Nutrient chapter

Beta-glucan

Beta-glucan. A family of glucose polymers defined by their linkage pattern rather than a single compound; the preparations in this collection differ in backbone, branching, molecular weight, conformation, solubility, particle size and purity, and each is recorded as its own entity with no family link joining them, because those differences determine which receptor engages and whether engagement signals at all. Species, exposure and limitations are retained in each linked claim.

44 recorded mechanisms · 4 availability situations · 1 preserved sources. Draft and verified records are labeled separately.

Read recorded mechanisms Open recursive mind map

The mechanisms

What the sources say this nutrient does, one relationship at a time. Plain wording comes first; the technical statement follows.

The carbohydrate polymers known as beta-1,3-D-glucans exert potent effects on the immune system, stimulating antitumour and antimicrobial activity for example, by binding to receptors on macrophages and other white blood cells and activating them, and although beta-glucans are known to bind to receptors such as complement receptor 3 there is evidence that another beta-glucan receptor is present on macrophages, which is identified here as dectin-1.
Dectin-1 / CLEC7A → Beta-glucan source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/glucan-research/11544516.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "14e7f5285cdda3bdcf3596e5e9517683d195dd4a4ae42ff1f9d07f1d3288bf1c", "start_char": 0, "end_char": 573, "text_sha256": "14e7f5285cdda3bdcf3596e5e9517683d195dd4a4ae42ff1f9d07f1d3288bf1c"}
experimental_model
Identification of the unknown macrophage beta-glucan receptor
exposure
Beta-1,3-D-glucans binding to macrophage surface receptors
limitations
A brief communication announcing the identification. It states that beta-glucans were already known to bind complement receptor 3, so it adds a receptor rather than replacing one.
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 and human cells
plain_language
A second receptor for these sugars was identified, alongside the complement receptor already known to bind them.
primary_references
[bg-p11544516] Immune recognition. A new receptor for beta-glucans. (2001). https://pubmed.ncbi.nlm.nih.gov/11544516/ DOI: 10.1038/35092620
tissue_or_cell_type
Macrophage
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 99–110
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Identification of the unknown macrophage beta-glucan receptor · source_derived_draft · unverified_draft
### bg-dectin1-is-the-unknown-receptor The carbohydrate polymers known as beta-1,3-D-glucans exert potent effects on the immune system, stimulating antitumour and antimicrobial activity for example, by binding to receptors on macrophages and other white blood cells and activating them, and although beta-glucans are known to bind to receptors such as complement receptor 3 there is evidence that another beta-glucan receptor is present on macrophages, which is identified here as dectin-1. 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: A second receptor for these sugars was identified, alongside the complement receptor already known to bind them. organism: Mouse and human cells tissue_or_cell_type: Macrophage experimental_model: Identification of the unknown macrophage beta-glucan receptor limitations: A brief communication announcing the identification. It states that beta-glucans were already known to bind complement receptor 3, so it adds a receptor rather than replacing one. exposure: Beta-1,3-D-glucans binding to macrophage surface receptors evidence_span: {"source_cache": "artifacts/glucan-research/11544516.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "14e7f5285cdda3bdcf3596e5e9517683d195dd4a4ae42ff1f9d07f1d3288bf1c", "start_char": 0, "end_char": 573, "text_sha256": "14e7f5285cdda3bdcf3596e5e9517683d195dd4a4ae42ff1f9d07f1d3288bf1c"} [bg-p11544516] Immune recognition. A new receptor for beta-glucans. (2001). https://pubmed.ncbi.nlm.nih.gov/11544516/ DOI: 10.1038/35092620
Complete structured claim and evidence
Non-opsonic zymosan binding was unaffected by genetic CD11b deficiency or a blocking monoclonal antibody against CR3, demonstrating that CR3 was not the beta-glucan receptor mediating this activity, and using the novel anti-Dectin-1 antibody 2A11 Dectin-1 was shown to be almost exclusively responsible for the beta-glucan-dependent non-opsonic recognition of zymosan by primary macrophages, defining Dectin-1 as the leukocyte beta-glucan receptor first described over 50 years ago and resolving the long-standing controversy regarding the identity of this important molecule.
Dectin-1 / CLEC7A → Non-opsonic recognition of a yeast particle source_derived_draftungraded
Experimental context and source evidence
evidence_span
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experimental_model
Carbohydrate inhibition, CD11b-deficient cells and a new anti-Dectin-1 monoclonal antibody applied to non-opsonic zymosan binding
exposure
Zymosan binding to primary macrophages with specific carbohydrate inhibitors, CD11b deficiency, a blocking anti-CR3 antibody and the novel anti-Dectin-1 antibody 2A11
limitations
The ligand is zymosan, which is a mannan-rich particle as well as a glucan one, and the readout is non-opsonic binding rather than every glucan response.
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
Removing the complement receptor entirely did not change how macrophages grabbed yeast particles; blocking the other receptor did.
primary_references
[bg-p12163569] Dectin-1 is a major beta-glucan receptor on macrophages. (2002). https://pubmed.ncbi.nlm.nih.gov/12163569/ DOI: 10.1084/jem.20020470
tissue_or_cell_type
Primary macrophage
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 112–123
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Carbohydrate inhibition, CD11b-deficient cells and a new anti-Dectin-1 monoclonal antibody applied to non-opsonic zymosan binding · source_derived_draft · unverified_draft
### bg-dectin1-not-cr3-binds-zymosan Non-opsonic zymosan binding was unaffected by genetic CD11b deficiency or a blocking monoclonal antibody against CR3, demonstrating that CR3 was not the beta-glucan receptor mediating this activity, and using the novel anti-Dectin-1 antibody 2A11 Dectin-1 was shown to be almost exclusively responsible for the beta-glucan-dependent non-opsonic recognition of zymosan by primary macrophages, defining Dectin-1 as the leukocyte beta-glucan receptor first described over 50 years ago and resolving the long-standing controversy regarding the identity of this important molecule. 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: Removing the complement receptor entirely did not change how macrophages grabbed yeast particles; blocking the other receptor did. organism: Mouse tissue_or_cell_type: Primary macrophage experimental_model: Carbohydrate inhibition, CD11b-deficient cells and a new anti-Dectin-1 monoclonal antibody applied to non-opsonic zymosan binding limitations: The ligand is zymosan, which is a mannan-rich particle as well as a glucan one, and the readout is non-opsonic binding rather than every glucan response. exposure: Zymosan binding to primary macrophages with specific carbohydrate inhibitors, CD11b deficiency, a blocking anti-CR3 antibody and the novel anti-Dectin-1 antibody 2A11 evidence_span: {"source_cache": "artifacts/glucan-research/12163569.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "533d8630c3d727db58869724825f47c5241cf9c3159acce359d3bc8b0fdb2a6a", "start_char": 0, "end_char": 1365, "text_sha256": "533d8630c3d727db58869724825f47c5241cf9c3159acce359d3bc8b0fdb2a6a"} [bg-p12163569] Dectin-1 is a major beta-glucan receptor on macrophages. (2002). https://pubmed.ncbi.nlm.nih.gov/12163569/ DOI: 10.1084/jem.20020470
Complete structured claim and evidence
Dectin-1 lacks residues involved in calcium ligation that mediates carbohydrate-binding by classical C-type lectins, and among 187 diverse sequence-defined oligosaccharide probes together with designer microarrays from a neutral soluble glucan from S. cerevisiae, curdlan from Alcaligenes faecalis and pustulan from Umbilicaria papullosa, Dectin-1 binding is detected exclusively to 1,3-linked glucose oligomers, the minimum length required for detectable binding being a 10- or 11-mer, and 11-13 gluco-oligomers in clustered form displayed on liposomes mimic the macromolecular beta-glucans and compete with zymosan binding and triggering of tumour necrosis factor alpha secretion.
Dectin-1 / CLEC7A → Beta-(1->3)-linked gluco-oligosaccharides source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/glucan-research/16371356.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "dd98941694dedd8e3e85766c0c299b54fbc29ca8cce7c61a333efceee796867f", "start_char": 0, "end_char": 1911, "text_sha256": "dd98941694dedd8e3e85766c0c299b54fbc29ca8cce7c61a333efceee796867f"}
experimental_model
Neoglycolipid oligosaccharide microarrays built from three glucan polysaccharides and screened against 187 sequence-defined probes
exposure
Dectin-1 binding to oligosaccharide probes generated from a soluble yeast glucan, curdlan and pustulan
limitations
A binding assignment on arrayed probes rather than on a cell surface. The clustered-ligand test uses liposomes and a Dectin-1-expressing cell line.
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
Recombinant protein and a macrophage cell line
plain_language
The receptor reads only one linkage, needs a run of about ten sugars to grip at all, and needs them clustered to fire.
primary_references
[bg-p16371356] Ligands for the beta-glucan receptor, Dectin-1, assigned using "designer" microarrays of oligosaccharide probes (neoglycolipids) generated from glucan polysaccharides. (2006). https://pubmed.ncbi.nlm.nih.gov/16371356/ DOI: 10.1074/jbc.m511461200
tissue_or_cell_type
Cell-free microarray and cultured cells
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 125–136
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Neoglycolipid oligosaccharide microarrays built from three glucan polysaccharides and screened against 187 sequence-defined probes · source_derived_draft · unverified_draft
### bg-only-beta-1-3-oligomers-bind Dectin-1 lacks residues involved in calcium ligation that mediates carbohydrate-binding by classical C-type lectins, and among 187 diverse sequence-defined oligosaccharide probes together with designer microarrays from a neutral soluble glucan from S. cerevisiae, curdlan from Alcaligenes faecalis and pustulan from Umbilicaria papullosa, Dectin-1 binding is detected exclusively to 1,3-linked glucose oligomers, the minimum length required for detectable binding being a 10- or 11-mer, and 11-13 gluco-oligomers in clustered form displayed on liposomes mimic the macromolecular beta-glucans and compete with zymosan binding and triggering of tumour necrosis factor alpha secretion. Condition category: normal nutrient_topic: Beta-glucan research collection; topical membership is not evidence of a direct clinical effect, and each preparation is recorded as its own entity with no family link joining any pair. plain_language: The receptor reads only one linkage, needs a run of about ten sugars to grip at all, and needs them clustered to fire. organism: Recombinant protein and a macrophage cell line tissue_or_cell_type: Cell-free microarray and cultured cells experimental_model: Neoglycolipid oligosaccharide microarrays built from three glucan polysaccharides and screened against 187 sequence-defined probes limitations: A binding assignment on arrayed probes rather than on a cell surface. The clustered-ligand test uses liposomes and a Dectin-1-expressing cell line. exposure: Dectin-1 binding to oligosaccharide probes generated from a soluble yeast glucan, curdlan and pustulan evidence_span: {"source_cache": "artifacts/glucan-research/16371356.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "dd98941694dedd8e3e85766c0c299b54fbc29ca8cce7c61a333efceee796867f", "start_char": 0, "end_char": 1911, "text_sha256": "dd98941694dedd8e3e85766c0c299b54fbc29ca8cce7c61a333efceee796867f"} [bg-p16371356] Ligands for the beta-glucan receptor, Dectin-1, assigned using "designer" microarrays of oligosaccharide probes (neoglycolipids) generated from glucan polysaccharides. (2006). https://pubmed.ncbi.nlm.nih.gov/16371356/ DOI: 10.1074/jbc.m511461200
Complete structured claim and evidence
Despite its ability to bind both soluble and particulate beta-glucan polymers, Dectin-1 signalling is only activated by particulate beta-glucans, which cluster the receptor in synapse-like structures from which the regulatory tyrosine phosphatases CD45 and CD148 are excluded, providing a model mechanism by which innate immune receptors can distinguish direct microbial contact from detection of microbes at a distance and initiate direct cellular antimicrobial responses only when they are required.
The phagocytic synapse, a receptor-rich contact that excludes CD45 and CD148 → Dectin-1 / CLEC7A source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/glucan-research/21525931.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5bb7dfc847efb60e644eeaf672d3277d18bca9c4fc75051c8d568d8e5dc450e0", "start_char": 0, "end_char": 1406, "text_sha256": "5bb7dfc847efb60e644eeaf672d3277d18bca9c4fc75051c8d568d8e5dc450e0"}
experimental_model
Comparison of soluble and particulate beta-glucan polymers on Dectin-1 signalling, with imaging of receptor and phosphatase distribution
exposure
Soluble against particulate beta-glucan polymers on Dectin-1-expressing phagocytes
limitations
The abstract reports the soluble-versus-particulate comparison and the phosphatase exclusion. It does not state what happens when a soluble glucan is immobilised, so no claim here rests on that.
