Component

Glycolysis

Glycolysis. Species, exposure and limitations are retained in each linked claim.

4 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

What it acts on

  1. Trained monocytes display high glucose consumption, high lactate production and a high ratio of NAD+ to NADH, reflecting a shift in metabolism with an increase in glycolysis dependent on the activation of mammalian target of rapamycin through a dectin-1-Akt-HIF-1 alpha pathway, inhibition of Akt, mTOR or HIF-1 alpha blocked monocyte induction of trained immunity whereas the AMP-activated protein kinase activator metformin inhibited the innate immune response to fungal infection, and mice with a myeloid cell-specific defect in HIF-1 alpha were unable to mount trained immunity against bacterial sepsis.

    Glycolysis → Trained immunity, an altered response to a later challenge after the first has ended source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/glucan-research/25258083.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "68c4cae9a0e4477a52864e63ecaf5ec977752b5d3246a9ba54aa22d160e41872", "start_char": 0, "end_char": 1225, "text_sha256": "68c4cae9a0e4477a52864e63ecaf5ec977752b5d3246a9ba54aa22d160e41872"}
    experimental_model
    Histone modification profiling and genome-wide transcriptome of trained human monocytes, with pathway inhibition and a myeloid conditional knockout
    exposure
    Beta-glucan training with inhibition of Akt, mTOR or HIF-1 alpha, and metformin as an AMPK activator
    limitations
    The metformin result is an experimental inhibition of an induced response, not a clinical interaction study.
    nutrient_topic
    Beta-glucan research collection; topical membership is not evidence of a direct clinical effect, and each preparation is recorded as its own entity with no family link joining any pair. · Beta-glucan
    organism
    Human cells and mouse
    plain_language
    The rewiring costs energy: block the cell from burning glucose the fast way and the training does not take.
    primary_references
    [bg-p25258083] mTOR- and HIF-1α-mediated aerobic glycolysis as metabolic basis for trained immunity. (2014). https://pubmed.ncbi.nlm.nih.gov/25258083/ DOI: 10.1126/science.1250684
    tissue_or_cell_type
    Monocyte

    Beta-glucan: a structural family rather than an agent, what decides whether a bound glucan actually signals, the complement route that a cereal and a yeast preparation share, and the unequal human evidence behind each (2026-09-22) · lines 437–448

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Histone modification profiling and genome-wide transcriptome of trained human monocytes, with pathway inhibition and a myeloid conditional knockout · source_derived_draft · unverified_draft

    ### bg-training-needs-aerobic-glycolysis Trained monocytes display high glucose consumption, high lactate production and a high ratio of NAD+ to NADH, reflecting a shift in metabolism with an increase in glycolysis dependent on the activation of mammalian target of rapamycin through a dectin-1-Akt-HIF-1 alpha pathway, inhibition of Akt, mTOR or HIF-1 alpha blocked monocyte induction of trained immunity whereas the AMP-activated protein kinase activator metformin inhibited the innate immune response to fungal infection, and mice with a myeloid cell-specific defect in HIF-1 alpha were unable to mount trained immunity against bacterial sepsis. Condition category: normal nutrient_topic: Beta-glucan research collection; topical membership is not evidence of a direct clinical effect, and each preparation is recorded as its own entity with no family link joining any pair. plain_language: The rewiring costs energy: block the cell from burning glucose the fast way and the training does not take. organism: Human cells and mouse tissue_or_cell_type: Monocyte experimental_model: Histone modification profiling and genome-wide transcriptome of trained human monocytes, with pathway inhibition and a myeloid conditional knockout limitations: The metformin result is an experimental inhibition of an induced response, not a clinical interaction study. exposure: Beta-glucan training with inhibition of Akt, mTOR or HIF-1 alpha, and metformin as an AMPK activator evidence_span: {"source_cache": "artifacts/glucan-research/25258083.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "68c4cae9a0e4477a52864e63ecaf5ec977752b5d3246a9ba54aa22d160e41872", "start_char": 0, "end_char": 1225, "text_sha256": "68c4cae9a0e4477a52864e63ecaf5ec977752b5d3246a9ba54aa22d160e41872"} [bg-p25258083] mTOR- and HIF-1α-mediated aerobic glycolysis as metabolic basis for trained immunity. (2014). https://pubmed.ncbi.nlm.nih.gov/25258083/ DOI: 10.1126/science.1250684
    Complete structured claim and evidence

