT1 and GPT; coupled kinetic assays · source_derived_draft · unverified_draft
### b6-met-got1-reaction Human GOT1 catalyzes reversible amino transfer between aspartate and 2-oxoglutarate, producing oxaloacetate and glutamate. Condition category: normal nutrient_topic: Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. plain_language: This B6-dependent enzyme links amino-acid and carbon metabolism. organism: Homo sapiens tissue_or_cell_type: Purified recombinant protein; no intact tissue experimental_model: Purified human cytosolic GOT1 and GPT; coupled kinetic assays limitations: Purified-enzyme evidence does not define dietary requirements or cellular PLP thresholds. exposure: Kinetic assays at pH 7.4 and 37 C [b6-transaminases-2022] Using Steady-State Kinetics to Quantitate Substrate Selectivity and Specificity: A Case Study with Two Human Transaminases. (2022). https://pmc.ncbi.nlm.nih.gov/articles/PMC8875635/ DOI: 10.3390/molecules27041398
Complete structured claim and evidence
Recombinant human NAGS catalyzed N-acetylglutamate formation from glutamate and acetyl-CoA.
Human N-acetylglutamate synthase / NAGS → N-Acetyl-L-glutamate source_derived_draftungraded
Experimental context and source evidence
evidence_span
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experimental_model
Purified recombinant NAGS kinetics
exposure
Glutamate, acetyl-CoA and arginine; mature and conserved-domain constructs
limitations
Construct-specific kinetics; no human B5-deficiency or arginine-repletion trial.
nutrient_topic
Citrulline research collection; topical membership is not evidence of a direct dietary effect. · L-Citrulline
organism
Human and mouse enzymes; human findings specified
plain_language
The activator for CPS1 has its own synthesis step.
primary_references
[citrulline-p16321554] Biochemical properties of recombinant human and mouse N-acetylglutamate synthase. (2006). https://pubmed.ncbi.nlm.nih.gov/16321554/ DOI: 10.1016/j.ymgme.2005.10.003
tissue_or_cell_type
N-acetylglutamate formation
Citrulline: arginine recycling, nitrogen disposal and nutrient connections (2026-09-17) · lines 255–266
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Purified recombinant NAGS kinetics · source_derived_draft · unverified_draft
### citrulline-nags-product Recombinant human NAGS catalyzed N-acetylglutamate formation from glutamate and acetyl-CoA. Condition category: normal nutrient_topic: Citrulline research collection; topical membership is not evidence of a direct dietary effect. plain_language: The activator for CPS1 has its own synthesis step. organism: Human and mouse enzymes; human findings specified tissue_or_cell_type: N-acetylglutamate formation experimental_model: Purified recombinant NAGS kinetics limitations: Construct-specific kinetics; no human B5-deficiency or arginine-repletion trial. exposure: Glutamate, acetyl-CoA and arginine; mature and conserved-domain constructs evidence_span: {"source_cache": "artifacts/citrulline-research/16321554.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5ce9d57aba8d7973c01de32ab7d5d0287858119fa75f0a372e3ed99523a861a5", "start_char": 0, "end_char": 1498, "text_sha256": "5ce9d57aba8d7973c01de32ab7d5d0287858119fa75f0a372e3ed99523a861a5"} [citrulline-p16321554] Biochemical properties of recombinant human and mouse N-acetylglutamate synthase. (2006). https://pubmed.ncbi.nlm.nih.gov/16321554/ DOI: 10.1016/j.ymgme.2005.10.003
Complete structured claim and evidence
N-acetylglutamate binding reshaped human CPS1 and established the channel linking its two phosphorylation sites.
N-Acetyl-L-glutamate → Human carbamoyl-phosphate synthetase 1 / CPS1 source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/citrulline-research/26592762.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "55b398f0f6c85b023e3eee96e6841df398d328bc8201dfb5207147aa871be581", "start_char": 0, "end_char": 1079, "text_sha256": "55b398f0f6c85b023e3eee96e6841df398d328bc8201dfb5207147aa871be581"}
experimental_model
Human recombinant enzyme crystallography and mutation analysis
exposure
Structures without NAG and with NAG plus nucleotides
limitations
Mechanism of enzyme activation; clinical effects of adding nutritional cofactors were not tested.
nutrient_topic
Citrulline research collection; topical membership is not evidence of a direct dietary effect. · L-Citrulline
organism
Human CPS1
plain_language
An activator switches the upstream nitrogen-handling enzyme into a functional shape.
primary_references