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
Binding was not enough: the receptor only fired when particles packed it into a patch that shut out the enzymes which switch it off.
primary_references
[bg-p21525931] Activation of the innate immune receptor Dectin-1 upon formation of a 'phagocytic synapse'. (2011). https://pubmed.ncbi.nlm.nih.gov/21525931/ DOI: 10.1038/nature10071
tissue_or_cell_type
Myeloid phagocytes
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 138–149
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Comparison of soluble and particulate beta-glucan polymers on Dectin-1 signalling, with imaging of receptor and phosphatase distribution · source_derived_draft · unverified_draft
### bg-only-particles-signal Despite its ability to bind both soluble and particulate beta-glucan polymers, Dectin-1 signalling is only activated by particulate beta-glucans, which cluster the receptor in synapse-like structures from which the regulatory tyrosine phosphatases CD45 and CD148 are excluded, providing a model mechanism by which innate immune receptors can distinguish direct microbial contact from detection of microbes at a distance and initiate direct cellular antimicrobial responses only when they are required. 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: Binding was not enough: the receptor only fired when particles packed it into a patch that shut out the enzymes which switch it off. organism: Mouse tissue_or_cell_type: Myeloid phagocytes experimental_model: Comparison of soluble and particulate beta-glucan polymers on Dectin-1 signalling, with imaging of receptor and phosphatase distribution limitations: The abstract reports the soluble-versus-particulate comparison and the phosphatase exclusion. It does not state what happens when a soluble glucan is immobilised, so no claim here rests on that. exposure: Soluble against particulate beta-glucan polymers on Dectin-1-expressing phagocytes evidence_span: {"source_cache": "artifacts/glucan-research/21525931.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5bb7dfc847efb60e644eeaf672d3277d18bca9c4fc75051c8d568d8e5dc450e0", "start_char": 0, "end_char": 1406, "text_sha256": "5bb7dfc847efb60e644eeaf672d3277d18bca9c4fc75051c8d568d8e5dc450e0"} [bg-p21525931] Activation of the innate immune receptor Dectin-1 upon formation of a 'phagocytic synapse'. (2011). https://pubmed.ncbi.nlm.nih.gov/21525931/ DOI: 10.1038/nature10071
Complete structured claim and evidence
Beta-glucans can adopt solution structures ranging from random coil to insoluble fibre due to tertiary helical and quaternary structure, and despite similar affinity for Dectin-1 the ability of glucans to induce Dectin-1A-mediated signalling correlates with degree of structure, with glucan denaturation experiments showing that glucan structure determines agonistic potential but not receptor binding affinity, while fluorescence measurements provided direct evidence of ligation-induced Dectin-1A aggregation which positively correlated with increasing glucan structure content.
Solution conformation of a glucan, from random coil to insoluble fibre → Ability of a bound glucan to produce a receptor signal source_derived_draftungraded
Experimental context and source evidence
availability_state
biomarker_context Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/glucan-research/37515324.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c5c602f96f0ff319650a47cb53c772df30c0dc267f6e82c46ae51bb5285b6d3f", "start_char": 0, "end_char": 1658, "text_sha256": "c5c602f96f0ff319650a47cb53c772df30c0dc267f6e82c46ae51bb5285b6d3f"}
experimental_model
Glucan denaturation, fluorescence measurement of receptor aggregation and diffusion, and fungal particle contact sites
exposure
Fungal beta-glucans of low, medium and high molecular weight differing in helical structure content, before and after denaturation
limitations
A single-receptor-isoform study using defined glucan conformations. The aggregates observed were small, a few engaged receptors rather than synapse-scale structures.
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 receptor in cultured cells
plain_language
What decides whether the receptor fires is the shape the sugar holds in solution, not how tightly it sticks and not whether it dissolves.
primary_references
[bg-p37515324] Dectin-1 multimerization and signaling depends on fungal β-glucan structure and exposure. (2023). https://pubmed.ncbi.nlm.nih.gov/37515324/ DOI: 10.1016/j.bpj.2023.07.021
tissue_or_cell_type
Dectin-1A-expressing cells and Candida cell wall
trigger_kind
biomarker_context Imported condition classification; unverified.
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 151–162
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Glucan denaturation, fluorescence measurement of receptor aggregation and diffusion, and fungal particle contact sites · source_derived_draft · unverified_draft
### bg-structure-not-solubility-signals Beta-glucans can adopt solution structures ranging from random coil to insoluble fibre due to tertiary helical and quaternary structure, and despite similar affinity for Dectin-1 the ability of glucans to induce Dectin-1A-mediated signalling correlates with degree of structure, with glucan denaturation experiments showing that glucan structure determines agonistic potential but not receptor binding affinity, while fluorescence measurements provided direct evidence of ligation-induced Dectin-1A aggregation which positively correlated with increasing glucan structure content. Condition category: biomarker_context 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: What decides whether the receptor fires is the shape the sugar holds in solution, not how tightly it sticks and not whether it dissolves. organism: Human receptor in cultured cells tissue_or_cell_type: Dectin-1A-expressing cells and Candida cell wall experimental_model: Glucan denaturation, fluorescence measurement of receptor aggregation and diffusion, and fungal particle contact sites limitations: A single-receptor-isoform study using defined glucan conformations. The aggregates observed were small, a few engaged receptors rather than synapse-scale structures. exposure: Fungal beta-glucans of low, medium and high molecular weight differing in helical structure content, before and after denaturation evidence_span: {"source_cache": "artifacts/glucan-research/37515324.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c5c602f96f0ff319650a47cb53c772df30c0dc267f6e82c46ae51bb5285b6d3f", "start_char": 0, "end_char": 1658, "text_sha256": "c5c602f96f0ff319650a47cb53c772df30c0dc267f6e82c46ae51bb5285b6d3f"} [bg-p37515324] Dectin-1 multimerization and signaling depends on fungal β-glucan structure and exposure. (2023). https://pubmed.ncbi.nlm.nih.gov/37515324/ DOI: 10.1016/j.bpj.2023.07.021
Complete structured claim and evidence
Laminarin is a (1->3, 1->6)-beta-glucan that is widely reported to be a Dectin-1 antagonist, however there are reports that laminarin is also a Dectin-1 agonist, and of five preparations from three commercial sources all contained laminarin although their molecular mass varied considerably from 4400 to 34,400 daltons, all were bound by recombinant human and mouse Dectin-1 but the affinity varied considerably and binding affinity did not correlate with Dectin-1 agonism, antagonism or potency, two laminarins were Dectin-1 antagonists and two were agonists, and the remaining laminarin was an antagonist but became an agonist when the low molecular weight moieties were removed.
Purity of a commercial glucan preparation → Ability of a bound glucan to produce a receptor signal source_derived_draftungraded
Experimental context and source evidence
availability_state
biomarker_context Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/glucan-research/29246954.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5afc1ddc8e49971759dcdc432cedb4c22cad267cace1e3909dd577c8ebb9eaa6", "start_char": 0, "end_char": 1760, "text_sha256": "5afc1ddc8e49971759dcdc432cedb4c22cad267cace1e3909dd577c8ebb9eaa6"}
experimental_model
Physical, structural, purity, binding and functional comparison of five commercial laminarin preparations from three suppliers
exposure
Five laminarin preparations of molecular mass 4400 to 34,400 daltons, before and after extensive dialysis
limitations
Five preparations of one named natural product. Removing low molecular weight contaminants explained the behaviour of one preparation and not the others, so purity is one cause of the variation rather than the whole of it.
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 and mouse cells
plain_language
Five bottles with the same name on the label: two blocked the receptor, two switched it on, and cleaning up a fifth flipped it.
primary_references
[bg-p29246954] Immunoregulatory Activity of the Natural Product Laminarin Varies Widely as a Result of Its Physical Properties. (2018). https://pubmed.ncbi.nlm.nih.gov/29246954/ DOI: 10.4049/jimmunol.1701258
tissue_or_cell_type
Recombinant receptor and primary cells
trigger_kind
biomarker_context Imported condition classification; unverified.
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 164–175
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Physical, structural, purity, binding and functional comparison of five commercial laminarin preparations from three suppliers · source_derived_draft · unverified_draft
### bg-same-name-opposite-activity Laminarin is a (1->3, 1->6)-beta-glucan that is widely reported to be a Dectin-1 antagonist, however there are reports that laminarin is also a Dectin-1 agonist, and of five preparations from three commercial sources all contained laminarin although their molecular mass varied considerably from 4400 to 34,400 daltons, all were bound by recombinant human and mouse Dectin-1 but the affinity varied considerably and binding affinity did not correlate with Dectin-1 agonism, antagonism or potency, two laminarins were Dectin-1 antagonists and two were agonists, and the remaining laminarin was an antagonist but became an agonist when the low molecular weight moieties were removed. Condition category: biomarker_context 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: Five bottles with the same name on the label: two blocked the receptor, two switched it on, and cleaning up a fifth flipped it. organism: Human and mouse cells tissue_or_cell_type: Recombinant receptor and primary cells experimental_model: Physical, structural, purity, binding and functional comparison of five commercial laminarin preparations from three suppliers limitations: Five preparations of one named natural product. Removing low molecular weight contaminants explained the behaviour of one preparation and not the others, so purity is one cause of the variation rather than the whole of it. exposure: Five laminarin preparations of molecular mass 4400 to 34,400 daltons, before and after extensive dialysis evidence_span: {"source_cache": "artifacts/glucan-research/29246954.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5afc1ddc8e49971759dcdc432cedb4c22cad267cace1e3909dd577c8ebb9eaa6", "start_char": 0, "end_char": 1760, "text_sha256": "5afc1ddc8e49971759dcdc432cedb4c22cad267cace1e3909dd577c8ebb9eaa6"} [bg-p29246954] Immunoregulatory Activity of the Natural Product Laminarin Varies Widely as a Result of Its Physical Properties. (2018). https://pubmed.ncbi.nlm.nih.gov/29246954/ DOI: 10.4049/jimmunol.1701258
Complete structured claim and evidence
Beta-glucans differ greatly in size, structure and ability to activate effector immune responses from dendritic cells and small particulate beta-glucans are thought to be poor activators of innate immunity, and large beta-glucan-stimulated human dendritic cells generate significantly more IL-1beta, IL-6 and IL-23 compared to those stimulated with the smaller beta-glucans, while in marked contrast the secretion of TSLP and CCL22 were found to be insensitive to beta-glucan particle size, with the capacity to induce phagocytosis and the relative IL-1beta production determined by beta-glucan size regulating the composition of the cytokine milieu.
Particle size of a glucan preparation → Interleukin-1 beta / IL1B source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/glucan-research/28736555.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9e9388d9e8263db85cdd17df9a497d9867627097a09ff8a0d630e5733e591e54", "start_char": 0, "end_char": 1128, "text_sha256": "9e9388d9e8263db85cdd17df9a497d9867627097a09ff8a0d630e5733e591e54"}
experimental_model
Comparison of large and small beta-glucan particles on human dendritic cell cytokine output
exposure
Large against small particulate beta-glucans, with assessment of phagocytosis
limitations
Human primary cells with a size comparison. The abstract reports the cytokine differences and the role of phagocytosis and IL-1beta; it does not report an oxidase dependence, so no claim here rests on that.
nutrient_topic
Beta-glucan research collection; topical membership is not evidence of a direct clinical effect, and each preparation is recorded as its own entity with no family link joining any pair. · Beta-glucan
organism
Human
plain_language
Bigger particles pulled three inflammatory signals out of the same cells; two other signals did not care about size at all.
primary_references
[bg-p28736555] β-Glucan Size Controls Dectin-1-Mediated Immune Responses in Human Dendritic Cells by Regulating IL-1β Production. (2017). https://pubmed.ncbi.nlm.nih.gov/28736555/ DOI: 10.3389/fimmu.2017.00791
tissue_or_cell_type
Monocyte-derived dendritic cell
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 177–188
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Comparison of large and small beta-glucan particles on human dendritic cell cytokine output · source_derived_draft · unverified_draft
### bg-particle-size-sets-the-cytokines Beta-glucans differ greatly in size, structure and ability to activate effector immune responses from dendritic cells and small particulate beta-glucans are thought to be poor activators of innate immunity, and large beta-glucan-stimulated human dendritic cells generate significantly more IL-1beta, IL-6 and IL-23 compared to those stimulated with the smaller beta-glucans, while in marked contrast the secretion of TSLP and CCL22 were found to be insensitive to beta-glucan particle size, with the capacity to induce phagocytosis and the relative IL-1beta production determined by beta-glucan size regulating the composition of the cytokine milieu. 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: Bigger particles pulled three inflammatory signals out of the same cells; two other signals did not care about size at all. organism: Human tissue_or_cell_type: Monocyte-derived dendritic cell experimental_model: Comparison of large and small beta-glucan particles on human dendritic cell cytokine output limitations: Human primary cells with a size comparison. The abstract reports the cytokine differences and the role of phagocytosis and IL-1beta; it does not report an oxidase dependence, so no claim here rests on that. exposure: Large against small particulate beta-glucans, with assessment of phagocytosis evidence_span: {"source_cache": "artifacts/glucan-research/28736555.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9e9388d9e8263db85cdd17df9a497d9867627097a09ff8a0d630e5733e591e54", "start_char": 0, "end_char": 1128, "text_sha256": "9e9388d9e8263db85cdd17df9a497d9867627097a09ff8a0d630e5733e591e54"} [bg-p28736555] β-Glucan Size Controls Dectin-1-Mediated Immune Responses in Human Dendritic Cells by Regulating IL-1β Production. (2017). https://pubmed.ncbi.nlm.nih.gov/28736555/ DOI: 10.3389/fimmu.2017.00791
Complete structured claim and evidence
Dectin-1 is recruited to phagosomes containing zymosan particles but not to phagosomes containing immunoglobulin G-opsonised particles, dectin-1 expression enhances Toll-like receptor-mediated activation of nuclear factor kappa B by beta-glucan-containing particles, and in macrophages and dendritic cells dectin-1 and Toll-like receptors are synergistic in mediating production of cytokines such as interleukin 12 and tumour necrosis factor alpha, while dectin-1 triggers production of reactive oxygen species, an inflammatory response that is primed by Toll-like receptor activation.
