Component
Taurine
Taurine. Species, exposure and limitations are retained in each linked claim.
81 recorded relationships. Experimental role, claim status and evidence remain attached to each record.
How nutrients influence it
Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
How nutrients reach it in more than one step
Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.
Tracing routes…
What it does
Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.
What it acts on
The 2023 study reported lower circulating taurine with age in its human samples, alongside corresponding age comparisons in mice and monkeys.
Experimental context and source evidence
- availability_state
- biomarker_context Imported condition classification; unverified.
- evidence_access
- Primary abstract
- experimental_model
- Human age-group observations; separate animal datasets.
- limitations
- Association alone does not establish deficiency as a cause or specify a universal threshold.
- nutrient_topic
- Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
- plain_language
- The original aging paper reported a fall in blood taurine.
- primary_references
- Taurine deficiency as a driver of aging. · 2023 · https://pubmed.ncbi.nlm.nih.gov/37289866/ · DOI 10.1126/science.abn9257
- trigger_kind
- biomarker_context Imported condition classification; unverified.
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 569–575
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human age-group observations; separate animal datasets. · source_derived_draft · unverified_draft
## taurine-aging-decline The original aging paper reported a fall in blood taurine. The 2023 study reported lower circulating taurine with age in its human samples, alongside corresponding age comparisons in mice and monkeys. Model: Human age-group observations; separate animal datasets. Limitations: Association alone does not establish deficiency as a cause or specify a universal threshold. Evidence access: Primary abstract Taurine deficiency as a driver of aging. · 2023 · https://pubmed.ncbi.nlm.nih.gov/37289866/ · DOI 10.1126/science.abn9257
Complete structured claim and evidenceIn 137 physically active and inactive men aged 20–93, circulating taurine was not associated with age, muscle mass, strength, physical performance or mitochondrial function.
Experimental context and source evidence
- availability_state
- biomarker_context Imported condition classification; unverified.
- evidence_access
- Primary abstract
- experimental_model
- Human observational study of men spanning adult ages.
- limitations
- No randomized taurine intervention; findings do not establish equivalence in women or every tissue.
- nutrient_topic
- Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
- plain_language
- Another human dataset did not support blood taurine as a simple aging signal.
- primary_references
- Experimental Evidence Against Taurine Deficiency as a Driver of Aging in Humans. · 2025 · https://pubmed.ncbi.nlm.nih.gov/41061678/ · DOI 10.1111/acel.70191
- trigger_kind
- biomarker_context Imported condition classification; unverified.
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 585–591
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human observational study of men spanning adult ages. · source_derived_draft · unverified_draft
## taurine-aging-men-null Another human dataset did not support blood taurine as a simple aging signal. In 137 physically active and inactive men aged 20–93, circulating taurine was not associated with age, muscle mass, strength, physical performance or mitochondrial function. Model: Human observational study of men spanning adult ages. Limitations: No randomized taurine intervention; findings do not establish equivalence in women or every tissue. Evidence access: Primary abstract Experimental Evidence Against Taurine Deficiency as a Driver of Aging in Humans. · 2025 · https://pubmed.ncbi.nlm.nih.gov/41061678/ · DOI 10.1111/acel.70191
Complete structured claim and evidenceTaurine treatment improved several measured health-related outcomes in monkeys in the 2023 study.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Nonhuman-primate supplementation arm.
- limitations
- The study did not establish longer primate or human lifespan; health measures should not be relabeled survival.
- nutrient_topic
- Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
- plain_language
- The primate arm measured health outcomes rather than lifespan extension.
- primary_references
- Taurine deficiency as a driver of aging. · 2023 · https://pubmed.ncbi.nlm.nih.gov/37289866/ · DOI 10.1126/science.abn9257
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 609–615
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Nonhuman-primate supplementation arm. · source_derived_draft · unverified_draft
## taurine-aging-monkey-health The primate arm measured health outcomes rather than lifespan extension. Taurine treatment improved several measured health-related outcomes in monkeys in the 2023 study. Model: Nonhuman-primate supplementation arm. Limitations: The study did not establish longer primate or human lifespan; health measures should not be relabeled survival. Evidence access: Primary abstract Taurine deficiency as a driver of aging. · 2023 · https://pubmed.ncbi.nlm.nih.gov/37289866/ · DOI 10.1126/science.abn9257
Complete structured claim and evidenceStarting 1000 mg/kg/day taurine at 14 months increased median lifespan by approximately 10–12% in the reported male and female mouse cohorts.
Experimental context and source evidence
- evidence_access
- Primary full text, lifespan results and Figure 1
- experimental_model
- C57BL/6J mice treated daily until death; same chow in both arms.
- limitations
- High animal exposure is not a human dose or proof of human lifespan extension.
- nutrient_topic
- Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
- plain_language
- The mouse intervention reported longer survival.
- primary_references
- Taurine deficiency as a driver of aging. · 2023 · https://pubmed.ncbi.nlm.nih.gov/37289866/ · DOI 10.1126/science.abn9257
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 593–599
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · C57BL/6J mice treated daily until death; same chow in both arms. · source_derived_draft · unverified_draft
## taurine-aging-mouse-lifespan The mouse intervention reported longer survival. Starting 1000 mg/kg/day taurine at 14 months increased median lifespan by approximately 10–12% in the reported male and female mouse cohorts. Model: C57BL/6J mice treated daily until death; same chow in both arms. Limitations: High animal exposure is not a human dose or proof of human lifespan extension. Evidence access: Primary full text, lifespan results and Figure 1 Taurine deficiency as a driver of aging. · 2023 · https://pubmed.ncbi.nlm.nih.gov/37289866/ · DOI 10.1126/science.abn9257
Complete structured claim and evidenceThe 2025 study found circulating taurine increased or remained unchanged with age in three geographically distinct human cohorts, with longitudinal and cross-sectional analyses and supporting nonhuman datasets.
Experimental context and source evidence
- availability_state
- biomarker_context Imported condition classification; unverified.
- evidence_access
- Primary abstract
- experimental_model
- Human cohorts plus nonhuman primates and mice; repeated and cross-sectional measurements.
- limitations
- A biomarker challenge does not by itself refute every animal supplementation outcome.
- nutrient_topic
- Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
- plain_language
- Later data did not reproduce a consistent age-related decline.
- primary_references
- Is taurine an aging biomarker? · 2025 · https://pubmed.ncbi.nlm.nih.gov/40472098/ · DOI 10.1126/science.adl2116
- trigger_kind
- biomarker_context Imported condition classification; unverified.
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 577–583
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human cohorts plus nonhuman primates and mice; repeated and cross-sectional measurements. · source_derived_draft · unverified_draft
## taurine-aging-not-universal Later data did not reproduce a consistent age-related decline. The 2025 study found circulating taurine increased or remained unchanged with age in three geographically distinct human cohorts, with longitudinal and cross-sectional analyses and supporting nonhuman datasets. Model: Human cohorts plus nonhuman primates and mice; repeated and cross-sectional measurements. Limitations: A biomarker challenge does not by itself refute every animal supplementation outcome. Evidence access: Primary abstract Is taurine an aging biomarker? · 2025 · https://pubmed.ncbi.nlm.nih.gov/40472098/ · DOI 10.1126/science.adl2116
Complete structured claim and evidenceTaurine supplementation extended C. elegans lifespan across the reported worm experiments, with dose-dependent effects.
Experimental context and source evidence
- evidence_access
- Primary full text, Figure 1 and supplementary-cohort description
- experimental_model
- C. elegans intervention cohorts in the 2023 study.
- limitations
- Organism-specific exposure and metabolism; not an additional human trial.
- nutrient_topic
- Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
- plain_language
- A separate organism also showed a survival response.
- primary_references
- Taurine deficiency as a driver of aging. · 2023 · https://pubmed.ncbi.nlm.nih.gov/37289866/ · DOI 10.1126/science.abn9257
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 601–607
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · C. elegans intervention cohorts in the 2023 study. · source_derived_draft · unverified_draft
## taurine-aging-worm-lifespan A separate organism also showed a survival response. Taurine supplementation extended C. elegans lifespan across the reported worm experiments, with dose-dependent effects. Model: C. elegans intervention cohorts in the 2023 study. Limitations: Organism-specific exposure and metabolism; not an additional human trial. Evidence access: Primary full text, Figure 1 and supplementary-cohort description Taurine deficiency as a driver of aging. · 2023 · https://pubmed.ncbi.nlm.nih.gov/37289866/ · DOI 10.1126/science.abn9257
Complete structured claim and evidenceIn 120 adults with prehypertension randomized to 1.6 g/day taurine or placebo for 12 weeks, clinic systolic pressure fell by 7.2 versus 2.6 mmHg and ambulatory systolic pressure by 3.8 versus 0.3 mmHg.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Randomized double-blind placebo-controlled human trial.
- limitations
- These are within-arm changes; the trial did not establish long-term cardiovascular-event reduction.
- nutrient_topic
- Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
- plain_language
- One controlled trial found a modest blood-pressure reduction.
- primary_references
- Taurine Supplementation Lowers Blood Pressure and Improves Vascular Function in Prehypertension: Randomized, Double-Blind, Placebo-Controlled Study. · 2016 · https://pubmed.ncbi.nlm.nih.gov/26781281/ · DOI 10.1161/HYPERTENSIONAHA.115.06624
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 473–479
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Randomized double-blind placebo-controlled human trial. · source_derived_draft · unverified_draft
## taurine-bp-trial One controlled trial found a modest blood-pressure reduction. In 120 adults with prehypertension randomized to 1.6 g/day taurine or placebo for 12 weeks, clinic systolic pressure fell by 7.2 versus 2.6 mmHg and ambulatory systolic pressure by 3.8 versus 0.3 mmHg. Model: Randomized double-blind placebo-controlled human trial. Limitations: These are within-arm changes; the trial did not establish long-term cardiovascular-event reduction. Evidence access: Primary abstract Taurine Supplementation Lowers Blood Pressure and Improves Vascular Function in Prehypertension: Randomized, Double-Blind, Placebo-Controlled Study. · 2016 · https://pubmed.ncbi.nlm.nih.gov/26781281/ · DOI 10.1161/HYPERTENSIONAHA.115.06624
Complete structured claim and evidenceTaurine at 10–100 micromolar reduced excitability of mouse thalamocortical neurons and evoked tonic currents consistent with extrasynaptic alpha4beta2delta GABA-A receptors.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Mouse ventrobasal thalamic neurons and recombinant receptor comparisons.
- limitations
- Bath concentration is not an oral dose; this does not establish treatment of human anxiety or insomnia.
- nutrient_topic
- Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
- plain_language
- A low concentration changed neuronal firing in this mouse brain region.
- primary_references
- Taurine is a potent activator of extrasynaptic GABA(A) receptors in the thalamus. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18171928/ · DOI 10.1523/JNEUROSCI.3996-07.2008
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 433–439
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse ventrobasal thalamic neurons and recombinant receptor comparisons. · source_derived_draft · unverified_draft
## taurine-gabaa-tonic A low concentration changed neuronal firing in this mouse brain region. Taurine at 10–100 micromolar reduced excitability of mouse thalamocortical neurons and evoked tonic currents consistent with extrasynaptic alpha4beta2delta GABA-A receptors. Model: Mouse ventrobasal thalamic neurons and recombinant receptor comparisons. Limitations: Bath concentration is not an oral dose; this does not establish treatment of human anxiety or insomnia. Evidence access: Primary abstract Taurine is a potent activator of extrasynaptic GABA(A) receptors in the thalamus. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18171928/ · DOI 10.1523/JNEUROSCI.3996-07.2008
Complete structured claim and evidenceApplied taurine activated recombinant human alpha1 homomeric glycine receptors in oocytes and HEK293 cells; its potency and efficacy varied with the experimental receptor response.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Human receptor expressed in Xenopus oocytes or human cells; electrophysiology.
- limitations
- Not a clinical sedative effect; chloride gradient and receptor composition shape cellular response.
- nutrient_topic
- Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
- plain_language
- Taurine can activate a receptor named for glycine.
- primary_references
- Activation of human alpha1 and alpha2 homomeric glycine receptors by taurine and GABA. · 2001 · https://pubmed.ncbi.nlm.nih.gov/11559772/ · DOI 10.1111/j.1469-7793.2001.t01-1-00741.x
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 417–423
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human receptor expressed in Xenopus oocytes or human cells; electrophysiology. · source_derived_draft · unverified_draft
## taurine-glycine-receptor-alpha1 Taurine can activate a receptor named for glycine. Applied taurine activated recombinant human alpha1 homomeric glycine receptors in oocytes and HEK293 cells; its potency and efficacy varied with the experimental receptor response. Model: Human receptor expressed in Xenopus oocytes or human cells; electrophysiology. Limitations: Not a clinical sedative effect; chloride gradient and receptor composition shape cellular response. Evidence access: Primary abstract Activation of human alpha1 and alpha2 homomeric glycine receptors by taurine and GABA. · 2001 · https://pubmed.ncbi.nlm.nih.gov/11559772/ · DOI 10.1111/j.1469-7793.2001.t01-1-00741.x
Complete structured claim and evidenceApplied taurine also activated human alpha2 homomeric glycine receptors, with efficacy varying from weak to full agonism across tested conditions.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Recombinant human alpha2 receptor electrophysiology.
- limitations
- Avoid labeling taurine a universally weak or full agonist.
- nutrient_topic
- Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
- plain_language
- The receptor subtype and cell setting change the strength of taurine signaling.
- primary_references
- Activation of human alpha1 and alpha2 homomeric glycine receptors by taurine and GABA. · 2001 · https://pubmed.ncbi.nlm.nih.gov/11559772/ · DOI 10.1111/j.1469-7793.2001.t01-1-00741.x
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 425–431
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Recombinant human alpha2 receptor electrophysiology. · source_derived_draft · unverified_draft
## taurine-glycine-receptor-alpha2 The receptor subtype and cell setting change the strength of taurine signaling. Applied taurine also activated human alpha2 homomeric glycine receptors, with efficacy varying from weak to full agonism across tested conditions. Model: Recombinant human alpha2 receptor electrophysiology. Limitations: Avoid labeling taurine a universally weak or full agonist. Evidence access: Primary abstract Activation of human alpha1 and alpha2 homomeric glycine receptors by taurine and GABA. · 2001 · https://pubmed.ncbi.nlm.nih.gov/11559772/ · DOI 10.1111/j.1469-7793.2001.t01-1-00741.x
Complete structured claim and evidenceTaurine supplementation increased measured plasma hydrogen sulfide in the blood-pressure trial; changes in pressure were negatively correlated with H2S and taurine concentrations.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Human randomized trial with biomarker correlations.
- limitations
- Correlation within the trial does not prove H2S mediated the clinical blood-pressure effect.
- nutrient_topic
- Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
- plain_language
- The study linked the response to a sulfur signaling molecule.