[citrulline-p26592762] Structure of human carbamoyl phosphate synthetase: deciphering the on/off switch of human ureagenesis. (2015). https://pubmed.ncbi.nlm.nih.gov/26592762/ DOI: 10.1038/srep16950
tissue_or_cell_type
Mitochondrial carbamoyl-phosphate synthesis
Citrulline: arginine recycling, nitrogen disposal and nutrient connections (2026-09-17) · lines 229–240
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human recombinant enzyme crystallography and mutation analysis · source_derived_draft · unverified_draft
### citrulline-cps1-nag N-acetylglutamate binding reshaped human CPS1 and established the channel linking its two phosphorylation sites. Condition category: normal nutrient_topic: Citrulline research collection; topical membership is not evidence of a direct dietary effect. plain_language: An activator switches the upstream nitrogen-handling enzyme into a functional shape. organism: Human CPS1 tissue_or_cell_type: Mitochondrial carbamoyl-phosphate synthesis experimental_model: Human recombinant enzyme crystallography and mutation analysis limitations: Mechanism of enzyme activation; clinical effects of adding nutritional cofactors were not tested. exposure: Structures without NAG and with NAG plus nucleotides evidence_span: {"source_cache": "artifacts/citrulline-research/26592762.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "55b398f0f6c85b023e3eee96e6841df398d328bc8201dfb5207147aa871be581", "start_char": 0, "end_char": 1079, "text_sha256": "55b398f0f6c85b023e3eee96e6841df398d328bc8201dfb5207147aa871be581"} [citrulline-p26592762] Structure of human carbamoyl phosphate synthetase: deciphering the on/off switch of human ureagenesis. (2015). https://pubmed.ncbi.nlm.nih.gov/26592762/ DOI: 10.1038/srep16950
Complete structured claim and evidence
Human glutamine synthetase catalyzes ATP-coupled ligation of glutamate and ammonia to make glutamine.
Glutamine synthetase / GLUL → L-Glutamine source_derived_draftungraded
Experimental context and source evidence
experimental_model
Human GLUL ligand-complex crystal structures; canine apoenzyme comparison
exposure
ADP/phosphate/Mn and ADP/phosphorylated-inhibitor/Mn complexes
limitations
Reaction identity does not determine the predominant metal in living human brain.
nutrient_topic
Manganese research collection; topical membership is not evidence of a direct dietary effect. · Manganese
organism
Homo sapiens protein
plain_language
GLUL combines glutamate and ammonia using ATP.
primary_references
[mn-enz-18005987] Crystal structures of mammalian glutamine synthetases illustrate substrate-induced conformational changes and provide opportunities for drug and herbicide design. (2008). https://pubmed.ncbi.nlm.nih.gov/18005987/ DOI: 10.1016/j.jmb.2007.10.029
tissue_or_cell_type
Purified GLUL
Manganese: enzyme cofactors, glycosylation, transport and nutrient interactions (2026-09-17) · lines 596–606
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human GLUL ligand-complex crystal structures; canine apoenzyme comparison · source_derived_draft · unverified_draft
### mn-enz-glul-reaction Human glutamine synthetase catalyzes ATP-coupled ligation of glutamate and ammonia to make glutamine. Condition category: normal nutrient_topic: Manganese research collection; topical membership is not evidence of a direct dietary effect. plain_language: GLUL combines glutamate and ammonia using ATP. organism: Homo sapiens protein tissue_or_cell_type: Purified GLUL experimental_model: Human GLUL ligand-complex crystal structures; canine apoenzyme comparison limitations: Reaction identity does not determine the predominant metal in living human brain. exposure: ADP/phosphate/Mn and ADP/phosphorylated-inhibitor/Mn complexes [mn-enz-18005987] Crystal structures of mammalian glutamine synthetases illustrate substrate-induced conformational changes and provide opportunities for drug and herbicide design. (2008). https://pubmed.ncbi.nlm.nih.gov/18005987/ DOI: 10.1016/j.jmb.2007.10.029
Complete structured claim and evidence
Reconstituted human glutamate carrier 1 supported glutamate transport coupled to a proton gradient.
Human mitochondrial glutamate carrier 1 / SLC25A22 → L-Glutamate source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Human carrier expressed in E. coli and reconstituted in phospholipid vesicles.
limitations
Glutamate/H+ cotransport and glutamate/OH− exchange are alternative descriptions in this assay; this is not the aspartate/glutamate exchanger.
nutrient_topic
L-Glutamate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Glutamate
