Component

Sodium butyrate

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

13 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

Read recorded mechanisms Open recursive mind map

How nutrients influence it

Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.

How nutrients reach it in more than one step

Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.

Tracing routes…

What it does

Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.

Recorded relationships

Where it participates (unsigned role)

  1. Hippocampal Bdnf siRNA blocked the memory-enabling effect of post-training sodium butyrate in the mouse task.

    Mouse brain-derived neurotrophic factor / Bdnf → Mouse object-location memory after injected sodium butyrate source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary abstract
    experimental_model
    Mouse hippocampal siRNA and object-location memory assay.
    limitations
    Task- and intervention-specific; not a universal mechanism for every memory effect of butyrate.
    nutrient_topic
    Butyrate collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Butyrate
    plain_language
    Reducing a neural growth-factor signal removed the measured benefit.
    primary_references
    Exercise and sodium butyrate transform a subthreshold learning event into long-term memory via a brain-derived neurotrophic factor-dependent mechanism. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23615664/ · DOI 10.1038/npp.2013.104
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Butyrate: microbial production, fuel use, signaling and nutrient interactions (2026-09-19) · lines 630–636

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse hippocampal siRNA and object-location memory assay. · source_derived_draft · unverified_draft

    ## butyrate-bdnf-knockdown Reducing a neural growth-factor signal removed the measured benefit. Hippocampal Bdnf siRNA blocked the memory-enabling effect of post-training sodium butyrate in the mouse task. Model: Mouse hippocampal siRNA and object-location memory assay. Limitations: Task- and intervention-specific; not a universal mechanism for every memory effect of butyrate. Evidence access: Primary abstract Exercise and sodium butyrate transform a subthreshold learning event into long-term memory via a brain-derived neurotrophic factor-dependent mechanism. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23615664/ · DOI 10.1038/npp.2013.104
    Complete structured claim and evidence

  2. Post-training sodium butyrate injection enabled 24-hour object-location memory after otherwise subthreshold training in mice, with increased hippocampal Bdnf transcripts.

    Butyrate → Mouse object-location memory after injected sodium butyrate source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Mouse behavioral and hippocampal transcription experiments.
    limitations
    Injected pharmacological exposure does not establish that ordinary microbial production or oral supplements improve human memory.
    nutrient_topic
    Butyrate collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Butyrate
    plain_language
    Injected treatment changed a learning response in mice.
    primary_references
    Exercise and sodium butyrate transform a subthreshold learning event into long-term memory via a brain-derived neurotrophic factor-dependent mechanism. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23615664/ · DOI 10.1038/npp.2013.104

    Butyrate: microbial production, fuel use, signaling and nutrient interactions (2026-09-19) · lines 622–628

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse behavioral and hippocampal transcription experiments. · source_derived_draft · unverified_draft

    ## butyrate-brain-memory Injected treatment changed a learning response in mice. Post-training sodium butyrate injection enabled 24-hour object-location memory after otherwise subthreshold training in mice, with increased hippocampal Bdnf transcripts. Model: Mouse behavioral and hippocampal transcription experiments. Limitations: Injected pharmacological exposure does not establish that ordinary microbial production or oral supplements improve human memory. Evidence access: Primary abstract Exercise and sodium butyrate transform a subthreshold learning event into long-term memory via a brain-derived neurotrophic factor-dependent mechanism. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23615664/ · DOI 10.1038/npp.2013.104
    Complete structured claim and evidence

  3. Sodium butyrate promoted store-operated calcium entry and activated the CaMKK-beta/AMPK pathway during Caco-2 tight-junction reassembly, without the change being explained by ATP concentration.