- primary_references
- Taurine Supplementation Lowers Blood Pressure and Improves Vascular Function in Prehypertension: Randomized, Double-Blind, Placebo-Controlled Study. · 2016 · https://pubmed.ncbi.nlm.nih.gov/26781281/ · DOI 10.1161/HYPERTENSIONAHA.115.06624
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 489–495
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human randomized trial with biomarker correlations. · source_derived_draft · unverified_draft
## taurine-human-h2s The study linked the response to a sulfur signaling molecule. Taurine supplementation increased measured plasma hydrogen sulfide in the blood-pressure trial; changes in pressure were negatively correlated with H2S and taurine concentrations. Model: Human randomized trial with biomarker correlations. Limitations: Correlation within the trial does not prove H2S mediated the clinical blood-pressure effect. Evidence access: Primary abstract Taurine Supplementation Lowers Blood Pressure and Improves Vascular Function in Prehypertension: Randomized, Double-Blind, Placebo-Controlled Study. · 2016 · https://pubmed.ncbi.nlm.nih.gov/26781281/ · DOI 10.1161/HYPERTENSIONAHA.115.06624
Complete structured claim and evidenceTaurine treatment reduced agonist-induced vascular reactivity through inhibition of TRPC3-mediated calcium influx in human mesenteric artery experiments.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Human artery preparations in the translational blood-pressure study.
- limitations
- Do not infer that oral taurine directly binds TRPC3; the signaling pathway and clinical mediation are distinct.
- nutrient_topic
- Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
- plain_language
- The mechanistic experiments implicated a calcium entry channel.
- primary_references
- Taurine Supplementation Lowers Blood Pressure and Improves Vascular Function in Prehypertension: Randomized, Double-Blind, Placebo-Controlled Study. · 2016 · https://pubmed.ncbi.nlm.nih.gov/26781281/ · DOI 10.1161/HYPERTENSIONAHA.115.06624
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 497–503
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human artery preparations in the translational blood-pressure study. · source_derived_draft · unverified_draft
## taurine-human-trpc3 The mechanistic experiments implicated a calcium entry channel. Taurine treatment reduced agonist-induced vascular reactivity through inhibition of TRPC3-mediated calcium influx in human mesenteric artery experiments. Model: Human artery preparations in the translational blood-pressure study. Limitations: Do not infer that oral taurine directly binds TRPC3; the signaling pathway and clinical mediation are distinct. Evidence access: Primary abstract Taurine Supplementation Lowers Blood Pressure and Improves Vascular Function in Prehypertension: Randomized, Double-Blind, Placebo-Controlled Study. · 2016 · https://pubmed.ncbi.nlm.nih.gov/26781281/ · DOI 10.1161/HYPERTENSIONAHA.115.06624
Complete structured claim and evidenceExogenous taurine increased leukemia-cell colony formation and accelerated disease progression in the tested immunocompetent mouse leukemia model.
Experimental context and source evidence
- evidence_access
- Primary full text, Extended Data Figure 5o–r and results
- experimental_model
- Mouse leukemia supplementation experiments, with separate patient-derived cell colony assays.
- limitations
- Not a human trial or proof that taurine initiates leukemia in healthy people.
- nutrient_topic
- Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
- plain_language
- Additional taurine worsened an existing malignancy in this experimental setting.
- primary_references
- Taurine from tumour niche drives glycolysis to promote leukaemogenesis. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40369079/ · DOI 10.1038/s41586-025-09018-7
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 553–559
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse leukemia supplementation experiments, with separate patient-derived cell colony assays. · source_derived_draft · unverified_draft
## taurine-leukemia-supplement Additional taurine worsened an existing malignancy in this experimental setting. Exogenous taurine increased leukemia-cell colony formation and accelerated disease progression in the tested immunocompetent mouse leukemia model. Model: Mouse leukemia supplementation experiments, with separate patient-derived cell colony assays. Limitations: Not a human trial or proof that taurine initiates leukemia in healthy people. Evidence access: Primary full text, Extended Data Figure 5o–r and results Taurine from tumour niche drives glycolysis to promote leukaemogenesis. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40369079/ · DOI 10.1038/s41586-025-09018-7
Complete structured claim and evidenceDuring the ten-patient 52-week open-label MELAS trial, six patients had no stroke-like episodes in the evaluation period and annual episode frequency fell from 2.22 to 0.72.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_access
- Primary abstract
- experimental_model
- Within-patient comparison without a placebo group.
- limitations
- The 60% response estimate had a wide 95% CI of 26.2–87.8%; no general anti-aging or energy inference.
- nutrient_topic
- Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
- plain_language
- The small disease-specific study reported fewer episodes during treatment.
- primary_references
- Taurine supplementation for prevention of stroke-like episodes in MELAS: a multicentre, open-label, 52-week phase III trial. · 2019 · https://pubmed.ncbi.nlm.nih.gov/29666206/ · DOI 10.1136/jnnp-2018-317964
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 289–295
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Within-patient comparison without a placebo group. · source_derived_draft · unverified_draft
## taurine-melas-episodes The small disease-specific study reported fewer episodes during treatment. During the ten-patient 52-week open-label MELAS trial, six patients had no stroke-like episodes in the evaluation period and annual episode frequency fell from 2.22 to 0.72. Model: Within-patient comparison without a placebo group. Limitations: The 60% response estimate had a wide 95% CI of 26.2–87.8%; no general anti-aging or energy inference. Evidence access: Primary abstract Taurine supplementation for prevention of stroke-like episodes in MELAS: a multicentre, open-label, 52-week phase III trial. · 2019 · https://pubmed.ncbi.nlm.nih.gov/29666206/ · DOI 10.1136/jnnp-2018-317964
Complete structured claim and evidenceFive patients in the ten-person MELAS trial showed a significant increase in leukocyte mitochondrial tRNA-Leu(UUR) taurine modification after high-dose taurine treatment.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_access
- Primary abstract
- experimental_model
- Open-label 52-week study; 9 or 12 g/day under clinical supervision.
- limitations
- Five molecular responders among ten patients; leukocyte measurements are not direct brain-tissue measurements.
- nutrient_topic
- Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
- plain_language
- A molecular response was measurable in a specific mitochondrial disease.
- primary_references
- Taurine supplementation for prevention of stroke-like episodes in MELAS: a multicentre, open-label, 52-week phase III trial. · 2019 · https://pubmed.ncbi.nlm.nih.gov/29666206/ · DOI 10.1136/jnnp-2018-317964
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 281–287
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Open-label 52-week study; 9 or 12 g/day under clinical supervision. · source_derived_draft · unverified_draft
## taurine-melas-rna-response A molecular response was measurable in a specific mitochondrial disease. Five patients in the ten-person MELAS trial showed a significant increase in leukocyte mitochondrial tRNA-Leu(UUR) taurine modification after high-dose taurine treatment. Model: Open-label 52-week study; 9 or 12 g/day under clinical supervision. Limitations: Five molecular responders among ten patients; leukocyte measurements are not direct brain-tissue measurements. Evidence access: Primary abstract Taurine supplementation for prevention of stroke-like episodes in MELAS: a multicentre, open-label, 52-week phase III trial. · 2019 · https://pubmed.ncbi.nlm.nih.gov/29666206/ · DOI 10.1136/jnnp-2018-317964
Complete structured claim and evidenceSupplying exogenous taurine enhanced microbiota-mediated resistance to subsequent enteric infection in mice.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Mouse infection, microbiota and taurine intervention experiments.
- limitations
- This outcome differs from Il10-null colitis; neither result is a universal rule about intestinal taurine.
- nutrient_topic
- Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
- plain_language
- In another setting, feeding microbes taurine improved pathogen resistance.
- primary_references
- Infection trains the host for microbiota-enhanced resistance to pathogens. · 2021 · https://pubmed.ncbi.nlm.nih.gov/33453153/ · DOI 10.1016/j.cell.2020.12.011
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 345–351
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse infection, microbiota and taurine intervention experiments. · source_derived_draft · unverified_draft
## taurine-microbial-protection In another setting, feeding microbes taurine improved pathogen resistance. Supplying exogenous taurine enhanced microbiota-mediated resistance to subsequent enteric infection in mice. Model: Mouse infection, microbiota and taurine intervention experiments. Limitations: This outcome differs from Il10-null colitis; neither result is a universal rule about intestinal taurine. Evidence access: Primary abstract Infection trains the host for microbiota-enhanced resistance to pathogens. · 2021 · https://pubmed.ncbi.nlm.nih.gov/33453153/ · DOI 10.1016/j.cell.2020.12.011
Complete structured claim and evidenceThe same study reported reduced TRPC3-mediated calcium influx and vascular reactivity in mouse mesenteric artery experiments after taurine treatment.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Mouse vascular experiments paired with the human study.
- limitations
- Mouse and human preparations are linked evidence, not identical biological records.
- nutrient_topic
- Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
- plain_language
- The vascular mechanism was also examined in mouse arteries.
- primary_references
- Taurine Supplementation Lowers Blood Pressure and Improves Vascular Function in Prehypertension: Randomized, Double-Blind, Placebo-Controlled Study. · 2016 · https://pubmed.ncbi.nlm.nih.gov/26781281/ · DOI 10.1161/HYPERTENSIONAHA.115.06624
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 505–511
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse vascular experiments paired with the human study. · source_derived_draft · unverified_draft
## taurine-mouse-trpc3 The vascular mechanism was also examined in mouse arteries. The same study reported reduced TRPC3-mediated calcium influx and vascular reactivity in mouse mesenteric artery experiments after taurine treatment. Model: Mouse vascular experiments paired with the human study. Limitations: Mouse and human preparations are linked evidence, not identical biological records. Evidence access: Primary abstract Taurine Supplementation Lowers Blood Pressure and Improves Vascular Function in Prehypertension: Randomized, Double-Blind, Placebo-Controlled Study. · 2016 · https://pubmed.ncbi.nlm.nih.gov/26781281/ · DOI 10.1161/HYPERTENSIONAHA.115.06624
Complete structured claim and evidenceTaurine slightly increased contractile calcium sensitivity in human type I fibers, but not type II fibers; maximum calcium-activated force was unchanged in both.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Same human skinned-fiber study.
- limitations
- Small preparation-specific effect; do not merge with rodent muscle or whole-person strength.
- nutrient_topic
- Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
- plain_language
- The contractile response differed between muscle fiber types.
- primary_references
- Acute effects of taurine on sarcoplasmic reticulum Ca2+ accumulation and contractility in human type I and type II skeletal muscle fibers. · 2014 · https://pubmed.ncbi.nlm.nih.gov/25123198/ · DOI 10.1152/japplphysiol.00494.2014
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 457–463
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Same human skinned-fiber study. · source_derived_draft · unverified_draft
## taurine-muscle-calcium-sensitivity The contractile response differed between muscle fiber types. Taurine slightly increased contractile calcium sensitivity in human type I fibers, but not type II fibers; maximum calcium-activated force was unchanged in both. Model: Same human skinned-fiber study. Limitations: Small preparation-specific effect; do not merge with rodent muscle or whole-person strength. Evidence access: Primary abstract Acute effects of taurine on sarcoplasmic reticulum Ca2+ accumulation and contractility in human type I and type II skeletal muscle fibers. · 2014 · https://pubmed.ncbi.nlm.nih.gov/25123198/ · DOI 10.1152/japplphysiol.00494.2014
Complete structured claim and evidenceExposing skinned human type I and II muscle fibers to taurine for more than ten minutes increased the SR calcium accumulation rate; 10 and 20 mM produced similar rates, while 5 mM was slower.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Mechanically skinned human vastus lateralis fibers.
- limitations
- Intracellular bath exposure bypasses absorption and transport; it does not prove oral performance benefits.
- nutrient_topic
- Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
- plain_language
- Taurine affected how quickly muscle stored calcium.
- primary_references
- Acute effects of taurine on sarcoplasmic reticulum Ca2+ accumulation and contractility in human type I and type II skeletal muscle fibers. · 2014 · https://pubmed.ncbi.nlm.nih.gov/25123198/ · DOI 10.1152/japplphysiol.00494.2014
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 449–455
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mechanically skinned human vastus lateralis fibers. · source_derived_draft · unverified_draft
## taurine-muscle-calcium-uptake Taurine affected how quickly muscle stored calcium. Exposing skinned human type I and II muscle fibers to taurine for more than ten minutes increased the SR calcium accumulation rate; 10 and 20 mM produced similar rates, while 5 mM was slower. Model: Mechanically skinned human vastus lateralis fibers. Limitations: Intracellular bath exposure bypasses absorption and transport; it does not prove oral performance benefits. Evidence access: Primary abstract Acute effects of taurine on sarcoplasmic reticulum Ca2+ accumulation and contractility in human type I and type II skeletal muscle fibers. · 2014 · https://pubmed.ncbi.nlm.nih.gov/25123198/ · DOI 10.1152/japplphysiol.00494.2014
Complete structured claim and evidenceAt 20 mM, taurine had no detectable effect on the responsiveness of SR calcium-release channels in either human fiber type.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Human skinned type I and II muscle fibers.
- limitations
- The proposed action inside the SR lumen was a hypothesis, not a demonstrated binding target.
- nutrient_topic
- Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
- plain_language
- Faster calcium accumulation did not mean every calcium process increased.
- primary_references
- Acute effects of taurine on sarcoplasmic reticulum Ca2+ accumulation and contractility in human type I and type II skeletal muscle fibers. · 2014 · https://pubmed.ncbi.nlm.nih.gov/25123198/ · DOI 10.1152/japplphysiol.00494.2014
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 465–471
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human skinned type I and II muscle fibers. · source_derived_draft · unverified_draft
## taurine-muscle-release-null Faster calcium accumulation did not mean every calcium process increased. At 20 mM, taurine had no detectable effect on the responsiveness of SR calcium-release channels in either human fiber type. Model: Human skinned type I and II muscle fibers. Limitations: The proposed action inside the SR lumen was a hypothesis, not a demonstrated binding target. Evidence access: Primary abstract Acute effects of taurine on sarcoplasmic reticulum Ca2+ accumulation and contractility in human type I and type II skeletal muscle fibers. · 2014 · https://pubmed.ncbi.nlm.nih.gov/25123198/ · DOI 10.1152/japplphysiol.00494.2014
Complete structured claim and evidenceTwo weeks of low-protein or low-sulfur-amino-acid feeding lowered plasma taurine and increased renal taurine uptake while reducing fractional urinary excretion in the studied mouse strains.
Experimental context and source evidence
- availability_state
- nutrient_deficiency Imported condition classification; unverified.
- evidence_access
- Primary abstract
- experimental_model
- C3H/HeJ and C57BL/6J mice; in-vivo excretion and renal membrane transport.
- limitations
- Strain-specific responses; precursor restriction is not isolated taurine withdrawal.
- nutrient_topic
- Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
- plain_language
- The kidney conserved taurine when dietary supply of its precursors was restricted.
- primary_references
- Renal transport of taurine adapts to perturbed taurine homeostasis. · 1982 · https://pubmed.ncbi.nlm.nih.gov/6952257/ · DOI 10.1073/pnas.79.6.2101
- trigger_kind
- nutrient_deficiency Imported condition classification; unverified.