plain_language
Cytosolic glutamate needs a carrier to reach mitochondrial reactions.
primary_references
Identification of the mitochondrial glutamate transporter. Bacterial expression, reconstitution, functional characterization, and tissue distribution of two human isoforms. · 2002 · https://pubmed.ncbi.nlm.nih.gov/11897791/ · DOI 10.1074/jbc.M201572200
transport_effect
depends The record names the proton coupling and not which way glutamate crossed the membrane.
transport_pool
the mitochondrial matrix The record names the proton coupling and not which way glutamate crossed the membrane.
L-Glutamate / L-glutamic acid: carbon and nitrogen allocation, signaling and cross-nutrient mechanisms (2026-09-19) · lines 82–88
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human carrier expressed in E. coli and reconstituted in phospholipid vesicles. · source_derived_draft · unverified_draft
## glutamate-mitochondrial-gc1 Cytosolic glutamate needs a carrier to reach mitochondrial reactions. Reconstituted human glutamate carrier 1 supported glutamate transport coupled to a proton gradient. Model: Human carrier expressed in E. coli and reconstituted in phospholipid vesicles. Limitations: Glutamate/H+ cotransport and glutamate/OH− exchange are alternative descriptions in this assay; this is not the aspartate/glutamate exchanger. Evidence access: Primary abstract Identification of the mitochondrial glutamate transporter. Bacterial expression, reconstitution, functional characterization, and tissue distribution of two human isoforms. · 2002 · https://pubmed.ncbi.nlm.nih.gov/11897791/ · DOI 10.1074/jbc.M201572200
Complete structured claim and evidence
The GLUD1 study identifies glutamate oxidation to 2-oxoglutarate as the enzyme reaction underlying its metabolic and regulatory investigation.
GLUD1 → 2-Oxoglutarate source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Established reaction described in a primary human GLUD1 genetic/functional study.
limitations
Reaction background is distinguished from the directly measured mutant regulation; this record does not quantify tissue flux.
nutrient_topic
L-Glutamate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Glutamate
plain_language
Removing amino nitrogen connects glutamate with the central carbon cycle.
primary_references
Hyperinsulinism and hyperammonemia in infants with regulatory mutations of the glutamate dehydrogenase gene. · 1998 · https://pubmed.ncbi.nlm.nih.gov/9571255/ · DOI 10.1056/NEJM199805073381904
L-Glutamate / L-glutamic acid: carbon and nitrogen allocation, signaling and cross-nutrient mechanisms (2026-09-19) · lines 162–168
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Established reaction described in a primary human GLUD1 genetic/functional study. · source_derived_draft · unverified_draft
## glutamate-gdh-oxidation Removing amino nitrogen connects glutamate with the central carbon cycle. The GLUD1 study identifies glutamate oxidation to 2-oxoglutarate as the enzyme reaction underlying its metabolic and regulatory investigation. Model: Established reaction described in a primary human GLUD1 genetic/functional study. Limitations: Reaction background is distinguished from the directly measured mutant regulation; this record does not quantify tissue flux. Evidence access: Primary abstract Hyperinsulinism and hyperammonemia in infants with regulatory mutations of the glutamate dehydrogenase gene. · 1998 · https://pubmed.ncbi.nlm.nih.gov/9571255/ · DOI 10.1056/NEJM199805073381904
Complete structured claim and evidence
Human P5CS links glutamate to P5C synthesis through ATP- and NADPH-dependent chemistry.
Human pyrroline-5-carboxylate synthase / ALDH18A1 → Delta-1-pyrroline-5-carboxylate / P5C source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/citrulline-research/11092761.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "09706fd9ec135c472473decaa612e06b3e5aa021c9b1493d77daf4fe98b8d5d2", "start_char": 0, "end_char": 1688, "text_sha256": "09706fd9ec135c472473decaa612e06b3e5aa021c9b1493d77daf4fe98b8d5d2"}
experimental_model
Patient genetics and recombinant variant expression
exposure
ALDH18A1 R84Q compared with wild-type isoforms
limitations
Rare inherited enzyme disorder; does not imply low dietary citrulline caused the clinical phenotype.
nutrient_topic
Citrulline research collection; topical membership is not evidence of a direct dietary effect. · L-Citrulline
organism
Human, two siblings and mammalian expression systems
plain_language