What acts on it

  1. In liver the concentration of xylulose-5-phosphate was significantly higher in the control group than in the acetic acid groups, and in gastrocnemius muscle the ratio of fructose-1,6-bisphosphate to fructose-6-phosphate was significantly higher in the control group; the authors proposed that acetic acid may activate gluconeogenesis and inactivate glycolysis in liver through suppression of xylulose-5-phosphate accumulation, and inhibit glycolysis in skeletal muscle by suppressing phosphofructokinase-1 activity.

    Acetic acid → Glycolysis source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/acetate-research/11435516.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "130bbe406429175feedf86bcfa4597f8f7f81ac1d27a5d299efc545e3225175e", "start_char": 0, "end_char": 1638, "text_sha256": "130bbe406429175feedf86bcfa4597f8f7f81ac1d27a5d299efc545e3225175e"}
    experimental_model
    Food-deprived rats given graded dietary acetic acid for 2 hours
    exposure
    0, 0.1, 0.2 or 0.4 g acetic acid per 100 g diet for 2 hours after 15 hours of food deprivation
    limitations
    Only the 0.2 g dose reached significance for glycogen, so the dose-response is not monotonic. The glycolytic mechanism is the authors’ inference from metabolite ratios, not a direct enzyme measurement.
    nutrient_topic
    Acetic acid research collection; topical membership is not evidence of a direct clinical effect, and the ingested acid is recorded separately from the circulating acetate anion. · Acetic acid
    organism
    Rat
    plain_language
    The acid appears to slow the burning of glucose, which is why more of it ends up stored.
    primary_references
    [acetate-p11435516] Acetic acid feeding enhances glycogen repletion in liver and skeletal muscle of rats. (2001). https://pubmed.ncbi.nlm.nih.gov/11435516/ DOI: 10.1093/jn/131.7.1973
    tissue_or_cell_type
    Liver and skeletal muscle

    Acetic acid: the ingested acid, the receptors acetate binds, the acetyl-CoA it becomes, and the acetyl groups that reach histones (2026-09-21) · lines 446–457

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Food-deprived rats given graded dietary acetic acid for 2 hours · source_derived_draft · unverified_draft

    ### acetate-acetate-inhibits-glycolysis In liver the concentration of xylulose-5-phosphate was significantly higher in the control group than in the acetic acid groups, and in gastrocnemius muscle the ratio of fructose-1,6-bisphosphate to fructose-6-phosphate was significantly higher in the control group; the authors proposed that acetic acid may activate gluconeogenesis and inactivate glycolysis in liver through suppression of xylulose-5-phosphate accumulation, and inhibit glycolysis in skeletal muscle by suppressing phosphofructokinase-1 activity. Condition category: normal nutrient_topic: Acetic acid research collection; topical membership is not evidence of a direct clinical effect, and the ingested acid is recorded separately from the circulating acetate anion. plain_language: The acid appears to slow the burning of glucose, which is why more of it ends up stored. organism: Rat tissue_or_cell_type: Liver and skeletal muscle experimental_model: Food-deprived rats given graded dietary acetic acid for 2 hours limitations: Only the 0.2 g dose reached significance for glycogen, so the dose-response is not monotonic. The glycolytic mechanism is the authors’ inference from metabolite ratios, not a direct enzyme measurement. exposure: 0, 0.1, 0.2 or 0.4 g acetic acid per 100 g diet for 2 hours after 15 hours of food deprivation evidence_span: {"source_cache": "artifacts/acetate-research/11435516.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "130bbe406429175feedf86bcfa4597f8f7f81ac1d27a5d299efc545e3225175e", "start_char": 0, "end_char": 1638, "text_sha256": "130bbe406429175feedf86bcfa4597f8f7f81ac1d27a5d299efc545e3225175e"} [acetate-p11435516] Acetic acid feeding enhances glycogen repletion in liver and skeletal muscle of rats. (2001). https://pubmed.ncbi.nlm.nih.gov/11435516/ DOI: 10.1093/jn/131.7.1973
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Administration of beta-glucan as a prototypical trained-immunity-inducing agonist to mice induced expansion of progenitors of the myeloid lineage which was associated with elevated signalling by innate immune mediators such as IL-1 beta and granulocyte-macrophage colony-stimulating factor and with adaptations in glucose metabolism and cholesterol biosynthesis, and the trained-immunity-related increase in myelopoiesis resulted in a beneficial response to secondary LPS challenge and protection from chemotherapy-induced myelosuppression in mice.