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 185–191
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · C3H/HeJ and C57BL/6J mice; in-vivo excretion and renal membrane transport. · source_derived_draft · unverified_draft
## taurine-renal-mouse-conservation The kidney conserved taurine when dietary supply of its precursors was restricted. Two weeks of low-protein or low-sulfur-amino-acid feeding lowered plasma taurine and increased renal taurine uptake while reducing fractional urinary excretion in the studied mouse strains. Model: C3H/HeJ and C57BL/6J mice; in-vivo excretion and renal membrane transport. Limitations: Strain-specific responses; precursor restriction is not isolated taurine withdrawal. Evidence access: Primary abstract Renal transport of taurine adapts to perturbed taurine homeostasis. · 1982 · https://pubmed.ncbi.nlm.nih.gov/6952257/ · DOI 10.1073/pnas.79.6.2101
Complete structured claim and evidenceA diet deficient in cysteine and methionine increased the Vmax of the rat high-affinity renal taurine uptake system without changing apparent Km.
Experimental context and source evidence
- availability_state
- nutrient_deficiency Imported condition classification; unverified.
- evidence_access
- Primary abstract
- experimental_model
- Rat dietary adaptation and renal transport assays.
- limitations
- Adaptation over days does not establish equivalent regulation in all human disease states.
- nutrient_topic
- Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
- plain_language
- Conservation involved more transport capacity rather than greater binding affinity.
- primary_references
- Renal adaptation to alteration in dietary amino acid intake. · 1983 · https://pubmed.ncbi.nlm.nih.gov/6881333/ · DOI 10.1152/ajprenal.1983.245.2.F159
- trigger_kind
- nutrient_deficiency Imported condition classification; unverified.
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 193–199
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Rat dietary adaptation and renal transport assays. · source_derived_draft · unverified_draft
## taurine-renal-rat-capacity Conservation involved more transport capacity rather than greater binding affinity. A diet deficient in cysteine and methionine increased the Vmax of the rat high-affinity renal taurine uptake system without changing apparent Km. Model: Rat dietary adaptation and renal transport assays. Limitations: Adaptation over days does not establish equivalent regulation in all human disease states. Evidence access: Primary abstract Renal adaptation to alteration in dietary amino acid intake. · 1983 · https://pubmed.ncbi.nlm.nih.gov/6881333/ · DOI 10.1152/ajprenal.1983.245.2.F159
Complete structured claim and evidenceTaurine starvation reduced mitochondrial tRNA taurine modification in cultured cells, with corresponding dietary-depletion observations in cat liver and flatfish tissues.
Experimental context and source evidence
- availability_state
- nutrient_deficiency Imported condition classification; unverified.
- evidence_access
- Primary abstract
- experimental_model
- Cultured-cell and dietary animal experiments.
- limitations
- Cats and flatfish differ from adult humans in endogenous taurine synthesis; no universal human plasma threshold was determined.
- nutrient_topic
- Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
- plain_language
- Insufficient taurine can leave fewer tRNAs carrying the normal mark.
- primary_references
- Metabolic and chemical regulation of tRNA modification associated with taurine deficiency and human disease. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29390138/ · DOI 10.1093/nar/gky068
- trigger_kind
- nutrient_deficiency Imported condition classification; unverified.
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 233–239
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Cultured-cell and dietary animal experiments. · source_derived_draft · unverified_draft
## taurine-taurine-starvation-rna Insufficient taurine can leave fewer tRNAs carrying the normal mark. Taurine starvation reduced mitochondrial tRNA taurine modification in cultured cells, with corresponding dietary-depletion observations in cat liver and flatfish tissues. Model: Cultured-cell and dietary animal experiments. Limitations: Cats and flatfish differ from adult humans in endogenous taurine synthesis; no universal human plasma threshold was determined. Evidence access: Primary abstract Metabolic and chemical regulation of tRNA modification associated with taurine deficiency and human disease. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29390138/ · DOI 10.1093/nar/gky068
Complete structured claim and evidenceIn two siblings with SLC6A6 p.Gly399Val and about 15% residual transport, supervised taurine treatment at 100 mg/kg/day normalized blood taurine and corrected cardiomyopathy after 24 months.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_access
- Primary abstract
- experimental_model
- Uncontrolled two-sibling longitudinal treatment report.
- limitations
- Not a dosing recommendation or evidence that all SLC6A6 variants respond; residual transport and timing matter.
- nutrient_topic
- Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
- plain_language
- A partially working transporter permitted a clinical treatment response in this family.
- primary_references
- Taurine treatment of retinal degeneration and cardiomyopathy in a consanguineous family with SLC6A6 taurine transporter deficiency. · 2020 · https://pubmed.ncbi.nlm.nih.gov/31903486/ · DOI 10.1093/hmg/ddz303
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 161–167
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Uncontrolled two-sibling longitudinal treatment report. · source_derived_draft · unverified_draft
## taurine-taut-heart-treatment A partially working transporter permitted a clinical treatment response in this family. In two siblings with SLC6A6 p.Gly399Val and about 15% residual transport, supervised taurine treatment at 100 mg/kg/day normalized blood taurine and corrected cardiomyopathy after 24 months. Model: Uncontrolled two-sibling longitudinal treatment report. Limitations: Not a dosing recommendation or evidence that all SLC6A6 variants respond; residual transport and timing matter. Evidence access: Primary abstract Taurine treatment of retinal degeneration and cardiomyopathy in a consanguineous family with SLC6A6 taurine transporter deficiency. · 2020 · https://pubmed.ncbi.nlm.nih.gov/31903486/ · DOI 10.1093/hmg/ddz303
Complete structured claim and evidenceIn the younger, six-year-old sibling in the p.Gly399Val family, taurine treatment was associated with arrested retinal degeneration and clinically improved vision over follow-up.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_access
- Primary abstract
- experimental_model
- Same two-sibling report; retinal response documented in the younger child.
- limitations
- Not proof that established retinal loss is generally reversible or that treatment works with complete transport loss.
- nutrient_topic
- Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
- plain_language
- Early retinal disease stabilized in one treated child.
- primary_references
- Taurine treatment of retinal degeneration and cardiomyopathy in a consanguineous family with SLC6A6 taurine transporter deficiency. · 2020 · https://pubmed.ncbi.nlm.nih.gov/31903486/ · DOI 10.1093/hmg/ddz303
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 169–175
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Same two-sibling report; retinal response documented in the younger child. · source_derived_draft · unverified_draft
## taurine-taut-retinal-treatment Early retinal disease stabilized in one treated child. In the younger, six-year-old sibling in the p.Gly399Val family, taurine treatment was associated with arrested retinal degeneration and clinically improved vision over follow-up. Model: Same two-sibling report; retinal response documented in the younger child. Limitations: Not proof that established retinal loss is generally reversible or that treatment works with complete transport loss. Evidence access: Primary abstract Taurine treatment of retinal degeneration and cardiomyopathy in a consanguineous family with SLC6A6 taurine transporter deficiency. · 2020 · https://pubmed.ncbi.nlm.nih.gov/31903486/ · DOI 10.1093/hmg/ddz303
Complete structured claim and evidenceThe taurine arm in the same prehypertension trial improved both endothelium-dependent and endothelium-independent vasodilation.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Same 120-person randomized study.
- limitations
- Clinical and vascular endpoints from one trial are not independent trials.
- nutrient_topic
- Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
- plain_language
- Blood-vessel function changed along with blood pressure.
- primary_references
- Taurine Supplementation Lowers Blood Pressure and Improves Vascular Function in Prehypertension: Randomized, Double-Blind, Placebo-Controlled Study. · 2016 · https://pubmed.ncbi.nlm.nih.gov/26781281/ · DOI 10.1161/HYPERTENSIONAHA.115.06624
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 481–487
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Same 120-person randomized study. · source_derived_draft · unverified_draft
## taurine-vascular-dilation Blood-vessel function changed along with blood pressure. The taurine arm in the same prehypertension trial improved both endothelium-dependent and endothelium-independent vasodilation. Model: Same 120-person randomized study. Limitations: Clinical and vascular endpoints from one trial are not independent trials. Evidence access: Primary abstract Taurine Supplementation Lowers Blood Pressure and Improves Vascular Function in Prehypertension: Randomized, Double-Blind, Placebo-Controlled Study. · 2016 · https://pubmed.ncbi.nlm.nih.gov/26781281/ · DOI 10.1161/HYPERTENSIONAHA.115.06624
Complete structured claim and evidenceTaurine pretreatment prevented the reported guanidinoacetate-related inhibition of complex II, complex II–III and sodium/potassium ATPase activity.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_span
- {"source_cache": "artifacts/creatine-research/17407807.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6174f6169ebf6ca7e61bc61642e38841a9089aecdd278ad8fb2f2221cf847c35", "start_char": 0, "end_char": 1929, "text_sha256": "6174f6169ebf6ca7e61bc61642e38841a9089aecdd278ad8fb2f2221cf847c35"}
- experimental_model
- Acute guanidinoacetate exposure with biochemical assays and antioxidant pretreatment
- exposure
- Intrastriatal guanidinoacetate and in-vitro assays; taurine or combined vitamins E plus C pretreatment
- limitations
- Acute experimental precursor toxicity is not a human supplement trial or proof that antioxidant treatment corrects GAMT deficiency. Vitamin E and C were combined.
- nutrient_topic
- Creatine research collection; topical membership is not evidence of a direct dietary effect. · Creatine
- organism
- Young rats and rat striatal preparations
- plain_language
- Taurine protected selected enzyme measurements in this rat experiment.
- primary_references
- [creatine-p17407807] Evidence that the inhibitory effects of guanidinoacetate on the activities of the respiratory chain, Na+,K+-ATPase and creatine kinase can be differentially prevented by taurine and vitamins E and C administration in rat striatum in vivo. (2007). https://pubmed.ncbi.nlm.nih.gov/17407807/ DOI: 10.1016/j.bbadis.2007.02.005
- tissue_or_cell_type
- Striatum
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Creatine: synthesis, transport, phosphocreatine energetics and nutrient interactions (2026-09-17) · lines 776–787
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Acute guanidinoacetate exposure with biochemical assays and antioxidant pretreatment · source_derived_draft · unverified_draft
### creatine-taurine-gaa-enzyme Taurine pretreatment prevented the reported guanidinoacetate-related inhibition of complex II, complex II–III and sodium/potassium ATPase activity. Condition category: machinery_impairment nutrient_topic: Creatine research collection; topical membership is not evidence of a direct dietary effect. plain_language: Taurine protected selected enzyme measurements in this rat experiment. organism: Young rats and rat striatal preparations tissue_or_cell_type: Striatum experimental_model: Acute guanidinoacetate exposure with biochemical assays and antioxidant pretreatment limitations: Acute experimental precursor toxicity is not a human supplement trial or proof that antioxidant treatment corrects GAMT deficiency. Vitamin E and C were combined. exposure: Intrastriatal guanidinoacetate and in-vitro assays; taurine or combined vitamins E plus C pretreatment evidence_span: {"source_cache": "artifacts/creatine-research/17407807.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6174f6169ebf6ca7e61bc61642e38841a9089aecdd278ad8fb2f2221cf847c35", "start_char": 0, "end_char": 1929, "text_sha256": "6174f6169ebf6ca7e61bc61642e38841a9089aecdd278ad8fb2f2221cf847c35"} [creatine-p17407807] Evidence that the inhibitory effects of guanidinoacetate on the activities of the respiratory chain, Na+,K+-ATPase and creatine kinase can be differentially prevented by taurine and vitamins E and C administration in rat striatum in vivo. (2007). https://pubmed.ncbi.nlm.nih.gov/17407807/ DOI: 10.1016/j.bbadis.2007.02.005
Complete structured claim and evidenceTaurine competed for GPR158 glycine binding and produced weaker cAMP suppression than glycine in the recombinant assays.
Experimental context and source evidence
- evidence_access
- Primary full text
- experimental_model
- Membrane ligand competition and cell signaling.
- limitations
- Shared binding is not proof of supplement synergy or the same neuronal response.
- nutrient_topic
- Glycine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Glycine
- plain_language
- Another nutrient-related molecule reaches the same receptor with a different response.
- primary_references
- Orphan receptor GPR158 serves as a metabotropic glycine receptor: mGlyR. · 2023 · https://pubmed.ncbi.nlm.nih.gov/36996198/ · DOI 10.1126/science.add7150
Glycine: supply, one-carbon allocation, receptors and cross-nutrient mechanisms (2026-09-19) · lines 242–248
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Membrane ligand competition and cell signaling. · source_derived_draft · unverified_draft
## glycine-gpr158-taurine Another nutrient-related molecule reaches the same receptor with a different response. Taurine competed for GPR158 glycine binding and produced weaker cAMP suppression than glycine in the recombinant assays. Model: Membrane ligand competition and cell signaling. Limitations: Shared binding is not proof of supplement synergy or the same neuronal response. Evidence access: Primary full text Orphan receptor GPR158 serves as a metabotropic glycine receptor: mGlyR. · 2023 · https://pubmed.ncbi.nlm.nih.gov/36996198/ · DOI 10.1126/science.add7150
Complete structured claim and evidence
What acts on it
Human CSAD also catalyzed L-cysteic-acid decarboxylation to taurine in vitro.
Experimental context and source evidence
- evidence_access
- Primary full text, substrate comparison
- experimental_model
- Recombinant human enzyme; L-cysteic-acid substrate assays.
- limitations
- This alternative reaction does not quantify its contribution to human whole-body synthesis.
- nutrient_topic
- Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
- plain_language
- The same enzyme can use a more oxidized substrate to make taurine directly.
- primary_references
- A Novel, Easy Assay Method for Human Cysteine Sulfinic Acid Decarboxylase. · 2021 · https://pubmed.ncbi.nlm.nih.gov/34068845/ · DOI 10.3390/life11050438
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 49–55
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Recombinant human enzyme; L-cysteic-acid substrate assays. · source_derived_draft · unverified_draft
## taurine-csad-cysteic-acid The same enzyme can use a more oxidized substrate to make taurine directly. Human CSAD also catalyzed L-cysteic-acid decarboxylation to taurine in vitro. Model: Recombinant human enzyme; L-cysteic-acid substrate assays. Limitations: This alternative reaction does not quantify its contribution to human whole-body synthesis. Evidence access: Primary full text, substrate comparison A Novel, Easy Assay Method for Human Cysteine Sulfinic Acid Decarboxylase. · 2021 · https://pubmed.ncbi.nlm.nih.gov/34068845/ · DOI 10.3390/life11050438
Complete structured claim and evidenceRecombinant human FMO1 catalyzed oxygenation of hypotaurine to taurine in vitro.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Human FMO1 enzyme assays.
- limitations
- This identifies an enzyme activity; it does not establish FMO1 as the only possible route in every tissue.
- nutrient_topic
- Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
- plain_language
- FMO1 completes the hypotaurine-to-taurine step.