This supplies a precursor route connected to ornithine and arginine production.
primary_references
[citrulline-p11092761] Hyperammonemia with reduced ornithine, citrulline, arginine and proline: a new inborn error caused by a mutation in the gene encoding delta(1)-pyrroline-5-carboxylate synthase. (2000). https://pubmed.ncbi.nlm.nih.gov/11092761/ DOI: 10.1093/hmg/9.19.2853
tissue_or_cell_type
Mitochondrial P5CS and circulating amino acids
Citrulline: arginine recycling, nitrogen disposal and nutrient connections (2026-09-17) · lines 294–305
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Patient genetics and recombinant variant expression · source_derived_draft · unverified_draft
### citrulline-p5cs-reaction Human P5CS links glutamate to P5C synthesis through ATP- and NADPH-dependent chemistry. Condition category: normal nutrient_topic: Citrulline research collection; topical membership is not evidence of a direct dietary effect. plain_language: This supplies a precursor route connected to ornithine and arginine production. organism: Human, two siblings and mammalian expression systems tissue_or_cell_type: Mitochondrial P5CS and circulating amino acids experimental_model: Patient genetics and recombinant variant expression limitations: Rare inherited enzyme disorder; does not imply low dietary citrulline caused the clinical phenotype. exposure: ALDH18A1 R84Q compared with wild-type isoforms evidence_span: {"source_cache": "artifacts/citrulline-research/11092761.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "09706fd9ec135c472473decaa612e06b3e5aa021c9b1493d77daf4fe98b8d5d2", "start_char": 0, "end_char": 1688, "text_sha256": "09706fd9ec135c472473decaa612e06b3e5aa021c9b1493d77daf4fe98b8d5d2"} [citrulline-p11092761] Hyperammonemia with reduced ornithine, citrulline, arginine and proline: a new inborn error caused by a mutation in the gene encoding delta(1)-pyrroline-5-carboxylate synthase. (2000). https://pubmed.ncbi.nlm.nih.gov/11092761/ DOI: 10.1093/hmg/9.19.2853
Complete structured claim and evidence
Purified human cytosolic FPGS used tetrahydrofolate as an effective substrate for polyglutamate synthesis.
Human cytosolic FPGS isoform → Tetrahydrofolate source_derived_draftungraded
Experimental context and source evidence
experimental_model
Purified human cytosolic FPGS expressed in bacteria
exposure
Comparative substrate enzyme assays
limitations
Purified substrate preference does not quantify intact-cell flux.
nutrient_topic
Folate and folic acid research collection; topical membership is not evidence of a direct dietary effect. · Folate (vitamin B9)
organism
Homo sapiens protein expressed in Escherichia coli
plain_language
FPGS adds tails that help retain usable folate.
primary_references
[chen1996] Purification and properties of human cytosolic folylpoly-gamma-glutamate synthetase and organization, localization, and differential splicing of its gene (1996). https://pubmed.ncbi.nlm.nih.gov/8662720/ DOI: 10.1074/jbc.271.22.13077
tissue_or_cell_type
Purified enzyme
Folate and folic acid: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 255–265
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Purified human cytosolic FPGS expressed in bacteria · source_derived_draft · unverified_draft
### folate-fpgs-thf-substrate Purified human cytosolic FPGS used tetrahydrofolate as an effective substrate for polyglutamate synthesis. Condition category: normal nutrient_topic: Folate and folic acid research collection; topical membership is not evidence of a direct dietary effect. plain_language: FPGS adds tails that help retain usable folate. organism: Homo sapiens protein expressed in Escherichia coli tissue_or_cell_type: Purified enzyme experimental_model: Purified human cytosolic FPGS expressed in bacteria limitations: Purified substrate preference does not quantify intact-cell flux. exposure: Comparative substrate enzyme assays [chen1996] Purification and properties of human cytosolic folylpoly-gamma-glutamate synthetase and organization, localization, and differential splicing of its gene (1996). https://pubmed.ncbi.nlm.nih.gov/8662720/ DOI: 10.1074/jbc.271.22.13077
Complete structured claim and evidence
Extracellular Mg caused voltage-dependent block of NMDA-type currents in cultured mouse neurons, stronger at hyperpolarized potentials.
Mg2+ → NMDA receptor-mediated current source_derived_draftungraded
Experimental context and source evidence
evidence-system
Single-channel patch clamp with glutamate/NMDA agonists and extracellular Mg changes