Dectin-1 / CLEC7A → Activation of nuclear factor kappa B source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/glucan-research/12719479.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "297eb222223ff6861d6890a273716f4cfb3f3c14f887c57c057c2af524f8b425", "start_char": 0, "end_char": 1588, "text_sha256": "297eb222223ff6861d6890a273716f4cfb3f3c14f887c57c057c2af524f8b425"}
experimental_model
Dectin-1 and Toll-like receptor co-expression with phagosome recruitment and cytokine measurement
exposure
Beta-glucan-containing zymosan particles on cells expressing dectin-1 with and without Toll-like receptor signalling
limitations
The particle is zymosan, which carries mannan and other yeast wall components as well as glucan, so a response to zymosan is not by itself a response to purified beta-glucan.
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 glucan receptor does not work alone; paired with a bacterial sensor the same particle produces far more than either would.
primary_references
[bg-p12719479] Collaborative induction of inflammatory responses by dectin-1 and Toll-like receptor 2. (2003). https://pubmed.ncbi.nlm.nih.gov/12719479/ DOI: 10.1084/jem.20021787
tissue_or_cell_type
Macrophage and dendritic cell
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 190–201
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Dectin-1 and Toll-like receptor co-expression with phagosome recruitment and cytokine measurement · source_derived_draft · unverified_draft
### bg-dectin1-works-with-tlr2 Dectin-1 is recruited to phagosomes containing zymosan particles but not to phagosomes containing immunoglobulin G-opsonised particles, dectin-1 expression enhances Toll-like receptor-mediated activation of nuclear factor kappa B by beta-glucan-containing particles, and in macrophages and dendritic cells dectin-1 and Toll-like receptors are synergistic in mediating production of cytokines such as interleukin 12 and tumour necrosis factor alpha, while dectin-1 triggers production of reactive oxygen species, an inflammatory response that is primed by Toll-like receptor activation. 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 glucan receptor does not work alone; paired with a bacterial sensor the same particle produces far more than either would. organism: Mouse tissue_or_cell_type: Macrophage and dendritic cell experimental_model: Dectin-1 and Toll-like receptor co-expression with phagosome recruitment and cytokine measurement limitations: The particle is zymosan, which carries mannan and other yeast wall components as well as glucan, so a response to zymosan is not by itself a response to purified beta-glucan. exposure: Beta-glucan-containing zymosan particles on cells expressing dectin-1 with and without Toll-like receptor signalling evidence_span: {"source_cache": "artifacts/glucan-research/12719479.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "297eb222223ff6861d6890a273716f4cfb3f3c14f887c57c057c2af524f8b425", "start_char": 0, "end_char": 1588, "text_sha256": "297eb222223ff6861d6890a273716f4cfb3f3c14f887c57c057c2af524f8b425"} [bg-p12719479] Collaborative induction of inflammatory responses by dectin-1 and Toll-like receptor 2. (2003). https://pubmed.ncbi.nlm.nih.gov/12719479/ DOI: 10.1084/jem.20021787
Complete structured claim and evidence
CR3 serves as the leukocyte beta-glucan receptor through a cation-independent lectin site located C-terminal to the I-domain of CD11b that contains the binding sites for iC3b, ICAM-1 and fibrinogen, a 10-kilodalton soluble zymosan polysaccharide consisting largely of mannose and approximately 5% glucose bound with high affinity of 6.7 x 10(-8) M, binding was blocked not only by pure beta-glucans from yeast, mushroom, seaweed or barley but also by N-acetyl-D-glucosamine and alpha- or beta-methylmannoside and alpha- or beta-methylglucoside, and its sugar specificity is broader than originally appreciated.
The lectin site of CD11b C-terminal to the I-domain → Beta-glucan source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/glucan-research/8558003.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "00a0fef65e91375066fe9920200032466aec1c0d85bf548d53f64c3d384106b7", "start_char": 0, "end_char": 1936, "text_sha256": "00a0fef65e91375066fe9920200032466aec1c0d85bf548d53f64c3d384106b7"}
experimental_model
Flow cytometry with labelled soluble polysaccharides, CR3 and CR4 chimeras, and a panel of domain-specific antibodies
exposure
Labelled beta-glucans from yeast, mushroom, seaweed and barley, and a 10-kilodalton soluble zymosan polysaccharide
limitations
Binding and inhibition rather than function. The highest-affinity ligand measured was not a pure beta-glucan but a mannose-rich zymosan polysaccharide, and the sugar specificity proved broader than beta-glucan alone.
nutrient_topic
Beta-glucan research collection; topical membership is not evidence of a direct clinical effect, and each preparation is recorded as its own entity with no family link joining any pair. · Beta-glucan
organism
Human
plain_language
The complement receptor grips sugars at a second site, separate from the one that grips the complement fragment.
primary_references
[bg-p8558003] Analysis of the sugar specificity and molecular location of the beta-glucan-binding lectin site of complement receptor type 3 (CD11b/CD18). (1996). https://pubmed.ncbi.nlm.nih.gov/8558003/ DOI: 10.4049/jimmunol.156.3.1235
tissue_or_cell_type
Leukocytes
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 203–214
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Flow cytometry with labelled soluble polysaccharides, CR3 and CR4 chimeras, and a panel of domain-specific antibodies · source_derived_draft · unverified_draft
### bg-cr3-has-a-lectin-site CR3 serves as the leukocyte beta-glucan receptor through a cation-independent lectin site located C-terminal to the I-domain of CD11b that contains the binding sites for iC3b, ICAM-1 and fibrinogen, a 10-kilodalton soluble zymosan polysaccharide consisting largely of mannose and approximately 5% glucose bound with high affinity of 6.7 x 10(-8) M, binding was blocked not only by pure beta-glucans from yeast, mushroom, seaweed or barley but also by N-acetyl-D-glucosamine and alpha- or beta-methylmannoside and alpha- or beta-methylglucoside, and its sugar specificity is broader than originally appreciated. 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 complement receptor grips sugars at a second site, separate from the one that grips the complement fragment. organism: Human tissue_or_cell_type: Leukocytes experimental_model: Flow cytometry with labelled soluble polysaccharides, CR3 and CR4 chimeras, and a panel of domain-specific antibodies limitations: Binding and inhibition rather than function. The highest-affinity ligand measured was not a pure beta-glucan but a mannose-rich zymosan polysaccharide, and the sugar specificity proved broader than beta-glucan alone. exposure: Labelled beta-glucans from yeast, mushroom, seaweed and barley, and a 10-kilodalton soluble zymosan polysaccharide evidence_span: {"source_cache": "artifacts/glucan-research/8558003.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "00a0fef65e91375066fe9920200032466aec1c0d85bf548d53f64c3d384106b7", "start_char": 0, "end_char": 1936, "text_sha256": "00a0fef65e91375066fe9920200032466aec1c0d85bf548d53f64c3d384106b7"} [bg-p8558003] Analysis of the sugar specificity and molecular location of the beta-glucan-binding lectin site of complement receptor type 3 (CD11b/CD18). (1996). https://pubmed.ncbi.nlm.nih.gov/8558003/ DOI: 10.4049/jimmunol.156.3.1235
Complete structured claim and evidence
When phagocyte or natural killer cell CR3 adheres to iC3b on erythrocytes or tumour cells that lack CR3-binding membrane polysaccharides neither lysis nor cytotoxicity are stimulated, but soluble CR3-specific polysaccharides such as beta-glucan induced a primed state of CR3 that could trigger killing of iC3b-target cells that were otherwise resistant to cytotoxicity, priming required tyrosine kinases and a magnesium-dependent conformational change of the I-domain that exposed the CBRM1/5 activation epitope, and unlike LPS or cytokines polysaccharides did not up-regulate neutrophil CR3 expression nor expose the high affinity ICAM-1-binding state.
Beta-glucan → The primed state of complement receptor 3 source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/glucan-research/8690804.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e6e6ce1cbb7d4a4d3170e4b86ac33d4b3220d59645c53d757fe3a2681397287e", "start_char": 0, "end_char": 1478, "text_sha256": "e6e6ce1cbb7d4a4d3170e4b86ac33d4b3220d59645c53d757fe3a2681397287e"}
experimental_model
Priming of neutrophil and natural killer cell CR3 with soluble polysaccharide, then challenge with iC3b-coated targets
exposure
Soluble CR3-specific polysaccharides including beta-glucan, with antibody blockade before or after the sugar
limitations
An in vitro cytotoxicity mechanism. It establishes how priming works and what it requires, not that the same sequence occurs in a treated patient.
nutrient_topic
Beta-glucan research collection; topical membership is not evidence of a direct clinical effect, and each preparation is recorded as its own entity with no family link joining any pair. · Beta-glucan
organism
Human
plain_language
The sugar does not make the killer cell find the tumour; it changes the receptor so that a target it was already touching becomes one it will kill.
primary_references
[bg-p8690804] Soluble beta-glucan polysaccharide binding to the lectin site of neutrophil or natural killer cell complement receptor type 3 (CD11b/CD18) generates a primed state of the receptor capable of mediating cytotoxicity of iC3b-opsonized target cells. (1996). https://pubmed.ncbi.nlm.nih.gov/8690804/ DOI: 10.1172/jci118777
tissue_or_cell_type
Neutrophil and natural killer cell
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 216–227
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Priming of neutrophil and natural killer cell CR3 with soluble polysaccharide, then challenge with iC3b-coated targets · source_derived_draft · unverified_draft
### bg-soluble-glucan-primes-cr3 When phagocyte or natural killer cell CR3 adheres to iC3b on erythrocytes or tumour cells that lack CR3-binding membrane polysaccharides neither lysis nor cytotoxicity are stimulated, but soluble CR3-specific polysaccharides such as beta-glucan induced a primed state of CR3 that could trigger killing of iC3b-target cells that were otherwise resistant to cytotoxicity, priming required tyrosine kinases and a magnesium-dependent conformational change of the I-domain that exposed the CBRM1/5 activation epitope, and unlike LPS or cytokines polysaccharides did not up-regulate neutrophil CR3 expression nor expose the high affinity ICAM-1-binding state. 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 sugar does not make the killer cell find the tumour; it changes the receptor so that a target it was already touching becomes one it will kill. organism: Human tissue_or_cell_type: Neutrophil and natural killer cell experimental_model: Priming of neutrophil and natural killer cell CR3 with soluble polysaccharide, then challenge with iC3b-coated targets limitations: An in vitro cytotoxicity mechanism. It establishes how priming works and what it requires, not that the same sequence occurs in a treated patient. exposure: Soluble CR3-specific polysaccharides including beta-glucan, with antibody blockade before or after the sugar evidence_span: {"source_cache": "artifacts/glucan-research/8690804.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e6e6ce1cbb7d4a4d3170e4b86ac33d4b3220d59645c53d757fe3a2681397287e", "start_char": 0, "end_char": 1478, "text_sha256": "e6e6ce1cbb7d4a4d3170e4b86ac33d4b3220d59645c53d757fe3a2681397287e"} [bg-p8690804] Soluble beta-glucan polysaccharide binding to the lectin site of neutrophil or natural killer cell complement receptor type 3 (CD11b/CD18) generates a primed state of the receptor capable of mediating cytotoxicity of iC3b-opsonized target cells. (1996). https://pubmed.ncbi.nlm.nih.gov/8690804/ DOI: 10.1172/jci118777
Complete structured claim and evidence
In comparison with antitumour monoclonal antibody or beta-glucan alone, combined treatment produced significantly greater tumour regression in all five models, tumour-free survival only occurred in models that incorporated stable expression of the target antigen, beta-glucan enhancement of the monoclonal antibody tumoricidal response did not occur in mice deficient in either leukocyte CR3 or serum C3 confirming the requirement for CR3 on leukocytes and iC3b on tumours, and granulocytes appeared to be primarily responsible for tumoricidal activity because beta-glucan therapeutic responses did not occur in granulocyte-depleted mice.
Beta-glucan → Complement-activating antitumour monoclonal antibodies source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/glucan-research/14695221.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "810d6af738d83f5bd304be109db27808437a1f7fb7398253366d88d0b258ccc5", "start_char": 0, "end_char": 1827, "text_sha256": "810d6af738d83f5bd304be109db27808437a1f7fb7398253366d88d0b258ccc5"}
experimental_model
Five mouse tumour models with antitumour monoclonal antibody, in CR3-deficient, C3-deficient and granulocyte-depleted animals
exposure
Intravenous beta-glucan combined with antitumour monoclonal antibodies in BALB/c and C57Bl/6 mice
limitations
Five models with genetic and depletion controls, which is what makes the requirement claim strong. Tumour-free survival occurred only where the target antigen was stably expressed.
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
Take away the complement protein, the receptor, or the granulocytes, and the effect disappears entirely.
primary_references
[bg-p14695221] Beta-glucan functions as an adjuvant for monoclonal antibody immunotherapy by recruiting tumoricidal granulocytes as killer cells. (2003). https://pubmed.ncbi.nlm.nih.gov/14695221/
tissue_or_cell_type
Mammary, subcutaneous and hepatic tumours
trigger_kind
machinery_impairment Imported condition classification; unverified.