- primary_references
- Flavin-Containing Monooxygenase 1 Catalyzes the Production of Taurine from Hypotaurine. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32156684/ · DOI 10.1124/dmd.119.089995
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 73–79
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human FMO1 enzyme assays. · source_derived_draft · unverified_draft
## taurine-fmo1-oxidation FMO1 completes the hypotaurine-to-taurine step. Recombinant human FMO1 catalyzed oxygenation of hypotaurine to taurine in vitro. Model: Human FMO1 enzyme assays. Limitations: This identifies an enzyme activity; it does not establish FMO1 as the only possible route in every tissue. Evidence access: Primary abstract Flavin-Containing Monooxygenase 1 Catalyzes the Production of Taurine from Hypotaurine. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32156684/ · DOI 10.1124/dmd.119.089995
Complete structured claim and evidenceHuman TauT structures captured beta-alanine and taurine as separately bound substrate analogues at the transporter binding site.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Human SLC6A6 cryo-EM structures and biochemical analysis.
- limitations
- Shared binding does not prove taurine depletion at typical beta-alanine supplement exposure.
- nutrient_topic
- Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
- plain_language
- Beta-alanine and taurine interact with the same molecular doorway.
- primary_references
- Molecular basis of human taurine transporter uptake and inhibition. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40789850/ · DOI 10.1038/s41467-025-62857-w
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 129–135
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human SLC6A6 cryo-EM structures and biochemical analysis. · source_derived_draft · unverified_draft
## taurine-taut-beta-alanine Beta-alanine and taurine interact with the same molecular doorway. Human TauT structures captured beta-alanine and taurine as separately bound substrate analogues at the transporter binding site. Model: Human SLC6A6 cryo-EM structures and biochemical analysis. Limitations: Shared binding does not prove taurine depletion at typical beta-alanine supplement exposure. Evidence access: Primary abstract Molecular basis of human taurine transporter uptake and inhibition. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40789850/ · DOI 10.1038/s41467-025-62857-w
Complete structured claim and evidenceHuman TauT structures and uptake assays characterized sodium- and chloride-dependent taurine transport and substrate recognition.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Human SLC6A6 cryo-EM structures plus biochemical transport assays.
- limitations
- Transport activity is distinct from oral absorption, blood concentration and tissue sufficiency.
- nutrient_topic
- Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
- plain_language
- Cells need a transporter to accumulate taurine.
- primary_references
- Molecular basis of human taurine transporter uptake and inhibition. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40789850/ · DOI 10.1038/s41467-025-62857-w
- transport_effect
- raises Uptake assays characterised sodium- and chloride-dependent taurine transport.
- transport_pool
- the expressing cell Uptake assays characterised sodium- and chloride-dependent taurine transport.
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 105–111
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human SLC6A6 cryo-EM structures plus biochemical transport assays. · source_derived_draft · unverified_draft
## taurine-taut-uptake Cells need a transporter to accumulate taurine. Human TauT structures and uptake assays characterized sodium- and chloride-dependent taurine transport and substrate recognition. Model: Human SLC6A6 cryo-EM structures plus biochemical transport assays. Limitations: Transport activity is distinct from oral absorption, blood concentration and tissue sufficiency. Evidence access: Primary abstract Molecular basis of human taurine transporter uptake and inhibition. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40789850/ · DOI 10.1038/s41467-025-62857-w
Complete structured claim and evidence
Where it participates (unsigned role)
RNA-mediated reduction of endogenous human ADO in HepG2/C3A cells decreased hypotaurine production from cysteamine.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Human liver-derived cultured cells.
- limitations
- Cysteamine can arise through CoA breakdown; this experiment does not show that B5 supplementation raises taurine.
- nutrient_topic
- Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
- plain_language
- Human-cell gene silencing supports the cysteamine pathway.
- primary_references
- Discovery and characterization of a second mammalian thiol dioxygenase, cysteamine dioxygenase. · 2007 · https://pubmed.ncbi.nlm.nih.gov/17581819/ · DOI 10.1074/jbc.M703089200
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 65–71
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human liver-derived cultured cells. · source_derived_draft · unverified_draft
## taurine-ado-human-knockdown Human-cell gene silencing supports the cysteamine pathway. RNA-mediated reduction of endogenous human ADO in HepG2/C3A cells decreased hypotaurine production from cysteamine. Model: Human liver-derived cultured cells. Limitations: Cysteamine can arise through CoA breakdown; this experiment does not show that B5 supplementation raises taurine. Evidence access: Primary abstract Discovery and characterization of a second mammalian thiol dioxygenase, cysteamine dioxygenase. · 2007 · https://pubmed.ncbi.nlm.nih.gov/17581819/ · DOI 10.1074/jbc.M703089200
Complete structured claim and evidenceRecombinant mouse Ado oxidized cysteamine to hypotaurine but did not oxidize cysteine in the tested assay.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Purified recombinant murine protein.
- limitations
- Do not assign the mouse enzyme kinetics directly to human ADO.
- nutrient_topic
- Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
- plain_language
- A separate enzyme provides a route from cysteamine.
- primary_references
- Discovery and characterization of a second mammalian thiol dioxygenase, cysteamine dioxygenase. · 2007 · https://pubmed.ncbi.nlm.nih.gov/17581819/ · DOI 10.1074/jbc.M703089200
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 57–63
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Purified recombinant murine protein. · source_derived_draft · unverified_draft
## taurine-ado-mouse-enzyme A separate enzyme provides a route from cysteamine. Recombinant mouse Ado oxidized cysteamine to hypotaurine but did not oxidize cysteine in the tested assay. Model: Purified recombinant murine protein. Limitations: Do not assign the mouse enzyme kinetics directly to human ADO. Evidence access: Primary abstract Discovery and characterization of a second mammalian thiol dioxygenase, cysteamine dioxygenase. · 2007 · https://pubmed.ncbi.nlm.nih.gov/17581819/ · DOI 10.1074/jbc.M703089200
Complete structured claim and evidenceThe same expressed human BAAT also catalyzed glycine conjugation of cholic acid.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Recombinant human enzyme.
- limitations
- Shared enzyme use does not establish clinical competition or a need to balance glycine and taurine supplements.
- nutrient_topic
- Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
- plain_language
- Glycine and taurine converge on the same bile-conjugating enzyme.
- primary_references
- Glycine and taurine conjugation of bile acids by a single enzyme. Molecular cloning and expression of human liver bile acid CoA:amino acid N-acyltransferase. · 1994 · https://pubmed.ncbi.nlm.nih.gov/8034703/
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 305–311
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Recombinant human enzyme. · source_derived_draft · unverified_draft
## taurine-baat-glycine Glycine and taurine converge on the same bile-conjugating enzyme. The same expressed human BAAT also catalyzed glycine conjugation of cholic acid. Model: Recombinant human enzyme. Limitations: Shared enzyme use does not establish clinical competition or a need to balance glycine and taurine supplements. Evidence access: Primary abstract Glycine and taurine conjugation of bile acids by a single enzyme. Molecular cloning and expression of human liver bile acid CoA:amino acid N-acyltransferase. · 1994 · https://pubmed.ncbi.nlm.nih.gov/8034703/
Complete structured claim and evidencePatients with defective bile acid amidation lacked glycine and taurine conjugates in urine, bile and serum; four homozygous BAAT mutations were identified among eight tested patients.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_access
- Primary abstract
- experimental_model
- Ten pediatric patients; bile chemistry and genetic investigation.
- limitations
- Not evidence that isolated dietary taurine shortage causes the same phenotype.
- nutrient_topic
- Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
- plain_language
- A broken conjugation enzyme affects both amino-acid routes.
- primary_references
- Genetic defects in bile acid conjugation cause fat-soluble vitamin deficiency. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23415802/ · DOI 10.1053/j.gastro.2013.02.004
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 313–319
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Ten pediatric patients; bile chemistry and genetic investigation. · source_derived_draft · unverified_draft
## taurine-baat-loss A broken conjugation enzyme affects both amino-acid routes. Patients with defective bile acid amidation lacked glycine and taurine conjugates in urine, bile and serum; four homozygous BAAT mutations were identified among eight tested patients. Model: Ten pediatric patients; bile chemistry and genetic investigation. Limitations: Not evidence that isolated dietary taurine shortage causes the same phenotype. Evidence access: Primary abstract Genetic defects in bile acid conjugation cause fat-soluble vitamin deficiency. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23415802/ · DOI 10.1053/j.gastro.2013.02.004
Complete structured claim and evidenceExpression of cloned human BAAT produced bile acid conjugation activity using taurine, establishing that the enzyme can make taurine-conjugated cholic acid from its activated CoA substrate.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Human liver cDNA expressed in bacteria; activity compared with purified liver enzyme.
- limitations
- Conjugated bile acid and free taurine are separate molecules.
- nutrient_topic
- Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
- plain_language
- Taurine becomes chemically attached to bile acids.
- primary_references
- Glycine and taurine conjugation of bile acids by a single enzyme. Molecular cloning and expression of human liver bile acid CoA:amino acid N-acyltransferase. · 1994 · https://pubmed.ncbi.nlm.nih.gov/8034703/
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 297–303
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human liver cDNA expressed in bacteria; activity compared with purified liver enzyme. · source_derived_draft · unverified_draft
## taurine-baat-taurine Taurine becomes chemically attached to bile acids. Expression of cloned human BAAT produced bile acid conjugation activity using taurine, establishing that the enzyme can make taurine-conjugated cholic acid from its activated CoA substrate. Model: Human liver cDNA expressed in bacteria; activity compared with purified liver enzyme. Limitations: Conjugated bile acid and free taurine are separate molecules. Evidence access: Primary abstract Glycine and taurine conjugation of bile acids by a single enzyme. Molecular cloning and expression of human liver bile acid CoA:amino acid N-acyltransferase. · 1994 · https://pubmed.ncbi.nlm.nih.gov/8034703/
Complete structured claim and evidenceThe pediatric bile acid amidation disorder was associated with insufficient effective duodenal bile acids, fat-soluble vitamin deficiency and growth failure in affected children.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_access
- Primary abstract
- experimental_model
- Human genetic disease cohort and biochemical characterization.
- limitations
- The study tests conjugation failure, not taurine supplement efficacy or one universal vitamin deficit.
- nutrient_topic
- Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
- plain_language
- Failed bile chemistry can make fat-soluble nutrient absorption fail downstream.
- primary_references
- Genetic defects in bile acid conjugation cause fat-soluble vitamin deficiency. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23415802/ · DOI 10.1053/j.gastro.2013.02.004
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 321–327
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human genetic disease cohort and biochemical characterization. · source_derived_draft · unverified_draft
## taurine-bile-vitamin-absorption Failed bile chemistry can make fat-soluble nutrient absorption fail downstream. The pediatric bile acid amidation disorder was associated with insufficient effective duodenal bile acids, fat-soluble vitamin deficiency and growth failure in affected children. Model: Human genetic disease cohort and biochemical characterization. Limitations: The study tests conjugation failure, not taurine supplement efficacy or one universal vitamin deficit. Evidence access: Primary abstract Genetic defects in bile acid conjugation cause fat-soluble vitamin deficiency. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23415802/ · DOI 10.1053/j.gastro.2013.02.004
Complete structured claim and evidencePurified human CSAD decarboxylated L-cysteine sulfinic acid to hypotaurine in PLP-containing enzyme assays.
Experimental context and source evidence
- evidence_access
- Primary full text, introduction and enzyme-assay results
- experimental_model
- Recombinant human enzyme; substrate kinetics and circular-dichroism assays.
- limitations
- Hypotaurine still needs oxidation to become taurine; this is not a human supplementation experiment.
- nutrient_topic
- Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
- plain_language
- Vitamin B6-dependent CSAD performs a step between cysteine and taurine.
- primary_references
- A Novel, Easy Assay Method for Human Cysteine Sulfinic Acid Decarboxylase. · 2021 · https://pubmed.ncbi.nlm.nih.gov/34068845/ · DOI 10.3390/life11050438
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 33–39
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Recombinant human enzyme; substrate kinetics and circular-dichroism assays. · source_derived_draft · unverified_draft
## taurine-csad-cysteinesulfinate Vitamin B6-dependent CSAD performs a step between cysteine and taurine. Purified human CSAD decarboxylated L-cysteine sulfinic acid to hypotaurine in PLP-containing enzyme assays. Model: Recombinant human enzyme; substrate kinetics and circular-dichroism assays. Limitations: Hypotaurine still needs oxidation to become taurine; this is not a human supplementation experiment. Evidence access: Primary full text, introduction and enzyme-assay results A Novel, Easy Assay Method for Human Cysteine Sulfinic Acid Decarboxylase. · 2021 · https://pubmed.ncbi.nlm.nih.gov/34068845/ · DOI 10.3390/life11050438
Complete structured claim and evidenceThe purified human CSAD characterized in this study was a PLP-dependent enzyme, linking its decarboxylation chemistry to the active cofactor form of vitamin B6.
Experimental context and source evidence
- evidence_access
- Primary full text, enzyme characterization
- experimental_model
- Human recombinant CSAD biochemical characterization.
- limitations
- Cofactor dependence does not establish that extra B6 increases taurine in a replete person.
- nutrient_topic
- Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
- plain_language
- CSAD needs the active B6 cofactor, not just its cysteine-derived substrate.
- primary_references
- A Novel, Easy Assay Method for Human Cysteine Sulfinic Acid Decarboxylase. · 2021 · https://pubmed.ncbi.nlm.nih.gov/34068845/ · DOI 10.3390/life11050438
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 41–47
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human recombinant CSAD biochemical characterization. · source_derived_draft · unverified_draft
## taurine-csad-plp CSAD needs the active B6 cofactor, not just its cysteine-derived substrate. The purified human CSAD characterized in this study was a PLP-dependent enzyme, linking its decarboxylation chemistry to the active cofactor form of vitamin B6. Model: Human recombinant CSAD biochemical characterization. Limitations: Cofactor dependence does not establish that extra B6 increases taurine in a replete person. Evidence access: Primary full text, enzyme characterization A Novel, Easy Assay Method for Human Cysteine Sulfinic Acid Decarboxylase. · 2021 · https://pubmed.ncbi.nlm.nih.gov/34068845/ · DOI 10.3390/life11050438
Complete structured claim and evidenceFmo1-null mice accumulated urinary hypotaurine and had less urinary taurine than wild-type mice.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_access
- Primary abstract
- experimental_model
- Mouse knockout; urinary proton NMR metabolomics.
- limitations
- Urine metabolites do not directly measure every tissue pool or prove human dietary deficiency.
- nutrient_topic
- Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
- plain_language
- Disabling the final enzyme changed the precursor/product pattern.