experimental_model
Single-channel patch clamp with glutamate/NMDA agonists and extracellular Mg changes
limitations
Native channel subunits were not resolved; no nutritional intake or clinical outcome was tested.
nutrient_topic
Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
organism
Mouse
plain_language
Magnesium restrains this excitatory current in a way that depends on membrane voltage.
primary_references
[nowak-1984-nmda] Magnesium gates glutamate-activated channels in mouse central neurones (1984). https://pubmed.ncbi.nlm.nih.gov/6320006/ DOI: 10.1038/307462a0
tissue
Cultured central neurons
tissue_or_cell_type
Cultured central neurons
Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1261–1272
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Single-channel patch clamp with glutamate/NMDA agonists and extracellular Mg changes · source_derived_draft · unverified_draft
### magnesium-voltage-dependent-nmda-block Extracellular Mg caused voltage-dependent block of NMDA-type currents in cultured mouse neurons, stronger at hyperpolarized potentials. Condition category: normal nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Magnesium restrains this excitatory current in a way that depends on membrane voltage. organism: Mouse tissue_or_cell_type: Cultured central neurons experimental_model: Single-channel patch clamp with glutamate/NMDA agonists and extracellular Mg changes limitations: Native channel subunits were not resolved; no nutritional intake or clinical outcome was tested. evidence-system: Single-channel patch clamp with glutamate/NMDA agonists and extracellular Mg changes tissue: Cultured central neurons [nowak-1984-nmda] Magnesium gates glutamate-activated channels in mouse central neurones (1984). https://pubmed.ncbi.nlm.nih.gov/6320006/ DOI: 10.1038/307462a0
Complete structured claim and evidence
Glycine increased opening frequency of NMDA-activated channels in cultured mouse brain neurons, with potentiation detected at 10 nM.
Glycine → Mouse NMDA-type receptors, subunits unresolved source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Mouse cultured neurons and outside-out patch recordings.
limitations
The effect was distinct from strychnine-sensitive glycine receptors; it does not define an oral glycine or glutamate response.
nutrient_topic
L-Glutamate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Glutamate
plain_language
An amino acid usually associated with inhibition can assist an excitatory receptor.
primary_references
Glycine potentiates the NMDA response in cultured mouse brain neurons. · 1987 · https://pubmed.ncbi.nlm.nih.gov/2433595/ · DOI 10.1038/325529a0
L-Glutamate / L-glutamic acid: carbon and nitrogen allocation, signaling and cross-nutrient mechanisms (2026-09-19) · lines 234–240
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse cultured neurons and outside-out patch recordings. · source_derived_draft · unverified_draft
## glutamate-nmda-glycine An amino acid usually associated with inhibition can assist an excitatory receptor. Glycine increased opening frequency of NMDA-activated channels in cultured mouse brain neurons, with potentiation detected at 10 nM. Model: Mouse cultured neurons and outside-out patch recordings. Limitations: The effect was distinct from strychnine-sensitive glycine receptors; it does not define an oral glycine or glutamate response. Evidence access: Primary abstract Glycine potentiates the NMDA response in cultured mouse brain neurons. · 1987 · https://pubmed.ncbi.nlm.nih.gov/2433595/ · DOI 10.1038/325529a0
Complete structured claim and evidence
Chloride activated glutamate uptake by purified rat VGLUT2 in reconstituted proteoliposomes.
Chloride ion → Rat vesicular glutamate transporter 2 / Slc17a6 source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text
experimental_model
Rat VGLUT2 expressed in insect cells, purified and reconstituted; membrane-potential-driven uptake.
limitations
Chloride regulation in vesicles is not equivalent to an effect of dietary salt.
nutrient_topic
L-Glutamate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Glutamate
plain_language
An ion regulates whether the vesicle-loading transporter works.
primary_references
Metabolic control of vesicular glutamate transport and release. · 2010 · https://pubmed.ncbi.nlm.nih.gov/20920794/ · DOI 10.1016/j.neuron.2010.09.002
L-Glutamate / L-glutamic acid: carbon and nitrogen allocation, signaling 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 · Rat VGLUT2 expressed in insect cells, purified and reconstituted; membrane-potential-driven uptake. · source_derived_draft · unverified_draft