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 229–240
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Five mouse tumour models with antitumour monoclonal antibody, in CR3-deficient, C3-deficient and granulocyte-depleted animals · source_derived_draft · unverified_draft
### bg-needs-cr3-c3-and-granulocytes In comparison with antitumour monoclonal antibody or beta-glucan alone, combined treatment produced significantly greater tumour regression in all five models, tumour-free survival only occurred in models that incorporated stable expression of the target antigen, beta-glucan enhancement of the monoclonal antibody tumoricidal response did not occur in mice deficient in either leukocyte CR3 or serum C3 confirming the requirement for CR3 on leukocytes and iC3b on tumours, and granulocytes appeared to be primarily responsible for tumoricidal activity because beta-glucan therapeutic responses did not occur in granulocyte-depleted mice. Condition category: machinery_impairment 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: Take away the complement protein, the receptor, or the granulocytes, and the effect disappears entirely. organism: Mouse tissue_or_cell_type: Mammary, subcutaneous and hepatic tumours experimental_model: Five mouse tumour models with antitumour monoclonal antibody, in CR3-deficient, C3-deficient and granulocyte-depleted animals limitations: Five models with genetic and depletion controls, which is what makes the requirement claim strong. Tumour-free survival occurred only where the target antigen was stably expressed. exposure: Intravenous beta-glucan combined with antitumour monoclonal antibodies in BALB/c and C57Bl/6 mice evidence_span: {"source_cache": "artifacts/glucan-research/14695221.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "810d6af738d83f5bd304be109db27808437a1f7fb7398253366d88d0b258ccc5", "start_char": 0, "end_char": 1827, "text_sha256": "810d6af738d83f5bd304be109db27808437a1f7fb7398253366d88d0b258ccc5"} [bg-p14695221] Beta-glucan functions as an adjuvant for monoclonal antibody immunotherapy by recruiting tumoricidal granulocytes as killer cells. (2003). https://pubmed.ncbi.nlm.nih.gov/14695221/
Complete structured claim and evidence
Recent data indicated that barley beta-1,3;1,4-glucan given orally potentiated the activity of antitumour monoclonal antibody leading to enhanced tumour regression and survival, and this investigation showed that orally administered yeast beta-1,3;1,6-glucan functioned similarly to barley beta-1,3;1,4-glucan with antitumour monoclonal antibody, with both oral beta-1,3-glucans a requirement for iC3b on tumours and CR3 on granulocytes being confirmed by demonstrating therapeutic failures in mice deficient in C3 or CR3.
Barley mixed-linkage beta-(1->3)/(1->4)-glucan → Yeast beta-(1->3)/(1->6)-glucan source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/glucan-research/15240666.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "eaff7297fa40df19ef82e5e1de433ec0cf34590a7e3fda6aa6061e0922666781", "start_char": 0, "end_char": 1454, "text_sha256": "eaff7297fa40df19ef82e5e1de433ec0cf34590a7e3fda6aa6061e0922666781"}
experimental_model
Fluorescein-labelled oral glucans tracked through macrophages to marrow, with therapy in C3-deficient and CR3-deficient mice
exposure
Orally administered barley beta-1,3;1,4-glucan and orally administered yeast beta-1,3;1,6-glucan, each with antitumour monoclonal antibody
limitations
The single experiment in this collection that tested a cereal mixed-linkage glucan and a yeast branched glucan side by side in the same protocol. It is a mouse tumour model, and oral uptake in mice does not establish the same uptake in people.
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
A cereal glucan and a yeast glucan did the same job by the same route, which is the result that refuses to let the two be filed apart.
primary_references
[bg-p15240666] Mechanism by which orally administered beta-1,3-glucans enhance the tumoricidal activity of antitumor monoclonal antibodies in murine tumor models. (2004). https://pubmed.ncbi.nlm.nih.gov/15240666/ DOI: 10.4049/jimmunol.173.2.797
tissue_or_cell_type
Gut, spleen, lymph node, bone marrow and tumour
trigger_kind
machinery_impairment Imported condition classification; unverified.
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 242–253
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Fluorescein-labelled oral glucans tracked through macrophages to marrow, with therapy in C3-deficient and CR3-deficient mice · source_derived_draft · unverified_draft
### bg-barley-and-yeast-converge Recent data indicated that barley beta-1,3;1,4-glucan given orally potentiated the activity of antitumour monoclonal antibody leading to enhanced tumour regression and survival, and this investigation showed that orally administered yeast beta-1,3;1,6-glucan functioned similarly to barley beta-1,3;1,4-glucan with antitumour monoclonal antibody, with both oral beta-1,3-glucans a requirement for iC3b on tumours and CR3 on granulocytes being confirmed by demonstrating therapeutic failures in mice deficient in C3 or CR3. Condition category: machinery_impairment 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: A cereal glucan and a yeast glucan did the same job by the same route, which is the result that refuses to let the two be filed apart. organism: Mouse tissue_or_cell_type: Gut, spleen, lymph node, bone marrow and tumour experimental_model: Fluorescein-labelled oral glucans tracked through macrophages to marrow, with therapy in C3-deficient and CR3-deficient mice limitations: The single experiment in this collection that tested a cereal mixed-linkage glucan and a yeast branched glucan side by side in the same protocol. It is a mouse tumour model, and oral uptake in mice does not establish the same uptake in people. exposure: Orally administered barley beta-1,3;1,4-glucan and orally administered yeast beta-1,3;1,6-glucan, each with antitumour monoclonal antibody evidence_span: {"source_cache": "artifacts/glucan-research/15240666.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "eaff7297fa40df19ef82e5e1de433ec0cf34590a7e3fda6aa6061e0922666781", "start_char": 0, "end_char": 1454, "text_sha256": "eaff7297fa40df19ef82e5e1de433ec0cf34590a7e3fda6aa6061e0922666781"} [bg-p15240666] Mechanism by which orally administered beta-1,3-glucans enhance the tumoricidal activity of antitumor monoclonal antibodies in murine tumor models. (2004). https://pubmed.ncbi.nlm.nih.gov/15240666/ DOI: 10.4049/jimmunol.173.2.797
Complete structured claim and evidence
Barley and yeast beta-1,3-glucan were labelled with fluorescein to track their oral uptake and processing in vivo, orally administered beta-1,3-glucans were taken up by macrophages that transported them to spleen, lymph nodes and bone marrow, within the bone marrow the macrophages degraded the large beta-1,3-glucans into smaller soluble beta-1,3-glucan fragments that were taken up by the CR3 of marginated granulocytes, and these granulocytes with CR3-bound beta-1,3-glucan-fluorescein were shown to kill iC3b-opsonized tumour cells following their recruitment to a site of complement activation resembling a tumour coated with monoclonal antibody.
Transport of ingested glucan by macrophages to spleen, lymph node and marrow → Beta-(1->3)-linked gluco-oligosaccharides source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/glucan-research/15240666.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "eaff7297fa40df19ef82e5e1de433ec0cf34590a7e3fda6aa6061e0922666781", "start_char": 0, "end_char": 1454, "text_sha256": "eaff7297fa40df19ef82e5e1de433ec0cf34590a7e3fda6aa6061e0922666781"}
experimental_model
Fluorescein-labelled oral glucans tracked through macrophages to marrow, with therapy in C3-deficient and CR3-deficient mice
exposure
Orally administered barley beta-1,3;1,4-glucan and orally administered yeast beta-1,3;1,6-glucan, each with antitumour monoclonal antibody
limitations
The single experiment in this collection that tested a cereal mixed-linkage glucan and a yeast branched glucan side by side in the same protocol. It is a mouse tumour model, and oral uptake in mice does not establish the same uptake in people.
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
Swallowed glucan is carried to the marrow inside macrophages, cut up there, and handed to granulocytes on the way out.
primary_references
[bg-p15240666] Mechanism by which orally administered beta-1,3-glucans enhance the tumoricidal activity of antitumor monoclonal antibodies in murine tumor models. (2004). https://pubmed.ncbi.nlm.nih.gov/15240666/ DOI: 10.4049/jimmunol.173.2.797
tissue_or_cell_type
Gut, spleen, lymph node, bone marrow and tumour
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 255–266
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Fluorescein-labelled oral glucans tracked through macrophages to marrow, with therapy in C3-deficient and CR3-deficient mice · source_derived_draft · unverified_draft
### bg-macrophages-carry-and-cut-it Barley and yeast beta-1,3-glucan were labelled with fluorescein to track their oral uptake and processing in vivo, orally administered beta-1,3-glucans were taken up by macrophages that transported them to spleen, lymph nodes and bone marrow, within the bone marrow the macrophages degraded the large beta-1,3-glucans into smaller soluble beta-1,3-glucan fragments that were taken up by the CR3 of marginated granulocytes, and these granulocytes with CR3-bound beta-1,3-glucan-fluorescein were shown to kill iC3b-opsonized tumour cells following their recruitment to a site of complement activation resembling a tumour coated with monoclonal antibody. 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: Swallowed glucan is carried to the marrow inside macrophages, cut up there, and handed to granulocytes on the way out. organism: Mouse tissue_or_cell_type: Gut, spleen, lymph node, bone marrow and tumour experimental_model: Fluorescein-labelled oral glucans tracked through macrophages to marrow, with therapy in C3-deficient and CR3-deficient mice limitations: The single experiment in this collection that tested a cereal mixed-linkage glucan and a yeast branched glucan side by side in the same protocol. It is a mouse tumour model, and oral uptake in mice does not establish the same uptake in people. exposure: Orally administered barley beta-1,3;1,4-glucan and orally administered yeast beta-1,3;1,6-glucan, each with antitumour monoclonal antibody evidence_span: {"source_cache": "artifacts/glucan-research/15240666.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "eaff7297fa40df19ef82e5e1de433ec0cf34590a7e3fda6aa6061e0922666781", "start_char": 0, "end_char": 1454, "text_sha256": "eaff7297fa40df19ef82e5e1de433ec0cf34590a7e3fda6aa6061e0922666781"} [bg-p15240666] Mechanism by which orally administered beta-1,3-glucans enhance the tumoricidal activity of antitumor monoclonal antibodies in murine tumor models. (2004). https://pubmed.ncbi.nlm.nih.gov/15240666/ DOI: 10.4049/jimmunol.173.2.797
Complete structured claim and evidence
Imprime-induced anti-cancer functionality is dependent on immune complex formation with naturally-occurring anti-beta glucan antibodies, the formation of Imprime-antibody complexes activates complement primarily via the classical complement pathway and is opsonised by iC3b, immune complex binding depends upon Complement Receptor 3 and Fc gamma Receptor IIa eliciting phenotypic activation of and enhanced chemokine production by neutrophils and monocytes enabling these effector cells to kill antibody-opsonized tumour cells, and importantly these innate immune cell changes were not evident in subjects with low antibody levels but could be rescued with exogenous antibody supplementation.
Naturally occurring anti-beta-glucan IgG antibodies → Imprime PGG / BTH1677, a soluble yeast beta-(1->3)/(1->6)-glucan source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/glucan-research/27812183.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "949fc5939bec2e3fab259b6b6161fba8cdd7779c7efa0261a1e7dbf1cab111cf", "start_char": 0, "end_char": 1493, "text_sha256": "949fc5939bec2e3fab259b6b6161fba8cdd7779c7efa0261a1e7dbf1cab111cf"}
experimental_model
Whole blood from healthy human subjects with antibody-depleted and antibody-supplemented conditions
exposure
Imprime PGG in whole blood across a range of naturally occurring anti-beta-glucan antibody levels
limitations
Ex vivo whole blood rather than treated patients. The antibody dependence is demonstrated both by absence in low-antibody donors and by rescue with added antibody.
nutrient_topic
Beta-glucan research collection; topical membership is not evidence of a direct clinical effect, and each preparation is recorded as its own entity with no family link joining any pair. · Beta-glucan
organism
Human
plain_language
This soluble glucan does nothing on its own; it has to be caught by an antibody the person already had.
primary_references
[bg-p27812183] Imprime PGG-Mediated Anti-Cancer Immune Activation Requires Immune Complex Formation. (2016). https://pubmed.ncbi.nlm.nih.gov/27812183/ DOI: 10.1371/journal.pone.0165909
tissue_or_cell_type
Whole blood, neutrophil and 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 268–279
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Whole blood from healthy human subjects with antibody-depleted and antibody-supplemented conditions · source_derived_draft · unverified_draft
### bg-imprime-needs-an-antibody-first Imprime-induced anti-cancer functionality is dependent on immune complex formation with naturally-occurring anti-beta glucan antibodies, the formation of Imprime-antibody complexes activates complement primarily via the classical complement pathway and is opsonised by iC3b, immune complex binding depends upon Complement Receptor 3 and Fc gamma Receptor IIa eliciting phenotypic activation of and enhanced chemokine production by neutrophils and monocytes enabling these effector cells to kill antibody-opsonized tumour cells, and importantly these innate immune cell changes were not evident in subjects with low antibody levels but could be rescued with exogenous antibody supplementation. 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: This soluble glucan does nothing on its own; it has to be caught by an antibody the person already had. organism: Human tissue_or_cell_type: Whole blood, neutrophil and monocyte experimental_model: Whole blood from healthy human subjects with antibody-depleted and antibody-supplemented conditions limitations: Ex vivo whole blood rather than treated patients. The antibody dependence is demonstrated both by absence in low-antibody donors and by rescue with added antibody. exposure: Imprime PGG in whole blood across a range of naturally occurring anti-beta-glucan antibody levels evidence_span: {"source_cache": "artifacts/glucan-research/27812183.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "949fc5939bec2e3fab259b6b6161fba8cdd7779c7efa0261a1e7dbf1cab111cf", "start_char": 0, "end_char": 1493, "text_sha256": "949fc5939bec2e3fab259b6b6161fba8cdd7779c7efa0261a1e7dbf1cab111cf"} [bg-p27812183] Imprime PGG-Mediated Anti-Cancer Immune Activation Requires Immune Complex Formation. (2016). https://pubmed.ncbi.nlm.nih.gov/27812183/ DOI: 10.1371/journal.pone.0165909
Complete structured claim and evidence
At the end of infusion free serum antibody levels decreased, circulating immune complex levels increased and complement activation was observed, at approximately 1 to 4 hours after end of infusion increased expression of cytokines and chemokines, a 1.5 to 4-fold increase in neutrophil and monocyte counts and a broad activation of innate immune genes were observed, low-antibody subjects with levels below 20 micrograms per millilitre typically showed minimal changes except when their levels rose above 20 micrograms per millilitre after repeated dosing, mild-to-moderate infusion-related reactions occurred in subjects with antibody at or above 20 micrograms per millilitre, and premedications alleviated some of the infusion-related reactions but also inhibited cytokine responses.