- primary_references
- Flavin-Containing Monooxygenase 1 Catalyzes the Production of Taurine from Hypotaurine. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32156684/ · DOI 10.1124/dmd.119.089995
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 89–95
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse knockout; urinary proton NMR metabolomics. · source_derived_draft · unverified_draft
## taurine-fmo1-deletion Disabling the final enzyme changed the precursor/product pattern. Fmo1-null mice accumulated urinary hypotaurine and had less urinary taurine than wild-type mice. Model: Mouse knockout; urinary proton NMR metabolomics. Limitations: Urine metabolites do not directly measure every tissue pool or prove human dietary deficiency. Evidence access: Primary abstract Flavin-Containing Monooxygenase 1 Catalyzes the Production of Taurine from Hypotaurine. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32156684/ · DOI 10.1124/dmd.119.089995
Complete structured claim and evidenceHuman FMO1 converted hypotaurine to taurine with either NADPH or NADH as the reducing cofactor in the reported assays.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Recombinant human FMO1 biochemistry.
- limitations
- NAD(P)H availability, FMO1 abundance and substrate availability are separate variables; no niacin repletion effect was tested.
- nutrient_topic
- Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
- plain_language
- Niacin-derived electron carriers support this synthetic reaction.
- primary_references
- Flavin-Containing Monooxygenase 1 Catalyzes the Production of Taurine from Hypotaurine. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32156684/ · DOI 10.1124/dmd.119.089995
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 81–87
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Recombinant human FMO1 biochemistry. · source_derived_draft · unverified_draft
## taurine-fmo1-reducing-cofactors Niacin-derived electron carriers support this synthetic reaction. Human FMO1 converted hypotaurine to taurine with either NADPH or NADH as the reducing cofactor in the reported assays. Model: Recombinant human FMO1 biochemistry. Limitations: NAD(P)H availability, FMO1 abundance and substrate availability are separate variables; no niacin repletion effect was tested. Evidence access: Primary abstract Flavin-Containing Monooxygenase 1 Catalyzes the Production of Taurine from Hypotaurine. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32156684/ · DOI 10.1124/dmd.119.089995
Complete structured claim and evidenceIsotope tracing supported the beta-carbon of serine entering the methylene group of mitochondrial taurine-modified uridine through 5,10-methylene-THF.
Experimental context and source evidence
- evidence_access
- Primary full text, Figure 1 and metabolic-labeling experiments
- experimental_model
- Human HeLa metabolic labeling plus biochemical reconstitution.
- limitations
- A folate connection is not evidence for a benefit from folic acid supplementation in replete people.
- nutrient_topic
- Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
- plain_language
- Folate chemistry contributes part of the RNA mark; taurine supplies a different part.
- primary_references
- Metabolic and chemical regulation of tRNA modification associated with taurine deficiency and human disease. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29390138/ · DOI 10.1093/nar/gky068
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 209–215
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human HeLa metabolic labeling plus biochemical reconstitution. · source_derived_draft · unverified_draft
## taurine-folate-carbon-donor Folate chemistry contributes part of the RNA mark; taurine supplies a different part. Isotope tracing supported the beta-carbon of serine entering the methylene group of mitochondrial taurine-modified uridine through 5,10-methylene-THF. Model: Human HeLa metabolic labeling plus biochemical reconstitution. Limitations: A folate connection is not evidence for a benefit from folic acid supplementation in replete people. Evidence access: Primary full text, Figure 1 and metabolic-labeling experiments Metabolic and chemical regulation of tRNA modification associated with taurine deficiency and human disease. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29390138/ · DOI 10.1093/nar/gky068
Complete structured claim and evidenceMitochondrial folate-transporter-mutant CHO cells showed reduced taurine modification of mitochondrial tRNA.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_access
- Primary full text, Figure 1F
- experimental_model
- Chinese hamster ovary Mft mutant cells.
- limitations
- Compartment-specific transport failure is different from low total blood folate.
- nutrient_topic
- Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
- plain_language
- Getting folate into the mitochondrial compartment matters.
- primary_references
- Metabolic and chemical regulation of tRNA modification associated with taurine deficiency and human disease. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29390138/ · DOI 10.1093/nar/gky068
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 225–231
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Chinese hamster ovary Mft mutant cells. · source_derived_draft · unverified_draft
## taurine-folate-carrier-mutation Getting folate into the mitochondrial compartment matters. Mitochondrial folate-transporter-mutant CHO cells showed reduced taurine modification of mitochondrial tRNA. Model: Chinese hamster ovary Mft mutant cells. Limitations: Compartment-specific transport failure is different from low total blood folate. Evidence access: Primary full text, Figure 1F Metabolic and chemical regulation of tRNA modification associated with taurine deficiency and human disease. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29390138/ · DOI 10.1093/nar/gky068
Complete structured claim and evidenceTaurine-evoked currents were absent in relay neurons from GABA-A-receptor alpha4-subunit knockout mice.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Mouse alpha4-knockout thalamic neuron recordings.
- limitations
- Subunit dependence is local to this experimental response.
- nutrient_topic
- Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
- plain_language
- Removing a receptor subunit tested dependence of the current.
- primary_references
- Taurine is a potent activator of extrasynaptic GABA(A) receptors in the thalamus. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18171928/ · DOI 10.1523/JNEUROSCI.3996-07.2008
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 441–447
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse alpha4-knockout thalamic neuron recordings. · source_derived_draft · unverified_draft
## taurine-gabaa-knockout Removing a receptor subunit tested dependence of the current. Taurine-evoked currents were absent in relay neurons from GABA-A-receptor alpha4-subunit knockout mice. Model: Mouse alpha4-knockout thalamic neuron recordings. Limitations: Subunit dependence is local to this experimental response. Evidence access: Primary abstract Taurine is a potent activator of extrasynaptic GABA(A) receptors in the thalamus. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18171928/ · DOI 10.1523/JNEUROSCI.3996-07.2008
Complete structured claim and evidenceTaurine-depleted cultured cells accumulated mitochondrial tRNA cmnm5U, whose glycine-derived group replaces the taurine-derived group of tau-m5U.
Experimental context and source evidence
- availability_state
- nutrient_deficiency Imported condition classification; unverified.
- evidence_access
- Primary abstract
- experimental_model
- Mass spectrometry of mitochondrial tRNAs from depleted cells.
- limitations
- Detection of an alternative mark does not establish complete functional rescue by glycine.
- nutrient_topic
- Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
- plain_language
- Low taurine changed the chemical identity of the RNA modification.
- primary_references
- Metabolic and chemical regulation of tRNA modification associated with taurine deficiency and human disease. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29390138/ · DOI 10.1093/nar/gky068
- trigger_kind
- nutrient_deficiency Imported condition classification; unverified.
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 241–247
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mass spectrometry of mitochondrial tRNAs from depleted cells. · source_derived_draft · unverified_draft
## taurine-glycine-substitution Low taurine changed the chemical identity of the RNA modification. Taurine-depleted cultured cells accumulated mitochondrial tRNA cmnm5U, whose glycine-derived group replaces the taurine-derived group of tau-m5U. Model: Mass spectrometry of mitochondrial tRNAs from depleted cells. Limitations: Detection of an alternative mark does not establish complete functional rescue by glycine. Evidence access: Primary abstract Metabolic and chemical regulation of tRNA modification associated with taurine deficiency and human disease. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29390138/ · DOI 10.1093/nar/gky068
Complete structured claim and evidencePurified mature human GTPBP3 exhibited GTPase activity, and functional experiments linked that activity to tRNA modification.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Human enzyme kinetics and cellular/yeast functional studies.
- limitations
- Results depend on the mature protein construct; do not infer benefit from dietary nucleotide supplements.
- nutrient_topic
- Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
- plain_language
- The modifying complex includes a GTP-powered component.
- primary_references
- The human tRNA taurine modification enzyme GTPBP3 is an active GTPase linked to mitochondrial diseases. · 2021 · https://pubmed.ncbi.nlm.nih.gov/33619562/ · DOI 10.1093/nar/gkab104
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 265–271
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human enzyme kinetics and cellular/yeast functional studies. · source_derived_draft · unverified_draft
## taurine-gtpbp3-gtpase The modifying complex includes a GTP-powered component. Purified mature human GTPBP3 exhibited GTPase activity, and functional experiments linked that activity to tRNA modification. Model: Human enzyme kinetics and cellular/yeast functional studies. Limitations: Results depend on the mature protein construct; do not infer benefit from dietary nucleotide supplements. Evidence access: Primary abstract The human tRNA taurine modification enzyme GTPBP3 is an active GTPase linked to mitochondrial diseases. · 2021 · https://pubmed.ncbi.nlm.nih.gov/33619562/ · DOI 10.1093/nar/gkab104
Complete structured claim and evidenceGTPBP3-knockout human cells exhibited impaired mitochondrial respiration alongside loss of taurine tRNA modification.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_access
- Primary abstract
- experimental_model
- Human cell knockout; respiratory measurements.
- limitations
- Same perturbation as the translation claim, not independent clinical evidence.
- nutrient_topic
- Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
- plain_language
- The RNA-processing defect reached the cell respiratory machinery.
- primary_references
- Metabolic and chemical regulation of tRNA modification associated with taurine deficiency and human disease. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29390138/ · DOI 10.1093/nar/gky068
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 257–263
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human cell knockout; respiratory measurements. · source_derived_draft · unverified_draft
## taurine-gtpbp3-respiration The RNA-processing defect reached the cell respiratory machinery. GTPBP3-knockout human cells exhibited impaired mitochondrial respiration alongside loss of taurine tRNA modification. Model: Human cell knockout; respiratory measurements. Limitations: Same perturbation as the translation claim, not independent clinical evidence. Evidence access: Primary abstract Metabolic and chemical regulation of tRNA modification associated with taurine deficiency and human disease. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29390138/ · DOI 10.1093/nar/gky068
Complete structured claim and evidenceDeleting GTPBP3 in human cells eliminated the normal taurine-containing wobble modification and reduced mitochondrial translation.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_access
- Primary abstract
- experimental_model
- Human GTPBP3-knockout cultured cells.
- limitations
- Adding substrate cannot be assumed to substitute for an absent enzyme.
- nutrient_topic
- Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
- plain_language
- Removing the modifying machinery impaired mitochondrial protein production.
- primary_references
- Metabolic and chemical regulation of tRNA modification associated with taurine deficiency and human disease. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29390138/ · DOI 10.1093/nar/gky068
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 249–255
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human GTPBP3-knockout cultured cells. · source_derived_draft · unverified_draft
## taurine-gtpbp3-translation Removing the modifying machinery impaired mitochondrial protein production. Deleting GTPBP3 in human cells eliminated the normal taurine-containing wobble modification and reduced mitochondrial translation. Model: Human GTPBP3-knockout cultured cells. Limitations: Adding substrate cannot be assumed to substitute for an absent enzyme. Evidence access: Primary abstract Metabolic and chemical regulation of tRNA modification associated with taurine deficiency and human disease. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29390138/ · DOI 10.1093/nar/gky068
Complete structured claim and evidenceLiver-specific Cdo1 deletion increased extrahepatic CDO abundance and hypotaurine; mice maintained taurine, glutathione and sulfate despite a taurine-free diet.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Conditional mouse liver knockout; kidney, adipose and pancreatic measurements.
- limitations
- This tissue-restricted deletion differs from complete pathway loss and from human deficiency.
- nutrient_topic
- Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
- plain_language
- Other tissues compensated when liver synthesis was impaired.
- primary_references
- Extrahepatic tissues compensate for loss of hepatic taurine synthesis in mice with liver-specific knockout of cysteine dioxygenase. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22414809/ · DOI 10.1152/ajpendo.00589.2011
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 97–103
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Conditional mouse liver knockout; kidney, adipose and pancreatic measurements. · source_derived_draft · unverified_draft
## taurine-hepatic-compensation Other tissues compensated when liver synthesis was impaired. Liver-specific Cdo1 deletion increased extrahepatic CDO abundance and hypotaurine; mice maintained taurine, glutathione and sulfate despite a taurine-free diet. Model: Conditional mouse liver knockout; kidney, adipose and pancreatic measurements. Limitations: This tissue-restricted deletion differs from complete pathway loss and from human deficiency. Evidence access: Primary abstract Extrahepatic tissues compensate for loss of hepatic taurine synthesis in mice with liver-specific knockout of cysteine dioxygenase. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22414809/ · DOI 10.1152/ajpendo.00589.2011
Complete structured claim and evidenceHO-1 inhibition, knockdown or genetic absence blocked the enhancement of macrophage phagocytosis by taurine chloramine, while overexpression augmented it.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Mouse macrophage pharmacological and genetic comparisons.
- limitations
- The mechanism concerns this phagocytosis assay, not all actions of taurine chloramine.
- nutrient_topic
- Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
- plain_language
- Removing HO-1 tested whether the observed effect needed that enzyme.
- primary_references
- Role of heme oxygenase-1 in potentiation of phagocytic activity of macrophages by taurine chloramine: Implications for the resolution of zymosan A-induced murine peritonitis. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29477410/ · DOI 10.1016/j.cellimm.2018.02.003
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 393–399
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse macrophage pharmacological and genetic comparisons. · source_derived_draft · unverified_draft
## taurine-ho1-required Removing HO-1 tested whether the observed effect needed that enzyme. HO-1 inhibition, knockdown or genetic absence blocked the enhancement of macrophage phagocytosis by taurine chloramine, while overexpression augmented it. Model: Mouse macrophage pharmacological and genetic comparisons. Limitations: The mechanism concerns this phagocytosis assay, not all actions of taurine chloramine. Evidence access: Primary abstract Role of heme oxygenase-1 in potentiation of phagocytic activity of macrophages by taurine chloramine: Implications for the resolution of zymosan A-induced murine peritonitis. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29477410/ · DOI 10.1016/j.cellimm.2018.02.003
Complete structured claim and evidenceSlc6a6 loss reduced RAG-GTP-dependent mTOR activation and downstream glycolysis in the mouse leukemia experiments.
Experimental context and source evidence
- evidence_access
- Primary full text, Figure 5
- experimental_model
- Mouse leukemia multiomics, signaling and metabolic experiments.
- limitations
- This pathway is not established as a universal response to taurine in healthy human cells.
- nutrient_topic
- Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
- plain_language
- Transport was connected to growth signaling and fuel use.
- primary_references
- Taurine from tumour niche drives glycolysis to promote leukaemogenesis. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40369079/ · DOI 10.1038/s41586-025-09018-7
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 537–543
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse leukemia multiomics, signaling and metabolic experiments. · source_derived_draft · unverified_draft
## taurine-leukemia-mtor Transport was connected to growth signaling and fuel use. Slc6a6 loss reduced RAG-GTP-dependent mTOR activation and downstream glycolysis in the mouse leukemia experiments. Model: Mouse leukemia multiomics, signaling and metabolic experiments. Limitations: This pathway is not established as a universal response to taurine in healthy human cells. Evidence access: Primary full text, Figure 5 Taurine from tumour niche drives glycolysis to promote leukaemogenesis. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40369079/ · DOI 10.1038/s41586-025-09018-7
Complete structured claim and evidenceExpression of constitutively active RAGA(Q66L) was used to restore mTOR signaling and growth-associated function downstream of taurine-uptake loss in mouse leukemia cells.