## glutamate-vglut2-chloride An ion regulates whether the vesicle-loading transporter works. Chloride activated glutamate uptake by purified rat VGLUT2 in reconstituted proteoliposomes. Model: Rat VGLUT2 expressed in insect cells, purified and reconstituted; membrane-potential-driven uptake. Limitations: Chloride regulation in vesicles is not equivalent to an effect of dietary salt. Evidence access: Primary full text Metabolic control of vesicular glutamate transport and release. · 2010 · https://pubmed.ncbi.nlm.nih.gov/20920794/ · DOI 10.1016/j.neuron.2010.09.002
Complete structured claim and evidence
Glutamate at 10 nM promoted integrin-mediated adhesion of tested human T cells to laminin and fibronectin; AMPA antagonists and relevant anti-integrin antibodies blocked the response.
L-Glutamate → Glutamate-evoked human T-cell adhesion source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Human T-cell receptor expression and adhesion assays.
limitations
Antagonist support does not uniquely prove GluA3 is the sole functional subunit; no dietary immune benefit is established.
nutrient_topic
L-Glutamate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Glutamate
plain_language
An extracellular amino acid changed immune-cell behavior in an assay.
primary_references
Human T cells express a functional ionotropic glutamate receptor GluR3, and glutamate by itself triggers integrin-mediated adhesion to laminin and fibronectin and chemotactic migration. · 2003 · https://pubmed.ncbi.nlm.nih.gov/12682273/ · DOI 10.4049/jimmunol.170.8.4362
L-Glutamate / L-glutamic acid: carbon and nitrogen allocation, signaling and cross-nutrient mechanisms (2026-09-19) · lines 354–360
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human T-cell receptor expression and adhesion assays. · source_derived_draft · unverified_draft
## glutamate-immune-adhesion An extracellular amino acid changed immune-cell behavior in an assay. Glutamate at 10 nM promoted integrin-mediated adhesion of tested human T cells to laminin and fibronectin; AMPA antagonists and relevant anti-integrin antibodies blocked the response. Model: Human T-cell receptor expression and adhesion assays. Limitations: Antagonist support does not uniquely prove GluA3 is the sole functional subunit; no dietary immune benefit is established. Evidence access: Primary abstract Human T cells express a functional ionotropic glutamate receptor GluR3, and glutamate by itself triggers integrin-mediated adhesion to laminin and fibronectin and chemotactic migration. · 2003 · https://pubmed.ncbi.nlm.nih.gov/12682273/ · DOI 10.4049/jimmunol.170.8.4362
Complete structured claim and evidence
Human mitochondrial glutamyl-tRNA synthetase attached glutamate to mitochondrial tRNA(Gln), generating the intermediate Glu-tRNA(Gln).
Human mitochondrial glutamyl-tRNA synthetase / EARS2 → Human mitochondrial glutamyl-tRNA(Gln) source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Recombinant human enzyme and mitochondrial tRNA biochemistry.
limitations
This intermediate is not glutamate being correctly incorporated at glutamine codons.
nutrient_topic
L-Glutamate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Glutamate
plain_language
A deliberately intermediate amino-acid attachment must be processed before translation.
primary_references
Biogenesis of glutaminyl-mt tRNAGln in human mitochondria. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19805282/ · DOI 10.1073/pnas.0907602106
L-Glutamate / L-glutamic acid: carbon and nitrogen allocation, signaling and cross-nutrient mechanisms (2026-09-19) · lines 370–376
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Recombinant human enzyme and mitochondrial tRNA biochemistry. · source_derived_draft · unverified_draft
## glutamate-ears2-intermediate A deliberately intermediate amino-acid attachment must be processed before translation. Human mitochondrial glutamyl-tRNA synthetase attached glutamate to mitochondrial tRNA(Gln), generating the intermediate Glu-tRNA(Gln). Model: Recombinant human enzyme and mitochondrial tRNA biochemistry. Limitations: This intermediate is not glutamate being correctly incorporated at glutamine codons. Evidence access: Primary abstract Biogenesis of glutaminyl-mt tRNAGln in human mitochondria. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19805282/ · DOI 10.1073/pnas.0907602106
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.