Naturally occurring anti-beta-glucan IgG antibodies → Imprime PGG / BTH1677, a soluble yeast beta-(1->3)/(1->6)-glucan source_derived_draftungraded
Experimental context and source evidence
availability_state
biomarker_context Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/glucan-research/30988115.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "bd9bd1b314472b30b2e3513ecb5e048178de145217473fa87379e0977d21f90d", "start_char": 0, "end_char": 1787, "text_sha256": "bd9bd1b314472b30b2e3513ecb5e048178de145217473fa87379e0977d21f90d"}
experimental_model
Single and multiple intravenous infusions in healthy volunteers stratified by pre-treatment antibody level, with and without premedication
exposure
Imprime PGG 4 milligrams per kilogram intravenously, with antihistamine and corticosteroid premedication in some subjects
limitations
Healthy volunteers and pharmacodynamic endpoints only. Nothing here measures a tumour outcome, so the antibody strata are not validated treatment-selection thresholds.
nutrient_topic
Beta-glucan research collection; topical membership is not evidence of a direct clinical effect, and each preparation is recorded as its own entity with no family link joining any pair. · Beta-glucan
organism
Human
plain_language
Below a certain antibody level almost nothing happened; above it, the drug worked and also caused the infusion reactions.
primary_references
[bg-p30988115] Immune Pharmacodynamic Responses of the Novel Cancer Immunotherapeutic Imprime PGG in Healthy Volunteers. (2019). https://pubmed.ncbi.nlm.nih.gov/30988115/ DOI: 10.4049/jimmunol.1801533
tissue_or_cell_type
Peripheral blood
trigger_kind
biomarker_context Imported condition classification; unverified.
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 281–292
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Single and multiple intravenous infusions in healthy volunteers stratified by pre-treatment antibody level, with and without premedication · source_derived_draft · unverified_draft
### bg-antibody-level-gates-the-response At the end of infusion free serum antibody levels decreased, circulating immune complex levels increased and complement activation was observed, at approximately 1 to 4 hours after end of infusion increased expression of cytokines and chemokines, a 1.5 to 4-fold increase in neutrophil and monocyte counts and a broad activation of innate immune genes were observed, low-antibody subjects with levels below 20 micrograms per millilitre typically showed minimal changes except when their levels rose above 20 micrograms per millilitre after repeated dosing, mild-to-moderate infusion-related reactions occurred in subjects with antibody at or above 20 micrograms per millilitre, and premedications alleviated some of the infusion-related reactions but also inhibited cytokine responses. Condition category: biomarker_context 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: Below a certain antibody level almost nothing happened; above it, the drug worked and also caused the infusion reactions. organism: Human tissue_or_cell_type: Peripheral blood experimental_model: Single and multiple intravenous infusions in healthy volunteers stratified by pre-treatment antibody level, with and without premedication limitations: Healthy volunteers and pharmacodynamic endpoints only. Nothing here measures a tumour outcome, so the antibody strata are not validated treatment-selection thresholds. exposure: Imprime PGG 4 milligrams per kilogram intravenously, with antihistamine and corticosteroid premedication in some subjects evidence_span: {"source_cache": "artifacts/glucan-research/30988115.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "bd9bd1b314472b30b2e3513ecb5e048178de145217473fa87379e0977d21f90d", "start_char": 0, "end_char": 1787, "text_sha256": "bd9bd1b314472b30b2e3513ecb5e048178de145217473fa87379e0977d21f90d"} [bg-p30988115] Immune Pharmacodynamic Responses of the Novel Cancer Immunotherapeutic Imprime PGG in Healthy Volunteers. (2019). https://pubmed.ncbi.nlm.nih.gov/30988115/ DOI: 10.4049/jimmunol.1801533
Complete structured claim and evidence
In two single-patient studies, one in a patient with metastatic colorectal cancer who received BTH1677 combined with the tumour targeting antibody cetuximab and a second in a patient with metastatic neuroendocrine tumour who received BTH1677 combined with the immune checkpoint inhibitor pembrolizumab, the patients had low serum titres of antibodies against beta-glucan and low innate immune effector functionality induced by BTH1677, and addition of intravenous immunoglobulins restored innate immune activity of BTH1677 and induced clinically meaningful anti-tumoural activity with long-term disease control.
Intravenous immunoglobulin → Imprime PGG / BTH1677, a soluble yeast beta-(1->3)/(1->6)-glucan source_derived_draftungraded
Experimental context and source evidence
availability_state
biomarker_context Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/glucan-research/32132045.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7dea757c889af10839a38a317d704760e7e15798bc15a5da3a1323ec4143cf42", "start_char": 0, "end_char": 1102, "text_sha256": "7dea757c889af10839a38a317d704760e7e15798bc15a5da3a1323ec4143cf42"}
experimental_model
Two single-patient reports of immunoglobulin infusion in patients with low anti-glucan antibody
exposure
BTH1677 with cetuximab or with pembrolizumab, plus intravenous immunoglobulin
limitations
Two patients. This is an anecdotal test of a mechanism, not evidence of treatment benefit, and no control condition exists for the tumour outcome.
nutrient_topic
Beta-glucan research collection; topical membership is not evidence of a direct clinical effect, and each preparation is recorded as its own entity with no family link joining any pair. · Beta-glucan
organism
Human
plain_language
Two patients who lacked the antibody were given antibody, and the drug started working.
primary_references
[bg-p32132045] Immunoglobulin Restores Immune Responses to BTH1677 in Patients With Low Levels of Antibodies to Beta-glucan. (2020). https://pubmed.ncbi.nlm.nih.gov/32132045/ DOI: 10.21873/anticanres.14090
tissue_or_cell_type
Peripheral blood and tumour
trigger_kind
biomarker_context Imported condition classification; unverified.
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 294–305
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Two single-patient reports of immunoglobulin infusion in patients with low anti-glucan antibody · source_derived_draft · unverified_draft
### bg-adding-antibody-restores-it In two single-patient studies, one in a patient with metastatic colorectal cancer who received BTH1677 combined with the tumour targeting antibody cetuximab and a second in a patient with metastatic neuroendocrine tumour who received BTH1677 combined with the immune checkpoint inhibitor pembrolizumab, the patients had low serum titres of antibodies against beta-glucan and low innate immune effector functionality induced by BTH1677, and addition of intravenous immunoglobulins restored innate immune activity of BTH1677 and induced clinically meaningful anti-tumoural activity with long-term disease control. Condition category: biomarker_context 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: Two patients who lacked the antibody were given antibody, and the drug started working. organism: Human tissue_or_cell_type: Peripheral blood and tumour experimental_model: Two single-patient reports of immunoglobulin infusion in patients with low anti-glucan antibody limitations: Two patients. This is an anecdotal test of a mechanism, not evidence of treatment benefit, and no control condition exists for the tumour outcome. exposure: BTH1677 with cetuximab or with pembrolizumab, plus intravenous immunoglobulin evidence_span: {"source_cache": "artifacts/glucan-research/32132045.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7dea757c889af10839a38a317d704760e7e15798bc15a5da3a1323ec4143cf42", "start_char": 0, "end_char": 1102, "text_sha256": "7dea757c889af10839a38a317d704760e7e15798bc15a5da3a1323ec4143cf42"} [bg-p32132045] Immunoglobulin Restores Immune Responses to BTH1677 in Patients With Low Levels of Antibodies to Beta-glucan. (2020). https://pubmed.ncbi.nlm.nih.gov/32132045/ DOI: 10.21873/anticanres.14090
Complete structured claim and evidence
Compared to control treatment the addition of BTH1677 numerically increased objective response rate by both investigator review at 47.8% versus 23.1% with p=0.0468 and central review at 36.6% versus 23.1% with p=0.2895, no other endpoints differed between arms, BTH1677 was well tolerated with adverse events expected of the backbone therapy predominating, and biomarker-positive patients displayed better objective response rate and overall survival than negative patients.
Imprime PGG / BTH1677, a soluble yeast beta-(1->3)/(1->6)-glucan → Objective tumour response rate source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/glucan-research/28303530.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1647608a80fde3f663b90783006859ae85ed15bc718a8d9031ba5acdb586eb7b", "start_char": 0, "end_char": 2002, "text_sha256": "1647608a80fde3f663b90783006859ae85ed15bc718a8d9031ba5acdb586eb7b"}
experimental_model
Randomised open-label multicentre phase II trial with both investigator and blinded central radiology review
exposure
BTH1677 4 milligrams per kilogram weekly with cetuximab, carboplatin and paclitaxel against the same backbone alone, randomised 2 to 1
limitations
Ninety patients, open-label, with the primary response endpoint read twice. The two reads disagree, which is the finding.
nutrient_topic
Beta-glucan research collection; topical membership is not evidence of a direct clinical effect, and each preparation is recorded as its own entity with no family link joining any pair. · Beta-glucan
organism
Human
plain_language
The doctors running the trial saw twice the response rate; the blinded reviewers saw a smaller difference that could have been chance.
primary_references
[bg-p28303530] A randomized, open-label, multicenter, phase II study evaluating the efficacy and safety of BTH1677 (1,3-1,6 beta glucan; Imprime PGG) in combination with cetuximab and chemotherapy in patients with advanced non-small cell lung cancer. (2017). https://pubmed.ncbi.nlm.nih.gov/28303530/ DOI: 10.1007/s10637-017-0450-3
tissue_or_cell_type
Advanced non-small cell lung cancer
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 307–318
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomised open-label multicentre phase II trial with both investigator and blinded central radiology review · source_derived_draft · unverified_draft
### bg-the-two-reads-disagree Compared to control treatment the addition of BTH1677 numerically increased objective response rate by both investigator review at 47.8% versus 23.1% with p=0.0468 and central review at 36.6% versus 23.1% with p=0.2895, no other endpoints differed between arms, BTH1677 was well tolerated with adverse events expected of the backbone therapy predominating, and biomarker-positive patients displayed better objective response rate and overall survival than negative patients. 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 doctors running the trial saw twice the response rate; the blinded reviewers saw a smaller difference that could have been chance. organism: Human tissue_or_cell_type: Advanced non-small cell lung cancer experimental_model: Randomised open-label multicentre phase II trial with both investigator and blinded central radiology review limitations: Ninety patients, open-label, with the primary response endpoint read twice. The two reads disagree, which is the finding. exposure: BTH1677 4 milligrams per kilogram weekly with cetuximab, carboplatin and paclitaxel against the same backbone alone, randomised 2 to 1 evidence_span: {"source_cache": "artifacts/glucan-research/28303530.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1647608a80fde3f663b90783006859ae85ed15bc718a8d9031ba5acdb586eb7b", "start_char": 0, "end_char": 2002, "text_sha256": "1647608a80fde3f663b90783006859ae85ed15bc718a8d9031ba5acdb586eb7b"} [bg-p28303530] A randomized, open-label, multicenter, phase II study evaluating the efficacy and safety of BTH1677 (1,3-1,6 beta glucan; Imprime PGG) in combination with cetuximab and chemotherapy in patients with advanced non-small cell lung cancer. (2017). https://pubmed.ncbi.nlm.nih.gov/28303530/ DOI: 10.1007/s10637-017-0450-3
Complete structured claim and evidence
Objective response rate based on blinded central radiology review was higher in the BTH1677 arm versus control but the difference between groups was not statistically significant at 60.4% versus 43.5% with P = .2096, all other clinical endpoints also favoured the BTH1677 arm but none statistically differed between arms, and although a higher incidence of Grade 3 or 4 adverse events occurred in the BTH1677 versus control arm at 93.2% versus 66.7% no unexpected adverse events were observed while serious adverse events and discontinuations due to adverse events were lower.