Experimental context and source evidence
- evidence_access
- Primary full text, Figure 5p–s and associated results
- experimental_model
- Mouse leukemia expression-rescue experiments.
- limitations
- Rescue does not identify taurine as a direct physical ligand of RAGA.
- nutrient_topic
- Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
- plain_language
- A downstream rescue tested the signaling chain.
- primary_references
- Taurine from tumour niche drives glycolysis to promote leukaemogenesis. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40369079/ · DOI 10.1038/s41586-025-09018-7
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 545–551
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse leukemia expression-rescue experiments. · source_derived_draft · unverified_draft
## taurine-leukemia-rag-rescue A downstream rescue tested the signaling chain. Expression of constitutively active RAGA(Q66L) was used to restore mTOR signaling and growth-associated function downstream of taurine-uptake loss in mouse leukemia cells. Model: Mouse leukemia expression-rescue experiments. Limitations: Rescue does not identify taurine as a direct physical ligand of RAGA. Evidence access: Primary full text, Figure 5p–s and associated results Taurine from tumour niche drives glycolysis to promote leukaemogenesis. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40369079/ · DOI 10.1038/s41586-025-09018-7
Complete structured claim and evidenceGenetic loss of Slc6a6 impaired progression in mouse myeloid leukemia models.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Mouse loss-of-function and in-vivo leukemia experiments.
- limitations
- This does not negate taurine requirements of normal retina and heart.
- nutrient_topic
- Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
- plain_language
- Leukemia cells needed taurine uptake in these models.
- primary_references
- Taurine from tumour niche drives glycolysis to promote leukaemogenesis. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40369079/ · DOI 10.1038/s41586-025-09018-7
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 529–535
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse loss-of-function and in-vivo leukemia experiments. · source_derived_draft · unverified_draft
## taurine-leukemia-taut-loss Leukemia cells needed taurine uptake in these models. Genetic loss of Slc6a6 impaired progression in mouse myeloid leukemia models. Model: Mouse loss-of-function and in-vivo leukemia experiments. Limitations: This does not negate taurine requirements of normal retina and heart. Evidence access: Primary abstract Taurine from tumour niche drives glycolysis to promote leukaemogenesis. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40369079/ · DOI 10.1038/s41586-025-09018-7
Complete structured claim and evidenceTAUT inhibition combined with venetoclax synergistically reduced growth of primary human AML cells in the reported experiments.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Ex-vivo human AML; venetoclax-resistance expression analyses.
- limitations
- Measured experimental combination effect, not a proven clinical interaction between taurine supplements and venetoclax.
- nutrient_topic
- Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
- plain_language
- Blocking nutrient uptake affected response to an anticancer drug in patient-derived cells.
- primary_references
- Taurine from tumour niche drives glycolysis to promote leukaemogenesis. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40369079/ · DOI 10.1038/s41586-025-09018-7
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 561–567
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Ex-vivo human AML; venetoclax-resistance expression analyses. · source_derived_draft · unverified_draft
## taurine-leukemia-venetoclax Blocking nutrient uptake affected response to an anticancer drug in patient-derived cells. TAUT inhibition combined with venetoclax synergistically reduced growth of primary human AML cells in the reported experiments. Model: Ex-vivo human AML; venetoclax-resistance expression analyses. Limitations: Measured experimental combination effect, not a proven clinical interaction between taurine supplements and venetoclax. Evidence access: Primary abstract Taurine from tumour niche drives glycolysis to promote leukaemogenesis. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40369079/ · DOI 10.1038/s41586-025-09018-7
Complete structured claim and evidenceAdding taurocholic acid, but not glycocholic acid, to a low-fat mouse diet promoted Bilophila wadsworthia expansion.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Mouse dietary experiments with conjugate comparison.
- limitations
- The intervention was taurocholate, not free taurine alone; microbial community and host genotype matter.
- nutrient_topic
- Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
- plain_language
- Taurine-conjugated bile supplies sulfur that certain microbes can exploit.
- primary_references
- Dietary-fat-induced taurocholic acid promotes pathobiont expansion and colitis in Il10-/- mice. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22722865/ · DOI 10.1038/nature11225
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 329–335
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse dietary experiments with conjugate comparison. · source_derived_draft · unverified_draft
## taurine-microbial-bilophila Taurine-conjugated bile supplies sulfur that certain microbes can exploit. Adding taurocholic acid, but not glycocholic acid, to a low-fat mouse diet promoted Bilophila wadsworthia expansion. Model: Mouse dietary experiments with conjugate comparison. Limitations: The intervention was taurocholate, not free taurine alone; microbial community and host genotype matter. Evidence access: Primary abstract Dietary-fat-induced taurocholic acid promotes pathobiont expansion and colitis in Il10-/- mice. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22722865/ · DOI 10.1038/nature11225
Complete structured claim and evidenceTaurocholic-acid feeding promoted colitis in Il10-null mice; milk-fat-associated microbial expansion and inflammation depended on host susceptibility.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Il10-deficient and wild-type mouse comparisons.
- limitations
- Not a demonstration that taurine causes human inflammatory bowel disease.
- nutrient_topic
- Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
- plain_language
- A sulfur-using microbial route worsened inflammation in this susceptible model.
- primary_references
- Dietary-fat-induced taurocholic acid promotes pathobiont expansion and colitis in Il10-/- mice. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22722865/ · DOI 10.1038/nature11225
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 337–343
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Il10-deficient and wild-type mouse comparisons. · source_derived_draft · unverified_draft
## taurine-microbial-colitis A sulfur-using microbial route worsened inflammation in this susceptible model. Taurocholic-acid feeding promoted colitis in Il10-null mice; milk-fat-associated microbial expansion and inflammation depended on host susceptibility. Model: Il10-deficient and wild-type mouse comparisons. Limitations: Not a demonstration that taurine causes human inflammatory bowel disease. Evidence access: Primary abstract Dietary-fat-induced taurocholic acid promotes pathobiont expansion and colitis in Il10-/- mice. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22722865/ · DOI 10.1038/nature11225
Complete structured claim and evidenceTaurine-supported microbiota increased sulfide production, which inhibited respiration important for invasion by the tested enteric pathogens; sulfide sequestration promoted invasion.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Mouse colonization-resistance study with microbial and sulfide interventions.
- limitations
- Local microbial sulfide, circulating host sulfide and systemic sulfide toxicity are distinct exposures.
- nutrient_topic
- Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
- plain_language
- The microbial product blocked a pathway that pathogens needed.
- primary_references
- Infection trains the host for microbiota-enhanced resistance to pathogens. · 2021 · https://pubmed.ncbi.nlm.nih.gov/33453153/ · DOI 10.1016/j.cell.2020.12.011
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 353–359
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse colonization-resistance study with microbial and sulfide interventions. · source_derived_draft · unverified_draft
## taurine-microbial-sulfide The microbial product blocked a pathway that pathogens needed. Taurine-supported microbiota increased sulfide production, which inhibited respiration important for invasion by the tested enteric pathogens; sulfide sequestration promoted invasion. Model: Mouse colonization-resistance study with microbial and sulfide interventions. Limitations: Local microbial sulfide, circulating host sulfide and systemic sulfide toxicity are distinct exposures. Evidence access: Primary abstract Infection trains the host for microbiota-enhanced resistance to pathogens. · 2021 · https://pubmed.ncbi.nlm.nih.gov/33453153/ · DOI 10.1016/j.cell.2020.12.011
Complete structured claim and evidencePurified myeloperoxidase plus hydrogen peroxide, chloride and taurine generated taurine chloramine; removing chloride or peroxide, or inhibiting MPO, blocked generation.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Purified human MPO system and stimulated human neutrophils.
- limitations
- Taurine chloramine remains an oxidant; free taurine is not equivalent to every chloramine effect.
- nutrient_topic
- Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
- plain_language
- An immune-cell oxidant reacts with taurine to make a different active molecule.
- primary_references
- Chlorination of taurine by human neutrophils. Evidence for hypochlorous acid generation. · 1982 · https://pubmed.ncbi.nlm.nih.gov/6286728/ · DOI 10.1172/jci110652
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 361–367
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Purified human MPO system and stimulated human neutrophils. · source_derived_draft · unverified_draft
## taurine-mpo-chlorination An immune-cell oxidant reacts with taurine to make a different active molecule. Purified myeloperoxidase plus hydrogen peroxide, chloride and taurine generated taurine chloramine; removing chloride or peroxide, or inhibiting MPO, blocked generation. Model: Purified human MPO system and stimulated human neutrophils. Limitations: Taurine chloramine remains an oxidant; free taurine is not equivalent to every chloramine effect. Evidence access: Primary abstract Chlorination of taurine by human neutrophils. Evidence for hypochlorous acid generation. · 1982 · https://pubmed.ncbi.nlm.nih.gov/6286728/ · DOI 10.1172/jci110652
Complete structured claim and evidenceReconstituting the human MTO1-GTPBP3 complex with hypomodified mitochondrial tRNA, taurine and 5,10-methylene-THF produced the taurine-containing U34 modification.
Experimental context and source evidence
- evidence_access
- Primary full text, in-vitro reconstitution methods and results
- experimental_model
- Human enzyme-complex reconstitution and mass spectrometry.
- limitations
- The reaction mixture also contained GTP, ATP, FAD, NADH, NADPH and magnesium; their presence alone does not demonstrate each is individually limiting.
- nutrient_topic
- Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
- plain_language
- Two proteins join taurine and a folate-derived carbon unit onto mitochondrial tRNA.
- primary_references
- Metabolic and chemical regulation of tRNA modification associated with taurine deficiency and human disease. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29390138/ · DOI 10.1093/nar/gky068
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 201–207
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human enzyme-complex reconstitution and mass spectrometry. · source_derived_draft · unverified_draft
## taurine-mto1-gtpbp3 Two proteins join taurine and a folate-derived carbon unit onto mitochondrial tRNA. Reconstituting the human MTO1-GTPBP3 complex with hypomodified mitochondrial tRNA, taurine and 5,10-methylene-THF produced the taurine-containing U34 modification. Model: Human enzyme-complex reconstitution and mass spectrometry. Limitations: The reaction mixture also contained GTP, ATP, FAD, NADH, NADPH and magnesium; their presence alone does not demonstrate each is individually limiting. Evidence access: Primary full text, in-vitro reconstitution methods and results Metabolic and chemical regulation of tRNA modification associated with taurine deficiency and human disease. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29390138/ · DOI 10.1093/nar/gky068
Complete structured claim and evidenceMto1-deficient experimental cells and mice showed defective mitochondrial translation with mistargeting and aggregation of nuclear-encoded mitochondrial proteins; chemical chaperones reduced cytotoxicity.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_access
- Primary abstract
- experimental_model
- Mto1 deficiency in experimental cells and mice.
- limitations
- The rescue used chemical chaperones, not proof that taurine treats absent Mto1.
- nutrient_topic
- Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
- plain_language
- Failure of mitochondrial translation can disturb protein handling beyond mitochondria.
- primary_references
- Defective Mitochondrial tRNA Taurine Modification Activates Global Proteostress and Leads to Mitochondrial Disease. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29320742/ · DOI 10.1016/j.celrep.2017.12.051
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 273–279
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mto1 deficiency in experimental cells and mice. · source_derived_draft · unverified_draft
## taurine-mto1-proteostress Failure of mitochondrial translation can disturb protein handling beyond mitochondria. Mto1-deficient experimental cells and mice showed defective mitochondrial translation with mistargeting and aggregation of nuclear-encoded mitochondrial proteins; chemical chaperones reduced cytotoxicity. Model: Mto1 deficiency in experimental cells and mice. Limitations: The rescue used chemical chaperones, not proof that taurine treats absent Mto1. Evidence access: Primary abstract Defective Mitochondrial tRNA Taurine Modification Activates Global Proteostress and Leads to Mitochondrial Disease. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29320742/ · DOI 10.1016/j.celrep.2017.12.051
Complete structured claim and evidenceInhibiting CDO1 in osteolineage cultures derived from AML patients reduced survival and colony formation of AML cells from the same patients.
Experimental context and source evidence
- evidence_access
- Primary full text, Figure 2h–i
- experimental_model
- Matched human stromal/AML cocultures.
- limitations
- Ex-vivo dependency does not establish an effective or safe clinical inhibitor.
- nutrient_topic
- Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
- plain_language
- Patient-derived support cells also provided a growth-supporting pathway.
- primary_references
- Taurine from tumour niche drives glycolysis to promote leukaemogenesis. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40369079/ · DOI 10.1038/s41586-025-09018-7
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 521–527
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Matched human stromal/AML cocultures. · source_derived_draft · unverified_draft
## taurine-niche-human-cdo1 Patient-derived support cells also provided a growth-supporting pathway. Inhibiting CDO1 in osteolineage cultures derived from AML patients reduced survival and colony formation of AML cells from the same patients. Model: Matched human stromal/AML cocultures. Limitations: Ex-vivo dependency does not establish an effective or safe clinical inhibitor. Evidence access: Primary full text, Figure 2h–i Taurine from tumour niche drives glycolysis to promote leukaemogenesis. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40369079/ · DOI 10.1038/s41586-025-09018-7
Complete structured claim and evidenceDeleting Cdo1 in mouse mesenchymal/osteolineage cells reduced support for leukemia growth and prolonged survival in the transplanted leukemia model.
Experimental context and source evidence
- evidence_access
- Primary full text, Figure 2 and niche experiments
- experimental_model
- Conditional mouse Cdo1 deletion, coculture and leukemia transplantation.
- limitations
- An established leukemia model does not measure cancer incidence in healthy supplement users.
- nutrient_topic
- Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
- plain_language
- The tumor-supporting tissue supplied taurine to leukemia cells.
- primary_references
- Taurine from tumour niche drives glycolysis to promote leukaemogenesis. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40369079/ · DOI 10.1038/s41586-025-09018-7
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 513–519
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Conditional mouse Cdo1 deletion, coculture and leukemia transplantation. · source_derived_draft · unverified_draft
## taurine-niche-mouse-cdo1 The tumor-supporting tissue supplied taurine to leukemia cells. Deleting Cdo1 in mouse mesenchymal/osteolineage cells reduced support for leukemia growth and prolonged survival in the transplanted leukemia model. Model: Conditional mouse Cdo1 deletion, coculture and leukemia transplantation. Limitations: An established leukemia model does not measure cancer incidence in healthy supplement users. Evidence access: Primary full text, Figure 2 and niche experiments Taurine from tumour niche drives glycolysis to promote leukaemogenesis. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40369079/ · DOI 10.1038/s41586-025-09018-7
Complete structured claim and evidenceTaurine uptake by reconstituted human placental membranes required chloride; chloride kinetics supported one chloride per taurine.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Human placental membrane proteoliposomes.
- limitations
- Alternative anions supported at most 30% of control uptake; this does not define a dietary chloride threshold.
- nutrient_topic
- Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
- plain_language
- Chloride is part of the transport cycle.