Blood exposure changes with meal composition and timing

Condition: biomarker_context · Acute oral loading with different carbohydrate conditions.

Normal role: Gut handling determines systemic exposure.

Recorded consequence: Different plasma responses, without equivalent red-cell changes.

Scope: Human short-term studies.

Present tastant, missing intracellular taste machinery

Condition: machinery_impairment · Mouse Plcb2 or Trpm5 deletion and selective rescue.

Normal role: Taste receptors require intracellular signaling.

Recorded consequence: Lost or selectively restored responses.

Scope: Mouse taste experiments.

Sensing survives but ATP transmission fails

Condition: machinery_impairment · Calhm1 or Calhm3 deletion.

Normal role: Taste cells transmit an ATP signal.

Recorded consequence: Impaired ATP release and perception.

Scope: Mouse knockout physiology.

Loss of one receptor leaves some detection

Condition: machinery_impairment · Mouse Tas1r3 knockout.

Normal role: T1R3 participates in umami recognition.

Recorded consequence: Diminished but residual responses.

Scope: Mouse receptor deletion.

Available glutamate cannot bypass a blocked gut relay

Condition: machinery_impairment · Serotonin depletion, receptor blockade or NOS inhibition.

Normal role: Local mediators connect luminal sensing to vagal firing.

Recorded consequence: Lost evoked nerve responses.

Scope: Rat gastric experiments.

Blocking mediators changes the mucosal response

Condition: machinery_impairment · Indomethacin or capsaicin pretreatment.

Normal role: Local glutamate signaling can affect mucus and pH.

Recorded consequence: Reduced measured response.

Scope: Rat duodenal perfusion.

The sources

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L-Glutamate / L-glutamic acid: carbon and nitrogen allocation, signaling and cross-nutrient mechanisms (2026-09-19)AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · unverified_draftRead preserved source
Magnesium: cross-nutrient mechanisms and deficiency (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
Manganese: enzyme cofactors, glycosylation, transport and nutrient interactions (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
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
Sulforaphane: formation, electrophile sensing and nutrient connections (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
Vitamin B6: mechanisms, deficiency and nutrient interactions (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

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.

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Monosodium L-glutamate

The mechanisms

MSG is the sodium salt of L-glutamate; the sensory study treats added MSG and NaCl as separate ingredients.

In eight adults receiving 150 mg/kg MSG in water, adding 1.1 g/kg hydrolyzed corn starch lowered mean peak plasma glutamate from 59.4 to 7.18 micromol/dL.

Erythrocyte glutamate and aspartate concentrations did not change in either arm of the eight-person MSG/carbohydrate experiment.

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.

Nine men received 150 mg/kg MSG capsules 30 minutes before a drink; plasma glutamate rose about tenfold without carbohydrate and sixfold with a 75 g carbohydrate drink.

The MSG-plus-carbohydrate condition had lower peak serum glucose than carbohydrate alone, 5.50 versus 7.69 mmol/L.

C-peptide-based insulin secretion did not differ on average: four participants increased and five decreased in the MSG-plus-carbohydrate condition.

Receptor chimeras, mutagenesis and modeling support glutamate binding near the hinge of the T1R1 Venus-flytrap domain.

The cooperative model places a 5-prime-ribonucleotide at an adjacent opening-side site, stabilizing the closed glutamate-bound receptor conformation.

Plcb2 knockout abolished tested sweet, amino-acid and bitter responses while sparing sour and salty responses in the reported mouse experiments.

Trpm5 knockout disrupted the same tested taste modalities in the mouse study.

Restoring Plcb2 only in bitter-receptor cells rescued bitter responses but not sweet or amino-acid responses.

Calhm1 knockout reduced taste-evoked ATP release without eliminating taste-cell excitability to the stimuli.

CALHM3 coassembly with CALHM1 conferred rapid voltage-dependent ATP-release-channel gating; the study connected this complex to type II taste-cell physiology.

Calhm3 deletion abolished taste-evoked ATP release and disrupted GPCR-mediated taste perception in mice.

Tas1r3-null mice retained diminished behavioral and nerve responses to umami compounds.

Glutamate taste with a consonant savory odor produced supralinear fMRI responses in medial orbitofrontal and pregenual cingulate regions, related to flavor pleasantness.

Serotonin depletion blocked glutamate-evoked gastric vagal firing in rats.

Blocking 5-HT3 receptors prevented the rat gastric vagal response to luminal glutamate.

NOS inhibition blocked glutamate-evoked vagal firing; an NO donor mimicked firing and its response was blocked by 5-HT3 antagonism.

Luminal L-glutamate increased epithelial pH in rat duodenum.

Glutamate increased rat duodenal mucus thickness without increasing measured blood flow.

mGluR4 agonists mimicked and an antagonist inhibited glutamate-associated pH and mucus responses.

Glutamate plus IMP enhanced bicarbonate secretion in rat duodenum.

Indomethacin or capsaicin pretreatment reduced glutamate-associated mucus and pH responses.