Imprime PGG / BTH1677, a soluble yeast beta-(1->3)/(1->6)-glucan → Objective tumour response rate source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/glucan-research/29486797.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7e4ff586490d7fdbefa5e817f7ee8b59c72e666bfb473620331f2fb178f46789", "start_char": 0, "end_char": 2024, "text_sha256": "7e4ff586490d7fdbefa5e817f7ee8b59c72e666bfb473620331f2fb178f46789"}
experimental_model
Randomised controlled phase II trial with blinded central radiology review as the primary read
exposure
BTH1677 4 milligrams per kilogram weekly with bevacizumab, carboplatin and paclitaxel against the same backbone alone
limitations
Ninety-two patients randomised 61 to 31, with response read centrally. A higher rate of grade 3 or 4 adverse events occurred on the glucan arm.
nutrient_topic
Beta-glucan research collection; topical membership is not evidence of a direct clinical effect, and each preparation is recorded as its own entity with no family link joining any pair. · Beta-glucan
organism
Human
plain_language
A second trial pointed the same way on every measure and reached statistical significance on none of them.
primary_references
[bg-p29486797] A randomized, controlled trial evaluating the efficacy and safety of BTH1677 in combination with bevacizumab, carboplatin, and paclitaxel in first-line treatment of advanced non-small cell lung cancer. (2018). https://pubmed.ncbi.nlm.nih.gov/29486797/ DOI: 10.1186/s40425-018-0324-z
tissue_or_cell_type
Untreated advanced non-small cell lung cancer
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 320–331
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomised controlled phase II trial with blinded central radiology review as the primary read · source_derived_draft · unverified_draft
### bg-second-trial-not-significant Objective response rate based on blinded central radiology review was higher in the BTH1677 arm versus control but the difference between groups was not statistically significant at 60.4% versus 43.5% with P = .2096, all other clinical endpoints also favoured the BTH1677 arm but none statistically differed between arms, and although a higher incidence of Grade 3 or 4 adverse events occurred in the BTH1677 versus control arm at 93.2% versus 66.7% no unexpected adverse events were observed while serious adverse events and discontinuations due to adverse events were lower. 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: A second trial pointed the same way on every measure and reached statistical significance on none of them. organism: Human tissue_or_cell_type: Untreated advanced non-small cell lung cancer experimental_model: Randomised controlled phase II trial with blinded central radiology review as the primary read limitations: Ninety-two patients randomised 61 to 31, with response read centrally. A higher rate of grade 3 or 4 adverse events occurred on the glucan arm. exposure: BTH1677 4 milligrams per kilogram weekly with bevacizumab, carboplatin and paclitaxel against the same backbone alone evidence_span: {"source_cache": "artifacts/glucan-research/29486797.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7e4ff586490d7fdbefa5e817f7ee8b59c72e666bfb473620331f2fb178f46789", "start_char": 0, "end_char": 2024, "text_sha256": "7e4ff586490d7fdbefa5e817f7ee8b59c72e666bfb473620331f2fb178f46789"} [bg-p29486797] A randomized, controlled trial evaluating the efficacy and safety of BTH1677 in combination with bevacizumab, carboplatin, and paclitaxel in first-line treatment of advanced non-small cell lung cancer. (2018). https://pubmed.ncbi.nlm.nih.gov/29486797/ DOI: 10.1186/s40425-018-0324-z
Complete structured claim and evidence
Confirmed objective response rate was 10% with one complete and two partial responses, median progression-free survival was 2.6 months and median overall survival was 11.1 months, prior immunotherapy negatively influenced overall survival with a hazard ratio of 2.95, and the combination of Imprime and pembrolizumab is tolerable but did not improve the outcome of advanced stage non-small cell lung cancer patients who previously progressed on anti-PD-1 or PD-L1 immunotherapies.
Imprime PGG / BTH1677, a soluble yeast beta-(1->3)/(1->6)-glucan → Progression-free survival in high-grade glioma source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/glucan-research/39670007.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2aad97fa3dcbfbdcedfc88a4fbcad902de0cbade16dcf3c94b26a9c6960ced38", "start_char": 0, "end_char": 2076, "text_sha256": "2aad97fa3dcbfbdcedfc88a4fbcad902de0cbade16dcf3c94b26a9c6960ced38"}
experimental_model
Investigator-initiated multi-institutional single-arm phase Ib/II trial in previously treated patients
exposure
Imprime PGG at the 4 milligram per kilogram maximum tolerated dose with pembrolizumab
limitations
Single-arm with no randomised comparator, in patients who had already progressed on checkpoint blockade. Thirty patients were evaluable for efficacy.
nutrient_topic
Beta-glucan research collection; topical membership is not evidence of a direct clinical effect, and each preparation is recorded as its own entity with no family link joining any pair. · Beta-glucan
organism
Human
plain_language
Added to a checkpoint drug in patients who had already failed one, it did not help.
primary_references
[bg-p39670007] Phase Ib/II study of imprime PGG and pembrolizumab in patients with previously treated advanced non-small cell lung cancer (NSCLC): BTCRC LUN 15-017. (2024). https://pubmed.ncbi.nlm.nih.gov/39670007/ DOI: 10.21037/tlcr-24-346
tissue_or_cell_type
Advanced non-small cell lung cancer
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 333–344
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Investigator-initiated multi-institutional single-arm phase Ib/II trial in previously treated patients · source_derived_draft · unverified_draft
### bg-no-benefit-with-pembrolizumab Confirmed objective response rate was 10% with one complete and two partial responses, median progression-free survival was 2.6 months and median overall survival was 11.1 months, prior immunotherapy negatively influenced overall survival with a hazard ratio of 2.95, and the combination of Imprime and pembrolizumab is tolerable but did not improve the outcome of advanced stage non-small cell lung cancer patients who previously progressed on anti-PD-1 or PD-L1 immunotherapies. 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: Added to a checkpoint drug in patients who had already failed one, it did not help. organism: Human tissue_or_cell_type: Advanced non-small cell lung cancer experimental_model: Investigator-initiated multi-institutional single-arm phase Ib/II trial in previously treated patients limitations: Single-arm with no randomised comparator, in patients who had already progressed on checkpoint blockade. Thirty patients were evaluable for efficacy. exposure: Imprime PGG at the 4 milligram per kilogram maximum tolerated dose with pembrolizumab evidence_span: {"source_cache": "artifacts/glucan-research/39670007.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2aad97fa3dcbfbdcedfc88a4fbcad902de0cbade16dcf3c94b26a9c6960ced38", "start_char": 0, "end_char": 2076, "text_sha256": "2aad97fa3dcbfbdcedfc88a4fbcad902de0cbade16dcf3c94b26a9c6960ced38"} [bg-p39670007] Phase Ib/II study of imprime PGG and pembrolizumab in patients with previously treated advanced non-small cell lung cancer (NSCLC): BTCRC LUN 15-017. (2024). https://pubmed.ncbi.nlm.nih.gov/39670007/ DOI: 10.21037/tlcr-24-346
Complete structured claim and evidence
One patient developed a dose-limiting toxicity of transient self-limiting hepatic transaminase elevation 5 days after starting beta-glucan at 120 milligrams per kilogram per day, overall 1, 3, 12 and 24 evaluable patients had complete response, partial response, stable and progressive disease respectively at the end of treatment, positive human anti-mouse antibody response and dectin-1 rs3901533 polymorphism were associated with better overall survival, and beta-glucan dose level and serum beta-glucan levels did not correlate with response.
Yeast beta-(1->3)/(1->6)-glucan → Objective tumour response rate source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/glucan-research/34944886.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ebbaee1e57b37044ff51d85d98d519101169e09a734d420c8bce53faab1d19f0", "start_char": 0, "end_char": 1471, "text_sha256": "ebbaee1e57b37044ff51d85d98d519101169e09a734d420c8bce53faab1d19f0"}
experimental_model
Phase I dose escalation of oral yeast glucan with an anti-GD2 antibody across cohorts of three to six patients
exposure
Oral yeast beta-glucan escalated from 10 to 200 milligrams per kilogram per day for 17 days with intravenous 3F8 antibody
limitations
A single-arm phase I with no control for the antibody alone, so the glucan contribution to any response cannot be isolated. Forty-four patients completed 141 cycles and forty were evaluable at end of treatment.
nutrient_topic
Beta-glucan research collection; topical membership is not evidence of a direct clinical effect, and each preparation is recorded as its own entity with no family link joining any pair. · Beta-glucan
organism
Human
plain_language
Across a twentyfold range of doses, how much was taken did not predict who responded; a receptor gene variant did.
primary_references
[bg-p34944886] Phase I Trial of Oral Yeast-Derived β-Glucan to Enhance Anti-GD2 Immunotherapy of Resistant High-Risk Neuroblastoma. (2021). https://pubmed.ncbi.nlm.nih.gov/34944886/ DOI: 10.3390/cancers13246265
tissue_or_cell_type
Relapsed or refractory high-risk neuroblastoma
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 346–357
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Phase I dose escalation of oral yeast glucan with an anti-GD2 antibody across cohorts of three to six patients · source_derived_draft · unverified_draft
### bg-dose-did-not-track-response One patient developed a dose-limiting toxicity of transient self-limiting hepatic transaminase elevation 5 days after starting beta-glucan at 120 milligrams per kilogram per day, overall 1, 3, 12 and 24 evaluable patients had complete response, partial response, stable and progressive disease respectively at the end of treatment, positive human anti-mouse antibody response and dectin-1 rs3901533 polymorphism were associated with better overall survival, and beta-glucan dose level and serum beta-glucan levels did not correlate with response. 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: Across a twentyfold range of doses, how much was taken did not predict who responded; a receptor gene variant did. organism: Human tissue_or_cell_type: Relapsed or refractory high-risk neuroblastoma experimental_model: Phase I dose escalation of oral yeast glucan with an anti-GD2 antibody across cohorts of three to six patients limitations: A single-arm phase I with no control for the antibody alone, so the glucan contribution to any response cannot be isolated. Forty-four patients completed 141 cycles and forty were evaluable at end of treatment. exposure: Oral yeast beta-glucan escalated from 10 to 200 milligrams per kilogram per day for 17 days with intravenous 3F8 antibody evidence_span: {"source_cache": "artifacts/glucan-research/34944886.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ebbaee1e57b37044ff51d85d98d519101169e09a734d420c8bce53faab1d19f0", "start_char": 0, "end_char": 1471, "text_sha256": "ebbaee1e57b37044ff51d85d98d519101169e09a734d420c8bce53faab1d19f0"} [bg-p34944886] Phase I Trial of Oral Yeast-Derived β-Glucan to Enhance Anti-GD2 Immunotherapy of Resistant High-Risk Neuroblastoma. (2021). https://pubmed.ncbi.nlm.nih.gov/34944886/ DOI: 10.3390/cancers13246265
Complete structured claim and evidence
Eligible patients receiving GD2/GD3 vaccine were randomly assigned to group 1 with 54 patients to receive no beta-glucan or group 2 with 53 patients to receive an oral beta-glucan regimen during the first 5 weeks of vaccine priming, and from week 6 onwards all 107 patients received oral beta-glucan during vaccine boost, adding oral beta-glucan during the first 5 weeks of vaccine priming elicited a higher anti-GD2 IgG1 antibody response in group 2 at 1.80 with 90% CI 0.12 to 3.39 and P = .08 against a planned type I error of 0.10, antibody titre correlated significantly with dectin-1 single nucleotide polymorphism, and the genotype frequency, seroconversion rates and vaccine-related toxic effects were similar in the 2 groups.
Yeast beta-(1->3)/(1->6)-glucan → Anti-GD2 IgG1 antibody titre source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/glucan-research/36547975.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "156766d12dba66e36fba78a5ca31f9c41f50f88f74817ba4d545a7a3ed5e23f2", "start_char": 0, "end_char": 2766, "text_sha256": "156766d12dba66e36fba78a5ca31f9c41f50f88f74817ba4d545a7a3ed5e23f2"}
experimental_model
Phase 2 randomised clinical trial isolating the adjuvant effect during the vaccine priming phase
exposure
Oral beta-glucan during the first 5 weeks of GD2/GD3 vaccine priming against none, with all patients receiving glucan from week 6 onward
limitations
A randomised design that isolates one adjuvant window, with a prespecified type I error of 0.10 rather than the conventional 0.05. The endpoint is an antibody titre, not survival.
nutrient_topic
Beta-glucan research collection; topical membership is not evidence of a direct clinical effect, and each preparation is recorded as its own entity with no family link joining any pair. · Beta-glucan
organism
Human
plain_language
Starting the glucan earlier raised the antibody the vaccine was meant to raise, at a significance bar the trial had set in advance at one in ten.
primary_references
[bg-p36547975] Effect of Oral β-Glucan on Antibody Response to Ganglioside Vaccine in Patients With High-Risk Neuroblastoma: A Phase 2 Randomized Clinical Trial. (2023). https://pubmed.ncbi.nlm.nih.gov/36547975/ DOI: 10.1001/jamaoncol.2022.5999
tissue_or_cell_type
High-risk neuroblastoma
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 359–370
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Phase 2 randomised clinical trial isolating the adjuvant effect during the vaccine priming phase · source_derived_draft · unverified_draft
### bg-immunogenicity-in-genetic-responders Eligible patients receiving GD2/GD3 vaccine were randomly assigned to group 1 with 54 patients to receive no beta-glucan or group 2 with 53 patients to receive an oral beta-glucan regimen during the first 5 weeks of vaccine priming, and from week 6 onwards all 107 patients received oral beta-glucan during vaccine boost, adding oral beta-glucan during the first 5 weeks of vaccine priming elicited a higher anti-GD2 IgG1 antibody response in group 2 at 1.80 with 90% CI 0.12 to 3.39 and P = .08 against a planned type I error of 0.10, antibody titre correlated significantly with dectin-1 single nucleotide polymorphism, and the genotype frequency, seroconversion rates and vaccine-related toxic effects were similar in the 2 groups. 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: Starting the glucan earlier raised the antibody the vaccine was meant to raise, at a significance bar the trial had set in advance at one in ten. organism: Human tissue_or_cell_type: High-risk neuroblastoma experimental_model: Phase 2 randomised clinical trial isolating the adjuvant effect during the vaccine priming phase limitations: A randomised design that isolates one adjuvant window, with a prespecified type I error of 0.10 rather than the conventional 0.05. The endpoint is an antibody titre, not survival. exposure: Oral beta-glucan during the first 5 weeks of GD2/GD3 vaccine priming against none, with all patients receiving glucan from week 6 onward evidence_span: {"source_cache": "artifacts/glucan-research/36547975.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "156766d12dba66e36fba78a5ca31f9c41f50f88f74817ba4d545a7a3ed5e23f2", "start_char": 0, "end_char": 2766, "text_sha256": "156766d12dba66e36fba78a5ca31f9c41f50f88f74817ba4d545a7a3ed5e23f2"} [bg-p36547975] Effect of Oral β-Glucan on Antibody Response to Ganglioside Vaccine in Patients With High-Risk Neuroblastoma: A Phase 2 Randomized Clinical Trial. (2023). https://pubmed.ncbi.nlm.nih.gov/36547975/ DOI: 10.1001/jamaoncol.2022.5999
Complete structured claim and evidence
Maximum plasma concentrations for glucan phosphate occurred at 4 hours while laminarin and scleroglucan showed two plasma peaks between 0.5 and 12 hours, at 24 hours 27 plus or minus 3% of the glucan phosphate and 20 plus or minus 7% of the laminarin remained in the serum, following oral administration glucans were bound and internalized by intestinal epithelial cells and gut-associated lymphoid tissue cells with internalization by intestinal epithelial cells not being Dectin-dependent, gut-associated lymphoid tissue expression of Dectin-1 and Toll-like receptor 2 but not Toll-like receptor 4 increased, oral glucan increased systemic levels of interleukin-12 by 151%, and oral glucan administration also increased survival in mice challenged with Staphylococcus aureus or Candida albicans.