    Butyrate → Store-operated calcium entry in butyrate-exposed Caco-2 cells source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Human Caco-2 calcium-switch model.
    limitations
    This does not show that dietary calcium or magnesium supplementation improves the response.
    nutrient_topic
    Butyrate collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Butyrate
    plain_language
    Calcium signaling helped connect butyrate to barrier repair.
    primary_references
    Sodium Butyrate Promotes Reassembly of Tight Junctions in Caco-2 Monolayers Involving Inhibition of MLCK/MLC2 Pathway and Phosphorylation of PKCβ2. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27735862/ · DOI 10.3390/ijms17101696

    Butyrate: microbial production, fuel use, signaling and nutrient interactions (2026-09-19) · lines 270–276

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human Caco-2 calcium-switch model. · source_derived_draft · unverified_draft

    ## butyrate-calcium-soce Calcium signaling helped connect butyrate to barrier repair. Sodium butyrate promoted store-operated calcium entry and activated the CaMKK-beta/AMPK pathway during Caco-2 tight-junction reassembly, without the change being explained by ATP concentration. Model: Human Caco-2 calcium-switch model. Limitations: This does not show that dietary calcium or magnesium supplementation improves the response. Evidence access: Primary abstract Sodium Butyrate Promotes Reassembly of Tight Junctions in Caco-2 Monolayers Involving Inhibition of MLCK/MLC2 Pathway and Phosphorylation of PKCβ2. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27735862/ · DOI 10.3390/ijms17101696
    Complete structured claim and evidence

  4. Oral sodium butyrate did not significantly increase brown-adipose glucose uptake in either lean or metabolic-syndrome men in the pilot.

    Butyrate → Human brown-adipose glucose uptake after oral butyrate source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Human FDG-PET/CT before/after measurements.
    limitations
    FDG uptake is a particular endpoint, not a complete assay of all thermogenesis.
    nutrient_topic
    Butyrate collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Butyrate
    plain_language
    The expected brown-fat response was not detected.
    primary_references
    Differential metabolic effects of oral butyrate treatment in lean versus metabolic syndrome subjects. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29799027/ · DOI 10.1038/s41424-018-0025-4

    Butyrate: microbial production, fuel use, signaling and nutrient interactions (2026-09-19) · lines 574–580

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human FDG-PET/CT before/after measurements. · source_derived_draft · unverified_draft

    ## butyrate-human-bat-null The expected brown-fat response was not detected. Oral sodium butyrate did not significantly increase brown-adipose glucose uptake in either lean or metabolic-syndrome men in the pilot. Model: Human FDG-PET/CT before/after measurements. Limitations: FDG uptake is a particular endpoint, not a complete assay of all thermogenesis. Evidence access: Primary abstract Differential metabolic effects of oral butyrate treatment in lean versus metabolic syndrome subjects. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29799027/ · DOI 10.1038/s41424-018-0025-4
    Complete structured claim and evidence

  5. Sodium butyrate reduced proteinuria, podocyte loss and renal injury in the mouse Adriamycin-nephropathy study.

    Butyrate → Mouse podocyte injury and proteinuria after butyrate source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Mouse induced-nephropathy intervention, with a separate butyrate-releasing starch arm.
    limitations
    Not evidence of efficacy in all human kidney diseases.
    nutrient_topic
    Butyrate collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Butyrate
    plain_language
    The experimental benefit extended beyond the gut to the kidney.
    primary_references
    Gut microbial metabolite butyrate protects against proteinuric kidney disease through epigenetic- and GPR109a-mediated mechanisms. · 2019 · https://pubmed.ncbi.nlm.nih.gov/31366236/ · DOI 10.1096/fj.201901080R

    Butyrate: microbial production, fuel use, signaling and nutrient interactions (2026-09-19) · lines 606–612

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse induced-nephropathy intervention, with a separate butyrate-releasing starch arm. · source_derived_draft · unverified_draft

    ## butyrate-kidney-protection The experimental benefit extended beyond the gut to the kidney. Sodium butyrate reduced proteinuria, podocyte loss and renal injury in the mouse Adriamycin-nephropathy study. Model: Mouse induced-nephropathy intervention, with a separate butyrate-releasing starch arm. Limitations: Not evidence of efficacy in all human kidney diseases. Evidence access: Primary abstract Gut microbial metabolite butyrate protects against proteinuric kidney disease through epigenetic- and GPR109a-mediated mechanisms. · 2019 · https://pubmed.ncbi.nlm.nih.gov/31366236/ · DOI 10.1096/fj.201901080R
    Complete structured claim and evidence

  6. In nine lean men, four weeks of 4 g/day oral sodium butyrate was associated with improved peripheral and hepatic insulin sensitivity.