MSG shortened the estimated half-emptying time of a protein-rich liquid meal in ten healthy men.

The same study found no significant MSG effect for carbohydrate-rich liquid or water meals in nine men.

In ten men, 60-minute gastric residual volume did not differ significantly between mixed liquid meals with and without 0.5% MSG, P=0.45.

Eight participants had faster emptying with MSG; two slowed. Duodenal wall-motion analysis in four of the eight showed increased motility.

In 584 participants, adding 0.3% MSG improved palatability ratings at tested 0.3%, 0.6% and 0.9% NaCl concentrations.

In 130 self-reported MSG-reactive volunteers given 5 g without food, 50 responded to MSG only, 17 to placebo only and 19 to both.

Repeated challenges did not establish consistent individual symptom patterns; the two final participants each reacted to only one of three MSG-with-food challenges.

A blinded crossover in twelve adults reporting MSG-associated asthma found no definite immediate or late asthmatic reaction to 1 g or 5 g MSG versus lactose placebo.

In postabsorptive healthy adults, tracer comparisons estimated 96 ± 1% first-pass splanchnic extraction of enterally delivered glutamate.

About 78 ± 3% of enterally delivered carbon-labeled glutamate tracer was recovered as exhaled CO2 in the study.

After six fasted adults ingested 100 mg nitrogen-labeled L-glutamic acid, most recovered circulating amino-acid label appeared in alanine and glutamine, with no significant amino-acid concentration changes during 150 minutes.

Coexpressed human T1R1/T1R3 responded to L-glutamate in receptor assays.

5-prime-ribonucleotides enhanced the human T1R1/T1R3 response to L-glutamate.

Human/mouse receptor chimeras and point mutants mapped acidic-amino-acid selectivity to the T1R1 ligand-binding region and identified other residues that broadened mouse-type responses.

Intragastric 150 mM MSG increased gastric vagal afferent discharge in anesthetized rats.

MSG-evoked celiac vagal and adrenal splanchnic efferent responses were abolished by gastric vagotomy in rats.

Current reversal measurements supported uptake of one glutamate anion with three sodium ions and one proton, coupled to outward movement of one potassium ion.

Bovine brain-capillary membrane preparations contained EAAT1/2/3 on the abluminal side and showed voltage- and potassium-dependent glutamate uptake.

Glutamate-cysteine ligase joins glutamate and cysteine to form gamma-glutamylcysteine in the first glutathione-synthesis step.

Added extracellular glutamate inhibited cystine uptake in N18-RE-105 neuronal hybrid cells, and toxicity tracked that inhibition.

PLP-bound human GAD67 catalyzes glutamate decarboxylation to GABA.

Human GPT catalyzes reversible amino transfer between alanine and 2-oxoglutarate, producing pyruvate and glutamate.

Human GOT1 catalyzes reversible amino transfer between aspartate and 2-oxoglutarate, producing oxaloacetate and glutamate.

Recombinant human NAGS catalyzed N-acetylglutamate formation from glutamate and acetyl-CoA.

N-acetylglutamate binding reshaped human CPS1 and established the channel linking its two phosphorylation sites.

Human glutamine synthetase catalyzes ATP-coupled ligation of glutamate and ammonia to make glutamine.

Reconstituted human glutamate carrier 1 supported glutamate transport coupled to a proton gradient.

The GLUD1 study identifies glutamate oxidation to 2-oxoglutarate as the enzyme reaction underlying its metabolic and regulatory investigation.

Human P5CS links glutamate to P5C synthesis through ATP- and NADPH-dependent chemistry.

Purified human cytosolic FPGS used tetrahydrofolate as an effective substrate for polyglutamate synthesis.

Extracellular Mg caused voltage-dependent block of NMDA-type currents in cultured mouse neurons, stronger at hyperpolarized potentials.

Glycine increased opening frequency of NMDA-activated channels in cultured mouse brain neurons, with potentiation detected at 10 nM.

Chloride activated glutamate uptake by purified rat VGLUT2 in reconstituted proteoliposomes.

Glutamate at 10 nM promoted integrin-mediated adhesion of tested human T cells to laminin and fibronectin; AMPA antagonists and relevant anti-integrin antibodies blocked the response.

Human mitochondrial glutamyl-tRNA synthetase attached glutamate to mitochondrial tRNA(Gln), generating the intermediate Glu-tRNA(Gln).

Availability and dependencies

The sources

Recorded disagreements

Open questions in this collection