    Beta-glucan → Expansion of myeloid-lineage progenitors in the bone marrow source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/glucan-research/29328910.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d81bb64ee275e9aef7d9a59be186b5082906172a79c6f0d943832662f226b0d5", "start_char": 0, "end_char": 1023, "text_sha256": "d81bb64ee275e9aef7d9a59be186b5082906172a79c6f0d943832662f226b0d5"}
    experimental_model
    Administration of beta-glucan to mice with assessment of haematopoietic stem and progenitor cells and two challenge models
    exposure
    Beta-glucan as a prototypical trained-immunity-inducing agonist, followed by secondary LPS challenge or chemotherapy
    limitations
    A mouse study with parenteral administration. It shows progenitors are modulated; it does not show that a swallowed glucan reaches human marrow.
    nutrient_topic
    Beta-glucan research collection; topical membership is not evidence of a direct clinical effect, and each preparation is recorded as its own entity with no family link joining any pair. · Beta-glucan
    organism
    Mouse
    plain_language
    The change is not only in the cells circulating now; it reaches the factory that makes the next ones.
    primary_references
    [bg-p29328910] Modulation of Myelopoiesis Progenitors Is an Integral Component of Trained Immunity. (2018). https://pubmed.ncbi.nlm.nih.gov/29328910/ DOI: 10.1016/j.cell.2017.11.034
    tissue_or_cell_type
    Bone marrow

    Beta-glucan: a structural family rather than an agent, what decides whether a bound glucan actually signals, the complement route that a cereal and a yeast preparation share, and the unequal human evidence behind each (2026-09-22) · lines 476–487

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Administration of beta-glucan to mice with assessment of haematopoietic stem and progenitor cells and two challenge models · source_derived_draft · unverified_draft

    ### bg-training-reaches-the-marrow Administration of beta-glucan as a prototypical trained-immunity-inducing agonist to mice induced expansion of progenitors of the myeloid lineage which was associated with elevated signalling by innate immune mediators such as IL-1 beta and granulocyte-macrophage colony-stimulating factor and with adaptations in glucose metabolism and cholesterol biosynthesis, and the trained-immunity-related increase in myelopoiesis resulted in a beneficial response to secondary LPS challenge and protection from chemotherapy-induced myelosuppression in mice. Condition category: normal nutrient_topic: Beta-glucan research collection; topical membership is not evidence of a direct clinical effect, and each preparation is recorded as its own entity with no family link joining any pair. plain_language: The change is not only in the cells circulating now; it reaches the factory that makes the next ones. organism: Mouse tissue_or_cell_type: Bone marrow experimental_model: Administration of beta-glucan to mice with assessment of haematopoietic stem and progenitor cells and two challenge models limitations: A mouse study with parenteral administration. It shows progenitors are modulated; it does not show that a swallowed glucan reaches human marrow. exposure: Beta-glucan as a prototypical trained-immunity-inducing agonist, followed by secondary LPS challenge or chemotherapy evidence_span: {"source_cache": "artifacts/glucan-research/29328910.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d81bb64ee275e9aef7d9a59be186b5082906172a79c6f0d943832662f226b0d5", "start_char": 0, "end_char": 1023, "text_sha256": "d81bb64ee275e9aef7d9a59be186b5082906172a79c6f0d943832662f226b0d5"} [bg-p29328910] Modulation of Myelopoiesis Progenitors Is an Integral Component of Trained Immunity. (2018). https://pubmed.ncbi.nlm.nih.gov/29328910/ DOI: 10.1016/j.cell.2017.11.034
    Complete structured claim and evidence