    Butyrate → Human insulin sensitivity after oral sodium butyrate source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Uncontrolled before/after pilot with clamp measurements.
    limitations
    No placebo group; the lean arm cannot establish efficacy in metabolic syndrome.
    nutrient_topic
    Butyrate collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Butyrate
    plain_language
    A small human pilot detected a metabolic change in lean participants.
    primary_references
    Differential metabolic effects of oral butyrate treatment in lean versus metabolic syndrome subjects. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29799027/ · DOI 10.1038/s41424-018-0025-4

    Butyrate: microbial production, fuel use, signaling and nutrient interactions (2026-09-19) · lines 558–564

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Uncontrolled before/after pilot with clamp measurements. · source_derived_draft · unverified_draft

    ## butyrate-lean-human-insulin A small human pilot detected a metabolic change in lean participants. In nine lean men, four weeks of 4 g/day oral sodium butyrate was associated with improved peripheral and hepatic insulin sensitivity. Model: Uncontrolled before/after pilot with clamp measurements. Limitations: No placebo group; the lean arm cannot establish efficacy in metabolic syndrome. Evidence access: Primary abstract Differential metabolic effects of oral butyrate treatment in lean versus metabolic syndrome subjects. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29799027/ · DOI 10.1038/s41424-018-0025-4
    Complete structured claim and evidence

  7. After preincubation with 2 mM sodium butyrate, AA/C1 cells increased the maximal butyrate uptake rate about fivefold without a significant change in apparent Km.

    Human monocarboxylate transporter 1 / SLC16A1 → Human colonic-cell butyrate transport source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Human colonic-cell radiotracer uptake.
    limitations
    An adaptive culture response does not establish oral bioavailability.
    nutrient_topic
    Butyrate collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Butyrate
    plain_language
    Transport capacity increased rather than measured substrate affinity.
    primary_references
    Substrate-induced regulation of the human colonic monocarboxylate transporter, MCT1. · 2002 · https://pubmed.ncbi.nlm.nih.gov/11882670/ · DOI 10.1113/jphysiol.2001.014241

    Butyrate: microbial production, fuel use, signaling and nutrient interactions (2026-09-19) · lines 134–140

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human colonic-cell radiotracer uptake. · source_derived_draft · unverified_draft

    ## butyrate-mct1-capacity Transport capacity increased rather than measured substrate affinity. After preincubation with 2 mM sodium butyrate, AA/C1 cells increased the maximal butyrate uptake rate about fivefold without a significant change in apparent Km. Model: Human colonic-cell radiotracer uptake. Limitations: An adaptive culture response does not establish oral bioavailability. Evidence access: Primary abstract Substrate-induced regulation of the human colonic monocarboxylate transporter, MCT1. · 2002 · https://pubmed.ncbi.nlm.nih.gov/11882670/ · DOI 10.1113/jphysiol.2001.014241
    Complete structured claim and evidence

  8. At 2 mM sodium butyrate, human AA/C1 colonic cells increased MCT1 mRNA and protein through transcription and greater mRNA stability.

    Butyrate → Human monocarboxylate transporter 1 / SLC16A1 source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Human colonic epithelial AA/C1 cultures.
    limitations
    Acetate and propionate did not reproduce this response; exposure and cell state matter.
    nutrient_topic
    Butyrate collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Butyrate
    plain_language
    Butyrate increased the capacity of one of its own uptake routes.
    primary_references
    Substrate-induced regulation of the human colonic monocarboxylate transporter, MCT1. · 2002 · https://pubmed.ncbi.nlm.nih.gov/11882670/ · DOI 10.1113/jphysiol.2001.014241

    Butyrate: microbial production, fuel use, signaling and nutrient interactions (2026-09-19) · lines 126–132

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human colonic epithelial AA/C1 cultures. · source_derived_draft · unverified_draft

    ## butyrate-mct1-expression Butyrate increased the capacity of one of its own uptake routes. At 2 mM sodium butyrate, human AA/C1 colonic cells increased MCT1 mRNA and protein through transcription and greater mRNA stability. Model: Human colonic epithelial AA/C1 cultures. Limitations: Acetate and propionate did not reproduce this response; exposure and cell state matter. Evidence access: Primary abstract Substrate-induced regulation of the human colonic monocarboxylate transporter, MCT1. · 2002 · https://pubmed.ncbi.nlm.nih.gov/11882670/ · DOI 10.1113/jphysiol.2001.014241
    Complete structured claim and evidence