Glucan phosphate → Serum beta-glucan concentration after oral dosing source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/glucan-research/15976018.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "19df013d426cc48180a1bc6bb1e1e359c1d8b1f923cc97be369f5ad9116c3b18", "start_char": 0, "end_char": 1617, "text_sha256": "19df013d426cc48180a1bc6bb1e1e359c1d8b1f923cc97be369f5ad9116c3b18"}
experimental_model
Oral pharmacokinetics of three water-soluble glucans in rats, with uptake, receptor expression and infectious challenge in mice
exposure
Glucan phosphate, laminarin and scleroglucan at 1 milligram per kilogram orally in rats, and 1 milligram orally in mice
limitations
Rodent pharmacokinetics and rodent challenge models. The reported figure for glucan phosphate at 24 hours is a percentage remaining in serum whose denominator the abstract does not state, so it is not read here as a fraction of the swallowed dose.
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
Rat and mouse
plain_language
In rodents the swallowed sugar does cross into the circulation, is taken up by the gut immune tissue, and leaves the animals better able to survive an infection.
primary_references
[bg-p15976018] Oral delivery and gastrointestinal absorption of soluble glucans stimulate increased resistance to infectious challenge. (2005). https://pubmed.ncbi.nlm.nih.gov/15976018/ DOI: 10.1124/jpet.105.085415
tissue_or_cell_type
Plasma, intestinal epithelium and gut-associated lymphoid tissue
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 372–383
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Oral pharmacokinetics of three water-soluble glucans in rats, with uptake, receptor expression and infectious challenge in mice · source_derived_draft · unverified_draft
### bg-oral-glucan-does-reach-the-blood Maximum plasma concentrations for glucan phosphate occurred at 4 hours while laminarin and scleroglucan showed two plasma peaks between 0.5 and 12 hours, at 24 hours 27 plus or minus 3% of the glucan phosphate and 20 plus or minus 7% of the laminarin remained in the serum, following oral administration glucans were bound and internalized by intestinal epithelial cells and gut-associated lymphoid tissue cells with internalization by intestinal epithelial cells not being Dectin-dependent, gut-associated lymphoid tissue expression of Dectin-1 and Toll-like receptor 2 but not Toll-like receptor 4 increased, oral glucan increased systemic levels of interleukin-12 by 151%, and oral glucan administration also increased survival in mice challenged with Staphylococcus aureus or Candida albicans. 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: In rodents the swallowed sugar does cross into the circulation, is taken up by the gut immune tissue, and leaves the animals better able to survive an infection. organism: Rat and mouse tissue_or_cell_type: Plasma, intestinal epithelium and gut-associated lymphoid tissue experimental_model: Oral pharmacokinetics of three water-soluble glucans in rats, with uptake, receptor expression and infectious challenge in mice limitations: Rodent pharmacokinetics and rodent challenge models. The reported figure for glucan phosphate at 24 hours is a percentage remaining in serum whose denominator the abstract does not state, so it is not read here as a fraction of the swallowed dose. exposure: Glucan phosphate, laminarin and scleroglucan at 1 milligram per kilogram orally in rats, and 1 milligram orally in mice evidence_span: {"source_cache": "artifacts/glucan-research/15976018.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "19df013d426cc48180a1bc6bb1e1e359c1d8b1f923cc97be369f5ad9116c3b18", "start_char": 0, "end_char": 1617, "text_sha256": "19df013d426cc48180a1bc6bb1e1e359c1d8b1f923cc97be369f5ad9116c3b18"} [bg-p15976018] Oral delivery and gastrointestinal absorption of soluble glucans stimulate increased resistance to infectious challenge. (2005). https://pubmed.ncbi.nlm.nih.gov/15976018/ DOI: 10.1124/jpet.105.085415
Complete structured claim and evidence
In a randomised open-label intervention pilot study in 15 healthy male volunteers, subjects in the beta-glucan group ingested beta-glucan 1000 milligrams once daily for 7 days, beta-glucan was barely detectable in serum of volunteers at all time-points, and neither cytokine production nor microbicidal activity of leukocytes were affected by orally administered beta-glucan, so the present study does not support the use of oral beta-glucan to enhance innate immune responses in humans.
Beta-glucan → Ex vivo cytokine production by stimulated leukocytes source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/glucan-research/25268806.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "b5a583c465284aae8e7d3e6dd9996fafe3b6ef389c61ee2a54f066fb4701e51b", "start_char": 0, "end_char": 1307, "text_sha256": "b5a583c465284aae8e7d3e6dd9996fafe3b6ef389c61ee2a54f066fb4701e51b"}
experimental_model
Randomised open-label intervention pilot study in 15 healthy male volunteers
exposure
Oral beta-glucan 1000 milligrams once daily for 7 days against no treatment, with serial sampling
limitations
Ten treated and five control subjects, one product, one dose, seven days, and ex vivo readouts. A negative pilot of this size does not establish that all oral preparations are inactive.
nutrient_topic
Beta-glucan research collection; topical membership is not evidence of a direct clinical effect, and each preparation is recorded as its own entity with no family link joining any pair. · Beta-glucan
organism
Human
plain_language
Ten healthy men took a gram a day for a week; almost none of it showed up in the blood and nothing measurable changed.
primary_references
[bg-p25268806] The effects of orally administered Beta-glucan on innate immune responses in humans, a randomized open-label intervention pilot-study. (2014). https://pubmed.ncbi.nlm.nih.gov/25268806/ DOI: 10.1371/journal.pone.0108794
tissue_or_cell_type
Serum and peripheral leukocytes
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 385–396
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomised open-label intervention pilot study in 15 healthy male volunteers · source_derived_draft · unverified_draft
### bg-in-people-nothing-was-detectable In a randomised open-label intervention pilot study in 15 healthy male volunteers, subjects in the beta-glucan group ingested beta-glucan 1000 milligrams once daily for 7 days, beta-glucan was barely detectable in serum of volunteers at all time-points, and neither cytokine production nor microbicidal activity of leukocytes were affected by orally administered beta-glucan, so the present study does not support the use of oral beta-glucan to enhance innate immune responses in humans. 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: Ten healthy men took a gram a day for a week; almost none of it showed up in the blood and nothing measurable changed. organism: Human tissue_or_cell_type: Serum and peripheral leukocytes experimental_model: Randomised open-label intervention pilot study in 15 healthy male volunteers limitations: Ten treated and five control subjects, one product, one dose, seven days, and ex vivo readouts. A negative pilot of this size does not establish that all oral preparations are inactive. exposure: Oral beta-glucan 1000 milligrams once daily for 7 days against no treatment, with serial sampling evidence_span: {"source_cache": "artifacts/glucan-research/25268806.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "b5a583c465284aae8e7d3e6dd9996fafe3b6ef389c61ee2a54f066fb4701e51b", "start_char": 0, "end_char": 1307, "text_sha256": "b5a583c465284aae8e7d3e6dd9996fafe3b6ef389c61ee2a54f066fb4701e51b"} [bg-p25268806] The effects of orally administered Beta-glucan on innate immune responses in humans, a randomized open-label intervention pilot-study. (2014). https://pubmed.ncbi.nlm.nih.gov/25268806/ DOI: 10.1371/journal.pone.0108794
Complete structured claim and evidence
Dectin-1 activates Syk in macrophages and is important for Dectin-1-stimulated reactive oxygen production but not for phagocytosis, Syk activation is restricted to a subpopulation of macrophages that is in equilibrium with cells that cannot activate the pathway, and the proportion of macrophages using this signalling pathway can be modulated by cytokine treatment, so Dectin-1 signalling reveals dynamic macrophage heterogeneity in inflammatory activation potential.
Dectin-1 / CLEC7A → Spleen tyrosine kinase / SYK source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/glucan-research/15956283.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "05fbe0dae04d44d8af5946504f066c104e7a294b29d35d70463d50874ec7b41c", "start_char": 0, "end_char": 990, "text_sha256": "05fbe0dae04d44d8af5946504f066c104e7a294b29d35d70463d50874ec7b41c"}
experimental_model
Measurement of Syk activation and reactive oxygen production in macrophage subpopulations
exposure
Dectin-1 stimulation with assessment of Syk activation, reactive oxygen production and phagocytosis
limitations
The heterogeneity finding is the important limit: the pathway operated in a subpopulation in equilibrium with cells that could not use it, and the proportion shifted with cytokine treatment.
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
One kinase carries the oxidative burst but not the swallowing, and only some of the cells can run it at any moment.
primary_references
[bg-p15956283] Dectin-1 activates Syk tyrosine kinase in a dynamic subset of macrophages for reactive oxygen production. (2005). https://pubmed.ncbi.nlm.nih.gov/15956283/ DOI: 10.1182/blood-2005-03-1239
tissue_or_cell_type
Macrophage
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 398–409
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Measurement of Syk activation and reactive oxygen production in macrophage subpopulations · source_derived_draft · unverified_draft
### bg-syk-carries-the-oxidative-burst Dectin-1 activates Syk in macrophages and is important for Dectin-1-stimulated reactive oxygen production but not for phagocytosis, Syk activation is restricted to a subpopulation of macrophages that is in equilibrium with cells that cannot activate the pathway, and the proportion of macrophages using this signalling pathway can be modulated by cytokine treatment, so Dectin-1 signalling reveals dynamic macrophage heterogeneity in inflammatory activation potential. 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: One kinase carries the oxidative burst but not the swallowing, and only some of the cells can run it at any moment. organism: Mouse tissue_or_cell_type: Macrophage experimental_model: Measurement of Syk activation and reactive oxygen production in macrophage subpopulations limitations: The heterogeneity finding is the important limit: the pathway operated in a subpopulation in equilibrium with cells that could not use it, and the proportion shifted with cytokine treatment. exposure: Dectin-1 stimulation with assessment of Syk activation, reactive oxygen production and phagocytosis evidence_span: {"source_cache": "artifacts/glucan-research/15956283.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "05fbe0dae04d44d8af5946504f066c104e7a294b29d35d70463d50874ec7b41c", "start_char": 0, "end_char": 990, "text_sha256": "05fbe0dae04d44d8af5946504f066c104e7a294b29d35d70463d50874ec7b41c"} [bg-p15956283] Dectin-1 activates Syk tyrosine kinase in a dynamic subset of macrophages for reactive oxygen production. (2005). https://pubmed.ncbi.nlm.nih.gov/15956283/ DOI: 10.1182/blood-2005-03-1239
Complete structured claim and evidence
All four affected family members had a homozygous point mutation in CARD9 resulting in a premature termination codon Q295X, healthy family members had wild-type expression of the CARD9 protein while the four patients lacked wild-type expression which was associated with low numbers of interleukin-17-producing helper T cells, and functional studies based on genetic reconstitution of myeloid cells from Card9-null mice showed that the Q295X mutation impairs innate signalling from the antifungal pattern-recognition receptor dectin-1.
The homozygous CARD9 Q295X premature termination variant → Dectin-1 / CLEC7A source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/glucan-research/19864672.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "41fdf4ca9e34eac18be47ed10f5eec82966269f2595759bc97a485f91d746de3", "start_char": 0, "end_char": 1842, "text_sha256": "41fdf4ca9e34eac18be47ed10f5eec82966269f2595759bc97a485f91d746de3"}
experimental_model
Homozygosity mapping and sequencing in a consanguineous five-generation family with 36 members enrolled
exposure
Naturally occurring homozygous CARD9 Q295X premature termination, with reconstitution in Card9-null mouse myeloid cells
limitations
Human genetics with a linkage score of 3.6 and functional confirmation. It establishes the importance of the pathway in host defence; it says nothing about beta-glucan as a supplement.
nutrient_topic
Beta-glucan research collection; topical membership is not evidence of a direct clinical effect, and each preparation is recorded as its own entity with no family link joining any pair. · Beta-glucan
organism
Human
plain_language
People born without this one signalling protein get persistent fungal infections, which is how much the pathway matters.
primary_references
[bg-p19864672] A homozygous CARD9 mutation in a family with susceptibility to fungal infections. (2009). https://pubmed.ncbi.nlm.nih.gov/19864672/ DOI: 10.1056/nejmoa0810719
tissue_or_cell_type
Leukocytes
trigger_kind
machinery_impairment Imported condition classification; unverified.