  2. At 4 hours after the start of feeding the acetic acid group had significantly greater liver and gastrocnemius muscle glycogen concentrations, and the authors concluded that a diet containing acetic acid may enhance glycogen repletion but not induce supercompensation, the large increase in glycogen that is beneficial in improving performance, by transitory inhibition of glycolysis.

    Acetic acid → Gastrocnemius muscle glycogen concentration source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/acetate-research/16277773.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "305aa81aca9908a350132a7c7dcc42c86be0b6030c70f51b5fe0c8971e75bcfe", "start_char": 0, "end_char": 1594, "text_sha256": "305aa81aca9908a350132a7c7dcc42c86be0b6030c70f51b5fe0c8971e75bcfe"}
    experimental_model
    Rats meal-fed once daily for 10 days, then sampled 4, 8 or 24 hours after feeding
    exposure
    0.7 g/kg-diet acetic acid in a 9 g meal, with sampling across the daily cycle
    limitations
    Adds the time dimension that single-timepoint studies miss. The effects were present at 4 hours and the authors explicitly rule out supercompensation.
    nutrient_topic
    Acetic acid research collection; topical membership is not evidence of a direct clinical effect, and the ingested acid is recorded separately from the circulating acetate anion. · Acetic acid
    organism
    Rat
    plain_language
    The stores refill faster but do not overfill, so this is not carbohydrate loading.
    primary_references
    [acetate-p16277773] Effect of acetic acid feeding on the circadian changes in glycogen and metabolites of glucose and lipid in liver and skeletal muscle of rats. (2005). https://pubmed.ncbi.nlm.nih.gov/16277773/ DOI: 10.1079/bjn20051545
    tissue_or_cell_type
    Liver and skeletal muscle

    Acetic acid: the ingested acid, the receptors acetate binds, the acetyl-CoA it becomes, and the acetyl groups that reach histones (2026-09-21) · lines 459–470

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rats meal-fed once daily for 10 days, then sampled 4, 8 or 24 hours after feeding · source_derived_draft · unverified_draft

    ### acetate-no-supercompensation At 4 hours after the start of feeding the acetic acid group had significantly greater liver and gastrocnemius muscle glycogen concentrations, and the authors concluded that a diet containing acetic acid may enhance glycogen repletion but not induce supercompensation, the large increase in glycogen that is beneficial in improving performance, by transitory inhibition of glycolysis. Condition category: normal nutrient_topic: Acetic acid research collection; topical membership is not evidence of a direct clinical effect, and the ingested acid is recorded separately from the circulating acetate anion. plain_language: The stores refill faster but do not overfill, so this is not carbohydrate loading. organism: Rat tissue_or_cell_type: Liver and skeletal muscle experimental_model: Rats meal-fed once daily for 10 days, then sampled 4, 8 or 24 hours after feeding limitations: Adds the time dimension that single-timepoint studies miss. The effects were present at 4 hours and the authors explicitly rule out supercompensation. exposure: 0.7 g/kg-diet acetic acid in a 9 g meal, with sampling across the daily cycle evidence_span: {"source_cache": "artifacts/acetate-research/16277773.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "305aa81aca9908a350132a7c7dcc42c86be0b6030c70f51b5fe0c8971e75bcfe", "start_char": 0, "end_char": 1594, "text_sha256": "305aa81aca9908a350132a7c7dcc42c86be0b6030c70f51b5fe0c8971e75bcfe"} [acetate-p16277773] Effect of acetic acid feeding on the circadian changes in glycogen and metabolites of glucose and lipid in liver and skeletal muscle of rats. (2005). https://pubmed.ncbi.nlm.nih.gov/16277773/ DOI: 10.1079/bjn20051545
    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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