  9. The same 4 g/day, four-week pilot found no insulin-sensitivity improvement in its ten men with metabolic syndrome.

    Butyrate → Human insulin sensitivity after oral sodium butyrate source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Human uncontrolled pilot; separate metabolic-syndrome group.
    limitations
    Population differences are observed; altered handling is a proposed explanation rather than established mediation.
    nutrient_topic
    Butyrate collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Butyrate
    plain_language
    The group with metabolic syndrome did not show the lean-group response.
    primary_references
    Differential metabolic effects of oral butyrate treatment in lean versus metabolic syndrome subjects. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29799027/ · DOI 10.1038/s41424-018-0025-4

    Butyrate: microbial production, fuel use, signaling and nutrient interactions (2026-09-19) · lines 566–572

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human uncontrolled pilot; separate metabolic-syndrome group. · source_derived_draft · unverified_draft

    ## butyrate-metabolic-syndrome-null The group with metabolic syndrome did not show the lean-group response. The same 4 g/day, four-week pilot found no insulin-sensitivity improvement in its ten men with metabolic syndrome. Model: Human uncontrolled pilot; separate metabolic-syndrome group. Limitations: Population differences are observed; altered handling is a proposed explanation rather than established mediation. Evidence access: Primary abstract Differential metabolic effects of oral butyrate treatment in lean versus metabolic syndrome subjects. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29799027/ · DOI 10.1038/s41424-018-0025-4
    Complete structured claim and evidence

  10. Feeding sodium butyrate at 5% of a high-fat diet increased thermogenesis and mitochondrial adaptation in mouse muscle and brown fat, with increased PGC-1alpha expression and insulin sensitivity.

    Butyrate → Mouse thermogenesis and mitochondrial adaptation after butyrate source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    High-fat-fed C57BL/6J mice.
    limitations
    Five percent of diet is not a human supplement dose; this study did not observe reduced food intake.
    nutrient_topic
    Butyrate collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Butyrate
    plain_language
    A high dietary exposure changed energy expenditure in mice.
    primary_references
    Butyrate improves insulin sensitivity and increases energy expenditure in mice. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19366864/ · DOI 10.2337/db08-1637

    Butyrate: microbial production, fuel use, signaling and nutrient interactions (2026-09-19) · lines 550–556

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · High-fat-fed C57BL/6J mice. · source_derived_draft · unverified_draft

    ## butyrate-mouse-thermogenesis A high dietary exposure changed energy expenditure in mice. Feeding sodium butyrate at 5% of a high-fat diet increased thermogenesis and mitochondrial adaptation in mouse muscle and brown fat, with increased PGC-1alpha expression and insulin sensitivity. Model: High-fat-fed C57BL/6J mice. Limitations: Five percent of diet is not a human supplement dose; this study did not observe reduced food intake. Evidence access: Primary abstract Butyrate improves insulin sensitivity and increases energy expenditure in mice. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19366864/ · DOI 10.2337/db08-1637
    Complete structured claim and evidence

  11. In 23 hypertensive adults, 3.9 g/day oral sodium butyrate for four weeks increased daytime systolic pressure by 9.63 mmHg and diastolic pressure by 5.08 mmHg versus sodium-matched placebo.

    Butyrate → Human blood pressure after butyrate administration source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary full text, intervention methods and primary results
    experimental_model
    Double-blind randomized trial after supervised antihypertensive washout; sodium chloride placebo matched the sodium load.
    limitations
    Small short trial; do not infer the increase was simply unmatched sodium or advise medication changes.
    nutrient_topic
    Butyrate collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Butyrate
    plain_language
    An oral human trial found higher blood pressure.
    primary_references
    Effects of Oral Butyrate on Blood Pressure in Patients With Hypertension: A Randomized, Placebo-Controlled Trial. · 2024 · https://pubmed.ncbi.nlm.nih.gov/39034917/ · DOI 10.1161/HYPERTENSIONAHA.123.22437

    Butyrate: microbial production, fuel use, signaling and nutrient interactions (2026-09-19) · lines 582–588

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Double-blind randomized trial after supervised antihypertensive washout; sodium chloride placebo matched the sodium load. · source_derived_draft · unverified_draft