- primary_references
- Solubilization and functional reconstitution of the human placental taurine transporter. · 1993 · https://pubmed.ncbi.nlm.nih.gov/8431457/ · DOI 10.1016/0005-2736(93)90296-c
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 121–127
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human placental membrane proteoliposomes. · source_derived_draft · unverified_draft
## taurine-placental-chloride Chloride is part of the transport cycle. Taurine uptake by reconstituted human placental membranes required chloride; chloride kinetics supported one chloride per taurine. Model: Human placental membrane proteoliposomes. Limitations: Alternative anions supported at most 30% of control uptake; this does not define a dietary chloride threshold. Evidence access: Primary abstract Solubilization and functional reconstitution of the human placental taurine transporter. · 1993 · https://pubmed.ncbi.nlm.nih.gov/8431457/ · DOI 10.1016/0005-2736(93)90296-c
Complete structured claim and evidenceReplacing sodium strongly reduced taurine uptake in reconstituted human placental membranes; uptake kinetics supported two sodium ions per taurine.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Human placental brush-border proteins reconstituted in proteoliposomes.
- limitations
- This was not purified SLC6A6 alone; the coupling estimate is assay-specific, not a reason to consume more sodium.
- nutrient_topic
- Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
- plain_language
- The sodium gradient helps power taurine entry.
- primary_references
- Solubilization and functional reconstitution of the human placental taurine transporter. · 1993 · https://pubmed.ncbi.nlm.nih.gov/8431457/ · DOI 10.1016/0005-2736(93)90296-c
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 113–119
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human placental brush-border proteins reconstituted in proteoliposomes. · source_derived_draft · unverified_draft
## taurine-placental-sodium The sodium gradient helps power taurine entry. Replacing sodium strongly reduced taurine uptake in reconstituted human placental membranes; uptake kinetics supported two sodium ions per taurine. Model: Human placental brush-border proteins reconstituted in proteoliposomes. Limitations: This was not purified SLC6A6 alone; the coupling estimate is assay-specific, not a reason to consume more sodium. Evidence access: Primary abstract Solubilization and functional reconstitution of the human placental taurine transporter. · 1993 · https://pubmed.ncbi.nlm.nih.gov/8431457/ · DOI 10.1016/0005-2736(93)90296-c
Complete structured claim and evidenceShmt2-mutant Chinese hamster ovary cells showed reduced mitochondrial tRNA taurine modification compared with wild type.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_access
- Primary full text, Figure 1F
- experimental_model
- CHO mutant-cell mass spectrometry.
- limitations
- This species-specific machinery defect is not a B6 or folate deprivation experiment.
- nutrient_topic
- Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
- plain_language
- One-carbon supply can affect the same RNA mark even when the taurine molecule is present.
- primary_references
- Metabolic and chemical regulation of tRNA modification associated with taurine deficiency and human disease. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29390138/ · DOI 10.1093/nar/gky068
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 217–223
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · CHO mutant-cell mass spectrometry. · source_derived_draft · unverified_draft
## taurine-shmt2-mutation One-carbon supply can affect the same RNA mark even when the taurine molecule is present. Shmt2-mutant Chinese hamster ovary cells showed reduced mitochondrial tRNA taurine modification compared with wild type. Model: CHO mutant-cell mass spectrometry. Limitations: This species-specific machinery defect is not a B6 or folate deprivation experiment. Evidence access: Primary full text, Figure 1F Metabolic and chemical regulation of tRNA modification associated with taurine deficiency and human disease. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29390138/ · DOI 10.1093/nar/gky068
Complete structured claim and evidenceTaurine chloramine treatment increased HO-1 expression in mouse peritoneal macrophages in the zymosan inflammation study.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Murine peritonitis, isolated macrophages and RAW264.7 cells.
- limitations
- This is a derivative and mouse immune-cell result, not evidence that taurine directly supplies or removes iron.
- nutrient_topic
- Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
- plain_language
- The derivative changed an enzyme involved in stress responses.
- primary_references
- Role of heme oxygenase-1 in potentiation of phagocytic activity of macrophages by taurine chloramine: Implications for the resolution of zymosan A-induced murine peritonitis. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29477410/ · DOI 10.1016/j.cellimm.2018.02.003
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 385–391
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Murine peritonitis, isolated macrophages and RAW264.7 cells. · source_derived_draft · unverified_draft
## taurine-taucl-ho1 The derivative changed an enzyme involved in stress responses. Taurine chloramine treatment increased HO-1 expression in mouse peritoneal macrophages in the zymosan inflammation study. Model: Murine peritonitis, isolated macrophages and RAW264.7 cells. Limitations: This is a derivative and mouse immune-cell result, not evidence that taurine directly supplies or removes iron. Evidence access: Primary abstract Role of heme oxygenase-1 in potentiation of phagocytic activity of macrophages by taurine chloramine: Implications for the resolution of zymosan A-induced murine peritonitis. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29477410/ · DOI 10.1016/j.cellimm.2018.02.003
Complete structured claim and evidenceAdding 0.5 mM taurine chloramine to activated RAW264.7 macrophages reduced measured nitrite output by 47%; cytosolic nitric-oxide-synthase activity was also inhibited by pretreatment.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Mouse RAW264.7 cells stimulated with interferon-gamma and LPS.
- limitations
- Millimolar derivative exposure does not establish the effect of oral taurine in humans.
- nutrient_topic
- Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
- plain_language
- The chlorinated derivative dampened one inflammatory output in cultured mouse cells.
- primary_references
- Taurine chloramine inhibits the synthesis of nitric oxide and the release of tumor necrosis factor in activated RAW 264.7 cells. · 1993 · https://pubmed.ncbi.nlm.nih.gov/7689627/ · DOI 10.1002/jlb.54.2.119
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 369–375
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse RAW264.7 cells stimulated with interferon-gamma and LPS. · source_derived_draft · unverified_draft
## taurine-taucl-no The chlorinated derivative dampened one inflammatory output in cultured mouse cells. Adding 0.5 mM taurine chloramine to activated RAW264.7 macrophages reduced measured nitrite output by 47%; cytosolic nitric-oxide-synthase activity was also inhibited by pretreatment. Model: Mouse RAW264.7 cells stimulated with interferon-gamma and LPS. Limitations: Millimolar derivative exposure does not establish the effect of oral taurine in humans. Evidence access: Primary abstract Taurine chloramine inhibits the synthesis of nitric oxide and the release of tumor necrosis factor in activated RAW 264.7 cells. · 1993 · https://pubmed.ncbi.nlm.nih.gov/7689627/ · DOI 10.1002/jlb.54.2.119
Complete structured claim and evidenceAdding 0.5 mM taurine chloramine to activated RAW264.7 cells reduced TNF release by 43% in the reported assay.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Same mouse-cell experiment as the nitric-oxide result.
- limitations
- Two endpoints from one paper are not independent replications.
- nutrient_topic
- Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
- plain_language
- A second inflammatory signal also fell.
- primary_references
- Taurine chloramine inhibits the synthesis of nitric oxide and the release of tumor necrosis factor in activated RAW 264.7 cells. · 1993 · https://pubmed.ncbi.nlm.nih.gov/7689627/ · DOI 10.1002/jlb.54.2.119
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 377–383
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Same mouse-cell experiment as the nitric-oxide result. · source_derived_draft · unverified_draft
## taurine-taucl-tnf A second inflammatory signal also fell. Adding 0.5 mM taurine chloramine to activated RAW264.7 cells reduced TNF release by 43% in the reported assay. Model: Same mouse-cell experiment as the nitric-oxide result. Limitations: Two endpoints from one paper are not independent replications. Evidence access: Primary abstract Taurine chloramine inhibits the synthesis of nitric oxide and the release of tumor necrosis factor in activated RAW 264.7 cells. · 1993 · https://pubmed.ncbi.nlm.nih.gov/7689627/ · DOI 10.1002/jlb.54.2.119
Complete structured claim and evidenceThe homozygous SLC6A6 p.Ala78Glu variant was associated with approximately 95% lower taurine uptake in patient peripheral blood mononuclear cells despite membrane localization of the variant protein.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_access
- Primary abstract
- experimental_model
- Two affected brothers; human genetic, cell and spectroscopy studies.
- limitations
- Variant-specific inherited disease, not a universal threshold for dietary taurine insufficiency.
- nutrient_topic
- Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
- plain_language
- A transporter can reach the membrane yet function poorly.
- primary_references
- Biallelic mutation of human SLC6A6 encoding the taurine transporter TAUT is linked to early retinal degeneration. · 2019 · https://pubmed.ncbi.nlm.nih.gov/31345061/ · DOI 10.1096/fj.201900914RR
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 145–151
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Two affected brothers; human genetic, cell and spectroscopy studies. · source_derived_draft · unverified_draft
## taurine-taut-a78e A transporter can reach the membrane yet function poorly. The homozygous SLC6A6 p.Ala78Glu variant was associated with approximately 95% lower taurine uptake in patient peripheral blood mononuclear cells despite membrane localization of the variant protein. Model: Two affected brothers; human genetic, cell and spectroscopy studies. Limitations: Variant-specific inherited disease, not a universal threshold for dietary taurine insufficiency. Evidence access: Primary abstract Biallelic mutation of human SLC6A6 encoding the taurine transporter TAUT is linked to early retinal degeneration. · 2019 · https://pubmed.ncbi.nlm.nih.gov/31345061/ · DOI 10.1096/fj.201900914RR
Complete structured claim and evidenceThe human TauT study captured guanidinoacetate-bound transporter structures as part of its substrate-recognition analysis.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Human SLC6A6 structural study.
- limitations
- Binding structures alone do not quantify net transport or competition in a living human.
- nutrient_topic
- Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
- plain_language
- A creatine precursor also connects to this transporter.
- primary_references
- Molecular basis of human taurine transporter uptake and inhibition. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40789850/ · DOI 10.1038/s41467-025-62857-w
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 137–143
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human SLC6A6 structural study. · source_derived_draft · unverified_draft
## taurine-taut-guanidinoacetate A creatine precursor also connects to this transporter. The human TauT study captured guanidinoacetate-bound transporter structures as part of its substrate-recognition analysis. Model: Human SLC6A6 structural study. Limitations: Binding structures alone do not quantify net transport or competition in a living human. Evidence access: Primary abstract Molecular basis of human taurine transporter uptake and inhibition. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40789850/ · DOI 10.1038/s41467-025-62857-w
Complete structured claim and evidenceSLC6A6 p.Thr249Ile and p.Ala294Thr missense variants showed complete loss of taurine transport in HEK293 cells and patient fibroblasts in the four-family study of seven affected individuals.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_access
- Primary abstract
- experimental_model
- Human multicenter genetic study; cellular transport experiments; final issue year 2026, online 2025.
- limitations
- Investigational supplementation was proposed, not proven effective by this study.
- nutrient_topic
- Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
- plain_language
- Some disease variants had no measurable transport in the tested cells.
- primary_references
- Early-Onset Retinopathy in Patients With Variants in SLC6A6 Leading to Impaired Taurine Transport. · 2026 · https://pubmed.ncbi.nlm.nih.gov/41343195/ · DOI 10.1001/jamaophthalmol.2025.4875
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 177–183
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human multicenter genetic study; cellular transport experiments; final issue year 2026, online 2025. · source_derived_draft · unverified_draft
## taurine-taut-new-variants Some disease variants had no measurable transport in the tested cells. SLC6A6 p.Thr249Ile and p.Ala294Thr missense variants showed complete loss of taurine transport in HEK293 cells and patient fibroblasts in the four-family study of seven affected individuals. Model: Human multicenter genetic study; cellular transport experiments; final issue year 2026, online 2025. Limitations: Investigational supplementation was proposed, not proven effective by this study. Evidence access: Primary abstract Early-Onset Retinopathy in Patients With Variants in SLC6A6 Leading to Impaired Taurine Transport. · 2026 · https://pubmed.ncbi.nlm.nih.gov/41343195/ · DOI 10.1001/jamaophthalmol.2025.4875
Complete structured claim and evidenceThe two brothers carrying homozygous SLC6A6 p.Ala78Glu had panretinal degeneration and markedly reduced taurine in plasma, muscle and brain.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_access
- Primary abstract
- experimental_model
- Rare human family; retinal examinations and in-vivo spectroscopy.
- limitations
- Absence of extraocular clinical signs at that time does not mean every organ was unaffected.
- nutrient_topic
- Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
- plain_language
- Transport failure affected taurine availability in multiple compartments.
- primary_references
- Biallelic mutation of human SLC6A6 encoding the taurine transporter TAUT is linked to early retinal degeneration. · 2019 · https://pubmed.ncbi.nlm.nih.gov/31345061/ · DOI 10.1096/fj.201900914RR
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 153–159
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Rare human family; retinal examinations and in-vivo spectroscopy. · source_derived_draft · unverified_draft
## taurine-taut-retina Transport failure affected taurine availability in multiple compartments. The two brothers carrying homozygous SLC6A6 p.Ala78Glu had panretinal degeneration and markedly reduced taurine in plasma, muscle and brain. Model: Rare human family; retinal examinations and in-vivo spectroscopy. Limitations: Absence of extraocular clinical signs at that time does not mean every organ was unaffected. Evidence access: Primary abstract Biallelic mutation of human SLC6A6 encoding the taurine transporter TAUT is linked to early retinal degeneration. · 2019 · https://pubmed.ncbi.nlm.nih.gov/31345061/ · DOI 10.1096/fj.201900914RR
Complete structured claim and evidenceLrrc8d knockdown also reduced swelling-evoked myo-inositol efflux in the same rat astrocyte experiments.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Primary rat astrocytes and labeled myo-inositol.
- limitations
- Shared channel dependence does not prove competitive depletion or supplement synergy.
- nutrient_topic
- Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
- plain_language
- Taurine and inositol share part of the cell-volume release machinery.
- primary_references
- Molecular composition and heterogeneity of the LRRC8-containing swelling-activated osmolyte channels in primary rat astrocytes. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28833202/ · DOI 10.1113/JP275053
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 409–415
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Primary rat astrocytes and labeled myo-inositol. · source_derived_draft · unverified_draft
## taurine-vrac-inositol Taurine and inositol share part of the cell-volume release machinery. Lrrc8d knockdown also reduced swelling-evoked myo-inositol efflux in the same rat astrocyte experiments. Model: Primary rat astrocytes and labeled myo-inositol. Limitations: Shared channel dependence does not prove competitive depletion or supplement synergy. Evidence access: Primary abstract Molecular composition and heterogeneity of the LRRC8-containing swelling-activated osmolyte channels in primary rat astrocytes. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28833202/ · DOI 10.1113/JP275053
Complete structured claim and evidenceRNAi knockdown of Lrrc8d strongly reduced swelling-evoked taurine release from primary rat astrocytes; Lrrc8a knockdown also suppressed release.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Primary rat astrocytes; 30% hypoosmotic challenge and radiotracers.
- limitations
- RNAi reduction, not whole-animal gene deletion; this is efflux rather than SLC6A6 uptake.
- nutrient_topic
- Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
- plain_language
- Swollen brain-support cells release taurine through a channel with specific subunits.