    ## butyrate-oral-bp-increase An oral human trial found higher blood pressure. In 23 hypertensive adults, 3.9 g/day oral sodium butyrate for four weeks increased daytime systolic pressure by 9.63 mmHg and diastolic pressure by 5.08 mmHg versus sodium-matched placebo. Model: Double-blind randomized trial after supervised antihypertensive washout; sodium chloride placebo matched the sodium load. Limitations: Small short trial; do not infer the increase was simply unmatched sodium or advise medication changes. Evidence access: Primary full text, intervention methods and primary results Effects of Oral Butyrate on Blood Pressure in Patients With Hypertension: A Randomized, Placebo-Controlled Trial. · 2024 · https://pubmed.ncbi.nlm.nih.gov/39034917/ · DOI 10.1161/HYPERTENSIONAHA.123.22437
    Complete structured claim and evidence

  12. Sodium butyrate increased PKC-beta2 Ser660 phosphorylation; PKC-beta inhibition blocked the promoted junction reassembly.

    Butyrate → Human protein kinase C beta II / PRKCB beta2 isoform source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Human Caco-2 signaling and inhibitor experiments.
    limitations
    Inhibitor sensitivity does not imply direct binding of butyrate to PKC-beta2.
    nutrient_topic
    Butyrate collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Butyrate
    plain_language
    A downstream kinase contributed to rebuilding the junction.
    primary_references
    Sodium Butyrate Promotes Reassembly of Tight Junctions in Caco-2 Monolayers Involving Inhibition of MLCK/MLC2 Pathway and Phosphorylation of PKCβ2. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27735862/ · DOI 10.3390/ijms17101696

    Butyrate: microbial production, fuel use, signaling and nutrient interactions (2026-09-19) · lines 278–284

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human Caco-2 signaling and inhibitor experiments. · source_derived_draft · unverified_draft

    ## butyrate-pkcb-junction A downstream kinase contributed to rebuilding the junction. Sodium butyrate increased PKC-beta2 Ser660 phosphorylation; PKC-beta inhibition blocked the promoted junction reassembly. Model: Human Caco-2 signaling and inhibitor experiments. Limitations: Inhibitor sensitivity does not imply direct binding of butyrate to PKC-beta2. Evidence access: Primary abstract Sodium Butyrate Promotes Reassembly of Tight Junctions in Caco-2 Monolayers Involving Inhibition of MLCK/MLC2 Pathway and Phosphorylation of PKCβ2. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27735862/ · DOI 10.3390/ijms17101696
    Complete structured claim and evidence

  13. Oral butyrate increased plasma butyrate without increasing fecal butyrate in the hypertension trial.

    Butyrate → Human circulating butyrate concentration source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    biomarker_context Imported condition classification; unverified.
    evidence_access
    Primary abstract
    experimental_model
    Same randomized human oral trial.
    limitations
    Neither compartment is a universal measure of intracellular sufficiency or total microbial production.
    nutrient_topic
    Butyrate collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Butyrate
    plain_language
    Blood and stool measurements did not change together.
    primary_references
    Effects of Oral Butyrate on Blood Pressure in Patients With Hypertension: A Randomized, Placebo-Controlled Trial. · 2024 · https://pubmed.ncbi.nlm.nih.gov/39034917/ · DOI 10.1161/HYPERTENSIONAHA.123.22437
    trigger_kind
    biomarker_context Imported condition classification; unverified.

    Butyrate: microbial production, fuel use, signaling and nutrient interactions (2026-09-19) · lines 598–604

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Same randomized human oral trial. · source_derived_draft · unverified_draft

    ## butyrate-plasma-feces-diverge Blood and stool measurements did not change together. Oral butyrate increased plasma butyrate without increasing fecal butyrate in the hypertension trial. Model: Same randomized human oral trial. Limitations: Neither compartment is a universal measure of intracellular sufficiency or total microbial production. Evidence access: Primary abstract Effects of Oral Butyrate on Blood Pressure in Patients With Hypertension: A Randomized, Placebo-Controlled Trial. · 2024 · https://pubmed.ncbi.nlm.nih.gov/39034917/ · DOI 10.1161/HYPERTENSIONAHA.123.22437
    Complete structured claim and evidence

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

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