- primary_references
- Molecular composition and heterogeneity of the LRRC8-containing swelling-activated osmolyte channels in primary rat astrocytes. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28833202/ · DOI 10.1113/JP275053
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 401–407
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Primary rat astrocytes; 30% hypoosmotic challenge and radiotracers. · source_derived_draft · unverified_draft
## taurine-vrac-taurine Swollen brain-support cells release taurine through a channel with specific subunits. RNAi knockdown of Lrrc8d strongly reduced swelling-evoked taurine release from primary rat astrocytes; Lrrc8a knockdown also suppressed release. Model: Primary rat astrocytes; 30% hypoosmotic challenge and radiotracers. Limitations: RNAi reduction, not whole-animal gene deletion; this is efflux rather than SLC6A6 uptake. Evidence access: Primary abstract Molecular composition and heterogeneity of the LRRC8-containing swelling-activated osmolyte channels in primary rat astrocytes. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28833202/ · DOI 10.1113/JP275053
Complete structured claim and evidenceGABA transport was studied by cellular uptake of tritiated GABA which was sodium-, chloride- and concentration-dependent with a Michaelis-Menten constant of 679 plus or minus 80 micromol per litre and a maximal uptake rate of 4,790 pmol per milligram protein per 5 minutes, uptake was significantly inhibited by betaine, beta-alanine, nipecotic acid, taurine and quinidine whereas probenecid, L-proline, creatine and glycine had no effect, and confocal immunofluorescent microscopy demonstrated colocalization of GAT2/BGT-1 with P-glycoprotein, a barrier-specific marker, on brain capillaries.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/gaba-research/11598501.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "97e62b677991c2535e9cd91c1283edc6415a64f66def965c17e478f7b676f708", "start_char": 0, "end_char": 1589, "text_sha256": "97e62b677991c2535e9cd91c1283edc6415a64f66def965c17e478f7b676f708"}
- experimental_model
- Reverse transcription PCR, Western blot and confocal immunostaining with uptake kinetics in an immortalised brain capillary endothelial line
- exposure
- Tritiated GABA uptake by a conditionally immortalised mouse brain capillary endothelial cell line used as an in vitro barrier model
- limitations
- An in vitro barrier model. It identifies the transporter and its kinetics; it does not establish the direction of net flux across an intact barrier.
- nutrient_topic
- GABA research collection; topical membership is not evidence of a direct clinical effect, and the sign of a GABA response depends on the chloride gradient of the cell it was measured in. · Gamma-aminobutyric acid
- organism
- Mouse
- plain_language
- The barrier has a dedicated carrier for this molecule, and its affinity is low enough that it only moves appreciable amounts at high concentrations.
- primary_references
- [gb-p11598501] GAT2/BGT-1 as a system responsible for the transport of gamma-aminobutyric acid at the mouse blood-brain barrier. (2001). https://pubmed.ncbi.nlm.nih.gov/11598501/ DOI: 10.1097/00004647-200110000-00012
- tissue_or_cell_type
- Brain capillary endothelium
- transport_effect
- raises Measured as cellular uptake of tritiated GABA, sodium- and chloride-dependent.
- transport_pool
- the expressing cell Measured as cellular uptake of tritiated GABA, sodium- and chloride-dependent.
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Reverse transcription PCR, Western blot and confocal immunostaining with uptake kinetics in an immortalised brain capillary endothelial line · source_derived_draft · unverified_draft
### gb-a-transporter-handles-gaba-at-the-barrier GABA transport was studied by cellular uptake of tritiated GABA which was sodium-, chloride- and concentration-dependent with a Michaelis-Menten constant of 679 plus or minus 80 micromol per litre and a maximal uptake rate of 4,790 pmol per milligram protein per 5 minutes, uptake was significantly inhibited by betaine, beta-alanine, nipecotic acid, taurine and quinidine whereas probenecid, L-proline, creatine and glycine had no effect, and confocal immunofluorescent microscopy demonstrated colocalization of GAT2/BGT-1 with P-glycoprotein, a barrier-specific marker, on brain capillaries. Condition category: normal nutrient_topic: GABA research collection; topical membership is not evidence of a direct clinical effect, and the sign of a GABA response depends on the chloride gradient of the cell it was measured in. plain_language: The barrier has a dedicated carrier for this molecule, and its affinity is low enough that it only moves appreciable amounts at high concentrations. organism: Mouse tissue_or_cell_type: Brain capillary endothelium experimental_model: Reverse transcription PCR, Western blot and confocal immunostaining with uptake kinetics in an immortalised brain capillary endothelial line limitations: An in vitro barrier model. It identifies the transporter and its kinetics; it does not establish the direction of net flux across an intact barrier. exposure: Tritiated GABA uptake by a conditionally immortalised mouse brain capillary endothelial cell line used as an in vitro barrier model evidence_span: {"source_cache": "artifacts/gaba-research/11598501.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "97e62b677991c2535e9cd91c1283edc6415a64f66def965c17e478f7b676f708", "start_char": 0, "end_char": 1589, "text_sha256": "97e62b677991c2535e9cd91c1283edc6415a64f66def965c17e478f7b676f708"} [gb-p11598501] GAT2/BGT-1 as a system responsible for the transport of gamma-aminobutyric acid at the mouse blood-brain barrier. (2001). https://pubmed.ncbi.nlm.nih.gov/11598501/ DOI: 10.1097/00004647-200110000-00012
Complete structured claim and evidenceA close relationship between vigabatrin-induced retinal toxicity and light exposure was observed, vigabatrin-treated mice reared in darkness preserved better visual function and retinal architectures as verified by optokinetic tests, optical coherence tomography and electroretinography, the retinal taurine level of vigabatrin-treated mice exposed to light was significantly lower than that of vigabatrin mice reared in darkness, and the vigabatrin-induced morphological and functional impairments could be partially alleviated by taurine treatment.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/gaba-research/27941319.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "92835398ef34fe87d3c084d1933722427a474b40c88c30ada21a6ede8f4d875a", "start_char": 0, "end_char": 1596, "text_sha256": "92835398ef34fe87d3c084d1933722427a474b40c88c30ada21a6ede8f4d875a"}
- experimental_model
- Electroretinography, optical coherence tomography and optokinetic testing in mice reared in light or darkness
- exposure
- Vigabatrin with and without light exposure, and with taurine supplementation
- limitations
- A mouse study. It identifies two contributing factors and shows partial rescue, not that taurine prevents the human visual field defect.
- nutrient_topic
- GABA research collection; topical membership is not evidence of a direct clinical effect, and the sign of a GABA response depends on the chloride gradient of the cell it was measured in. · Gamma-aminobutyric acid
- organism
- Mouse
- plain_language
- The retinal damage needed light to happen, went with a fall in retinal taurine, and was partly undone by giving taurine back.
- primary_references
- [gb-p27941319] The Vigabatrin Induced Retinal Toxicity is Associated with Photopic Exposure and Taurine Deficiency: An In Vivo Study. (2016). https://pubmed.ncbi.nlm.nih.gov/27941319/ DOI: 10.1159/000453143
- tissue_or_cell_type
- Retina
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Electroretinography, optical coherence tomography and optokinetic testing in mice reared in light or darkness · source_derived_draft · unverified_draft
### gb-light-and-taurine-both-matter A close relationship between vigabatrin-induced retinal toxicity and light exposure was observed, vigabatrin-treated mice reared in darkness preserved better visual function and retinal architectures as verified by optokinetic tests, optical coherence tomography and electroretinography, the retinal taurine level of vigabatrin-treated mice exposed to light was significantly lower than that of vigabatrin mice reared in darkness, and the vigabatrin-induced morphological and functional impairments could be partially alleviated by taurine treatment. Condition category: normal nutrient_topic: GABA research collection; topical membership is not evidence of a direct clinical effect, and the sign of a GABA response depends on the chloride gradient of the cell it was measured in. plain_language: The retinal damage needed light to happen, went with a fall in retinal taurine, and was partly undone by giving taurine back. organism: Mouse tissue_or_cell_type: Retina experimental_model: Electroretinography, optical coherence tomography and optokinetic testing in mice reared in light or darkness limitations: A mouse study. It identifies two contributing factors and shows partial rescue, not that taurine prevents the human visual field defect. exposure: Vigabatrin with and without light exposure, and with taurine supplementation evidence_span: {"source_cache": "artifacts/gaba-research/27941319.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "92835398ef34fe87d3c084d1933722427a474b40c88c30ada21a6ede8f4d875a", "start_char": 0, "end_char": 1596, "text_sha256": "92835398ef34fe87d3c084d1933722427a474b40c88c30ada21a6ede8f4d875a"} [gb-p27941319] The Vigabatrin Induced Retinal Toxicity is Associated with Photopic Exposure and Taurine Deficiency: An In Vivo Study. (2016). https://pubmed.ncbi.nlm.nih.gov/27941319/ DOI: 10.1159/000453143
Complete structured claim and evidenceHuman AGMAT R105 hydrolyzed taurocyamine more efficiently than guanidinobutyrate in the tested concentration range; R105 and G105 differed in substrate preferences.
Experimental context and source evidence
- evidence_access
- Primary full text; Figures 2 and 3
- experimental_model
- Purified human variants; 10 mM substrate comparison and concentration series.
- limitations
- This does not establish a clinically meaningful taurine deficit or a supplementation response.
- nutrient_topic
- Agmatine Sulfate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Agmatine Sulfate
- plain_language
- A variant can alter which related metabolic pool is processed.
- primary_references
- Guanidino acid hydrolysis by the human enzyme annotated as agmatinase. · 2022 · https://pubmed.ncbi.nlm.nih.gov/36543883/ · DOI 10.1038/s41598-022-26655-4
Agmatine Sulfate: transport, guanidino metabolism, ion channels and cross-nutrient mechanisms (2026-09-20) · lines 132–138
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Purified human variants; 10 mM substrate comparison and concentration series. · source_derived_draft · unverified_draft
## agmatine-sulfate-agmat-taurocyamine A variant can alter which related metabolic pool is processed. Human AGMAT R105 hydrolyzed taurocyamine more efficiently than guanidinobutyrate in the tested concentration range; R105 and G105 differed in substrate preferences. Model: Purified human variants; 10 mM substrate comparison and concentration series. Limitations: This does not establish a clinically meaningful taurine deficit or a supplementation response. Evidence access: Primary full text; Figures 2 and 3 Guanidino acid hydrolysis by the human enzyme annotated as agmatinase. · 2022 · https://pubmed.ncbi.nlm.nih.gov/36543883/ · DOI 10.1038/s41598-022-26655-4
Complete structured claim and evidencePurified human GATM transferred an amidino group from arginine to taurine, producing taurocyamine in vitro.
Experimental context and source evidence
- evidence_access
- Primary full text; Figure 4B
- experimental_model
- Recombinant human GATM substrate comparison.
- limitations
- Taurine is a secondary substrate in this assay; tissue flux and clinically important depletion were not established.
- nutrient_topic
- Agmatine Sulfate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Agmatine Sulfate
- plain_language
- Creatine-synthesis machinery also accepts a taurine-related side reaction.
- primary_references
- Guanidino acid hydrolysis by the human enzyme annotated as agmatinase. · 2022 · https://pubmed.ncbi.nlm.nih.gov/36543883/ · DOI 10.1038/s41598-022-26655-4
Agmatine Sulfate: transport, guanidino metabolism, ion channels and cross-nutrient mechanisms (2026-09-20) · lines 188–194
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Recombinant human GATM substrate comparison. · source_derived_draft · unverified_draft
## agmatine-sulfate-gatm-taurine Creatine-synthesis machinery also accepts a taurine-related side reaction. Purified human GATM transferred an amidino group from arginine to taurine, producing taurocyamine in vitro. Model: Recombinant human GATM substrate comparison. Limitations: Taurine is a secondary substrate in this assay; tissue flux and clinically important depletion were not established. Evidence access: Primary full text; Figure 4B Guanidino acid hydrolysis by the human enzyme annotated as agmatinase. · 2022 · https://pubmed.ncbi.nlm.nih.gov/36543883/ · DOI 10.1038/s41598-022-26655-4
Complete structured claim and evidenceAt saturating 30 mM agonist, human alpha1 glycine-receptor activation rose faster with glycine than beta-alanine or taurine, and glycine responses decayed more slowly after removal.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Human recombinant receptor comparison using high agonist concentrations.
- limitations
- Not equivalent to relative sedative potency after oral intake.
- nutrient_topic
- Glycine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Glycine
- plain_language
- Related molecules activate the same receptor with different timing.
- primary_references
- Kinetic determinants of agonist action at the recombinant human glycine receptor. · 2003 · https://pubmed.ncbi.nlm.nih.gov/12679369/ · DOI 10.1113/jphysiol.2002.037796
Glycine: supply, one-carbon allocation, receptors and cross-nutrient mechanisms (2026-09-19) · lines 202–208
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human recombinant receptor comparison using high agonist concentrations. · source_derived_draft · unverified_draft
## glycine-glyr-ligand-kinetics Related molecules activate the same receptor with different timing. At saturating 30 mM agonist, human alpha1 glycine-receptor activation rose faster with glycine than beta-alanine or taurine, and glycine responses decayed more slowly after removal. Model: Human recombinant receptor comparison using high agonist concentrations. Limitations: Not equivalent to relative sedative potency after oral intake. Evidence access: Primary abstract Kinetic determinants of agonist action at the recombinant human glycine receptor. · 2003 · https://pubmed.ncbi.nlm.nih.gov/12679369/ · DOI 10.1113/jphysiol.2002.037796
Complete structured claim and evidenceTen weeks of beta-alanine supplementation did not change muscle taurine in this study.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Human muscle-biopsy study.
- limitations
- Does not exclude effects under other exposures or in other species.
- nutrient_topic
- Carnosine collection; isomer, preparation, species, exposure and manipulation remain explicit. · L-Carnosine / beta-alanyl-L-histidine
- plain_language
- A proposed precursor interaction did not cause measurable depletion here.
- primary_references
- Influence of beta-alanine supplementation on skeletal muscle carnosine concentrations and high intensity cycling capacity. · 2007 · https://pubmed.ncbi.nlm.nih.gov/16868650/ · DOI 10.1007/s00726-006-0364-4
Carnosine: synthesis, transport, carbonyl chemistry and nutrient interactions (2026-09-19) · lines 220–226
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human muscle-biopsy study. · source_derived_draft · unverified_draft
## carnosine-taurine-negative A proposed precursor interaction did not cause measurable depletion here. Ten weeks of beta-alanine supplementation did not change muscle taurine in this study. Model: Human muscle-biopsy study. Limitations: Does not exclude effects under other exposures or in other species. Evidence access: Primary abstract Influence of beta-alanine supplementation on skeletal muscle carnosine concentrations and high intensity cycling capacity. · 2007 · https://pubmed.ncbi.nlm.nih.gov/16868650/ · DOI 10.1007/s00726-006-0364-4
Complete structured claim and evidence
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.