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 411–422
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Homozygosity mapping and sequencing in a consanguineous five-generation family with 36 members enrolled · source_derived_draft · unverified_draft
### bg-losing-card9-costs-antifungal-defence All four affected family members had a homozygous point mutation in CARD9 resulting in a premature termination codon Q295X, healthy family members had wild-type expression of the CARD9 protein while the four patients lacked wild-type expression which was associated with low numbers of interleukin-17-producing helper T cells, and functional studies based on genetic reconstitution of myeloid cells from Card9-null mice showed that the Q295X mutation impairs innate signalling from the antifungal pattern-recognition receptor dectin-1. Condition category: machinery_impairment nutrient_topic: Beta-glucan research collection; topical membership is not evidence of a direct clinical effect, and each preparation is recorded as its own entity with no family link joining any pair. plain_language: People born without this one signalling protein get persistent fungal infections, which is how much the pathway matters. organism: Human tissue_or_cell_type: Leukocytes experimental_model: Homozygosity mapping and sequencing in a consanguineous five-generation family with 36 members enrolled limitations: Human genetics with a linkage score of 3.6 and functional confirmation. It establishes the importance of the pathway in host defence; it says nothing about beta-glucan as a supplement. exposure: Naturally occurring homozygous CARD9 Q295X premature termination, with reconstitution in Card9-null mouse myeloid cells evidence_span: {"source_cache": "artifacts/glucan-research/19864672.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "41fdf4ca9e34eac18be47ed10f5eec82966269f2595759bc97a485f91d746de3", "start_char": 0, "end_char": 1842, "text_sha256": "41fdf4ca9e34eac18be47ed10f5eec82966269f2595759bc97a485f91d746de3"} [bg-p19864672] A homozygous CARD9 mutation in a family with susceptibility to fungal infections. (2009). https://pubmed.ncbi.nlm.nih.gov/19864672/ DOI: 10.1056/nejmoa0810719
Complete structured claim and evidence
Mice lacking functional T and B lymphocytes are protected against reinfection with Candida albicans in a monocyte-dependent manner, C. albicans and fungal cell wall beta-glucans induced functional reprogramming of monocytes leading to enhanced cytokine production in vivo and in vitro, the training required the beta-glucan receptor dectin-1 and the noncanonical Raf-1 pathway, and monocyte training by beta-glucans was associated with stable changes in histone trimethylation at H3K4 which suggests the involvement of epigenetic mechanisms.
Beta-glucan → Trained immunity, an altered response to a later challenge after the first has ended source_derived_draftungraded
Experimental context and source evidence
evidence_span
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experimental_model
Reinfection protection in mice lacking functional T and B lymphocytes, with monocyte reprogramming in vitro and in vivo
exposure
Candida albicans and fungal cell wall beta-glucans as the training stimulus, with the first exposure resolved before rechallenge
limitations
The Raf-1 dependence belongs to this training protocol. It does not establish that every beta-glucan training protocol is independent of the canonical Syk route.
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
Animals with no adaptive immune system at all were still protected the second time, because their monocytes had been rewired.
primary_references
[bg-p22901542] Candida albicans infection affords protection against reinfection via functional reprogramming of monocytes. (2012). https://pubmed.ncbi.nlm.nih.gov/22901542/ DOI: 10.1016/j.chom.2012.06.006
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 424–435
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Reinfection protection in mice lacking functional T and B lymphocytes, with monocyte reprogramming in vitro and in vivo · source_derived_draft · unverified_draft
### bg-training-runs-through-raf1 Mice lacking functional T and B lymphocytes are protected against reinfection with Candida albicans in a monocyte-dependent manner, C. albicans and fungal cell wall beta-glucans induced functional reprogramming of monocytes leading to enhanced cytokine production in vivo and in vitro, the training required the beta-glucan receptor dectin-1 and the noncanonical Raf-1 pathway, and monocyte training by beta-glucans was associated with stable changes in histone trimethylation at H3K4 which suggests the involvement of epigenetic mechanisms. 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: Animals with no adaptive immune system at all were still protected the second time, because their monocytes had been rewired. organism: Mouse tissue_or_cell_type: Monocyte experimental_model: Reinfection protection in mice lacking functional T and B lymphocytes, with monocyte reprogramming in vitro and in vivo limitations: The Raf-1 dependence belongs to this training protocol. It does not establish that every beta-glucan training protocol is independent of the canonical Syk route. exposure: Candida albicans and fungal cell wall beta-glucans as the training stimulus, with the first exposure resolved before rechallenge evidence_span: {"source_cache": "artifacts/glucan-research/22901542.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "75bc4bedb7017f3d94d8f7441862392ddca229ed16f93eb528d3f9df3da66408", "start_char": 0, "end_char": 1067, "text_sha256": "75bc4bedb7017f3d94d8f7441862392ddca229ed16f93eb528d3f9df3da66408"} [bg-p22901542] Candida albicans infection affords protection against reinfection via functional reprogramming of monocytes. (2012). https://pubmed.ncbi.nlm.nih.gov/22901542/ DOI: 10.1016/j.chom.2012.06.006
Complete structured claim and evidence
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
Network-level integration of transcriptomics and metabolomics data identifies glycolysis, glutaminolysis and the cholesterol synthesis pathway as indispensable for the induction of trained immunity by beta-glucan in monocytes, accumulation of fumarate due to glutamine replenishment of the TCA cycle integrates immune and metabolic circuits to induce monocyte epigenetic reprogramming by inhibiting KDM5 histone demethylases, fumarate itself induced an epigenetic program similar to beta-glucan-induced trained immunity, and inhibition of glutaminolysis and cholesterol synthesis in mice reduced the induction of trained immunity by beta-glucan.
Fumarate → KDM5 histone demethylases source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/glucan-research/27866838.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c67ca385f9dd5e9e97432aa9141a594b7121acca8eea6eba3d0738fed75deba8", "start_char": 0, "end_char": 1031, "text_sha256": "c67ca385f9dd5e9e97432aa9141a594b7121acca8eea6eba3d0738fed75deba8"}
experimental_model
Network integration of transcriptomics and metabolomics with pathway inhibition in monocytes and in mice
exposure
Beta-glucan training with inhibition of glutaminolysis and cholesterol synthesis, and fumarate given alone
limitations
Fumarate reproducing the epigenetic programme on its own is the strongest part. The link runs through inhibition of a demethylase, which is not the same modification as an acetylation mark.
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
A metabolite piles up and jams the enzyme that would strip the marks off, so the marks stay.
primary_references
[bg-p27866838] Glutaminolysis and Fumarate Accumulation Integrate Immunometabolic and Epigenetic Programs in Trained Immunity. (2016). https://pubmed.ncbi.nlm.nih.gov/27866838/ DOI: 10.1016/j.cmet.2016.10.008
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 450–461
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Network integration of transcriptomics and metabolomics with pathway inhibition in monocytes and in mice · source_derived_draft · unverified_draft
### bg-fumarate-blocks-a-demethylase Network-level integration of transcriptomics and metabolomics data identifies glycolysis, glutaminolysis and the cholesterol synthesis pathway as indispensable for the induction of trained immunity by beta-glucan in monocytes, accumulation of fumarate due to glutamine replenishment of the TCA cycle integrates immune and metabolic circuits to induce monocyte epigenetic reprogramming by inhibiting KDM5 histone demethylases, fumarate itself induced an epigenetic program similar to beta-glucan-induced trained immunity, and inhibition of glutaminolysis and cholesterol synthesis in mice reduced the induction of trained immunity by beta-glucan. 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: A metabolite piles up and jams the enzyme that would strip the marks off, so the marks stay. organism: Human cells and mouse tissue_or_cell_type: Monocyte experimental_model: Network integration of transcriptomics and metabolomics with pathway inhibition in monocytes and in mice limitations: Fumarate reproducing the epigenetic programme on its own is the strongest part. The link runs through inhibition of a demethylase, which is not the same modification as an acetylation mark. exposure: Beta-glucan training with inhibition of glutaminolysis and cholesterol synthesis, and fumarate given alone evidence_span: {"source_cache": "artifacts/glucan-research/27866838.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c67ca385f9dd5e9e97432aa9141a594b7121acca8eea6eba3d0738fed75deba8", "start_char": 0, "end_char": 1031, "text_sha256": "c67ca385f9dd5e9e97432aa9141a594b7121acca8eea6eba3d0738fed75deba8"} [bg-p27866838] Glutaminolysis and Fumarate Accumulation Integrate Immunometabolic and Epigenetic Programs in Trained Immunity. (2016). https://pubmed.ncbi.nlm.nih.gov/27866838/ DOI: 10.1016/j.cmet.2016.10.008
Complete structured claim and evidence
Activation of the cholesterol synthesis pathway but not the synthesis of cholesterol itself is essential for training of myeloid cells, rather the metabolite mevalonate is the mediator of training via activation of IGF1-R and mTOR and subsequent histone modifications in inflammatory pathways, statins which block mevalonate generation prevent trained immunity induction, and monocytes of patients with hyper immunoglobulin D syndrome who are mevalonate kinase deficient and accumulate mevalonate have a constitutive trained immunity phenotype at both immunological and epigenetic levels.
Mevalonate → 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/29328908.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c7d8052926f6be1dad87fedf0023f60ac5441b04f9b8e180c4b1e07edc83eb03", "start_char": 0, "end_char": 1173, "text_sha256": "c7d8052926f6be1dad87fedf0023f60ac5441b04f9b8e180c4b1e07edc83eb03"}
experimental_model
Pharmacological and genetic dissection of the cholesterol synthesis pathway, with monocytes from patients accumulating mevalonate
exposure
Training of myeloid cells with statins to block mevalonate generation, and monocytes from mevalonate kinase deficient patients
limitations
The patient arm is a natural experiment in the opposite direction, which is what makes the mevalonate assignment convincing. The statin result is inhibition of an induced laboratory response.
nutrient_topic
Beta-glucan research collection; topical membership is not evidence of a direct clinical effect, and each preparation is recorded as its own entity with no family link joining any pair. · Beta-glucan
organism
Human
plain_language
It is the intermediate and not the cholesterol that does the training, and people who cannot clear that intermediate are permanently trained.
primary_references
[bg-p29328908] Metabolic Induction of Trained Immunity through the Mevalonate Pathway. (2018). https://pubmed.ncbi.nlm.nih.gov/29328908/ DOI: 10.1016/j.cell.2017.11.025
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 463–474
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Pharmacological and genetic dissection of the cholesterol synthesis pathway, with monocytes from patients accumulating mevalonate · source_derived_draft · unverified_draft
### bg-mevalonate-not-cholesterol-trains Activation of the cholesterol synthesis pathway but not the synthesis of cholesterol itself is essential for training of myeloid cells, rather the metabolite mevalonate is the mediator of training via activation of IGF1-R and mTOR and subsequent histone modifications in inflammatory pathways, statins which block mevalonate generation prevent trained immunity induction, and monocytes of patients with hyper immunoglobulin D syndrome who are mevalonate kinase deficient and accumulate mevalonate have a constitutive trained immunity phenotype at both immunological and epigenetic levels. 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: It is the intermediate and not the cholesterol that does the training, and people who cannot clear that intermediate are permanently trained. organism: Human tissue_or_cell_type: Monocyte experimental_model: Pharmacological and genetic dissection of the cholesterol synthesis pathway, with monocytes from patients accumulating mevalonate limitations: The patient arm is a natural experiment in the opposite direction, which is what makes the mevalonate assignment convincing. The statin result is inhibition of an induced laboratory response. exposure: Training of myeloid cells with statins to block mevalonate generation, and monocytes from mevalonate kinase deficient patients evidence_span: {"source_cache": "artifacts/glucan-research/29328908.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c7d8052926f6be1dad87fedf0023f60ac5441b04f9b8e180c4b1e07edc83eb03", "start_char": 0, "end_char": 1173, "text_sha256": "c7d8052926f6be1dad87fedf0023f60ac5441b04f9b8e180c4b1e07edc83eb03"} [bg-p29328908] Metabolic Induction of Trained Immunity through the Mevalonate Pathway. (2018). https://pubmed.ncbi.nlm.nih.gov/29328908/ DOI: 10.1016/j.cell.2017.11.025
Complete structured claim and evidence
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
Oat beta-glucan in doses at or above 3 grams per day reduced low-density lipoprotein and total cholesterol relative to control by 0.25 mmol/L with 95% CI 0.20 to 0.30 and 0.30 mmol/L with 95% CI 0.24 to 0.35 respectively, there was no significant effect on high-density lipoprotein cholesterol or triglycerides and no evidence that dose across a range of 3.0 to 12.4 grams per day or duration of treatment from 2 to 12 weeks influenced the results, and LDL cholesterol lowering was significantly greater with higher baseline LDL cholesterol.
Oat mixed-linkage beta-(1->3)/(1->4)-glucan → LDL cholesterol concentration source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/glucan-research/25411276.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "33075c61a20f22975ba8719b6ef8834ce254f1d4e3ede6ca5d89cd4d81a82b28", "start_char": 0, "end_char": 2072, "text_sha256": "33075c61a20f22975ba8719b6ef8834ce254f1d4e3ede6ca5d89cd4d81a82b28"}
experimental_model
Random-effects meta-analysis and meta-regression of 28 randomised controlled trials at or above 3 grams per day
exposure
Oat beta-glucan at 3.0 to 12.4 grams per day against an appropriate control for 2 to 12 weeks
limitations
A meta-analysis with some indication of heterogeneity. The diabetes subgroup rests on few studies, and in-house study reports from a commercial source were among those searched.
nutrient_topic
Beta-glucan research collection; topical membership is not evidence of a direct clinical effect, and each preparation is recorded as its own entity with no family link joining any pair. · Beta-glucan
organism
Human
plain_language
Three grams a day takes about a quarter of a millimole off the harmful cholesterol and leaves the other lipids alone.
primary_references
[bg-p25411276] Cholesterol-lowering effects of oat β-glucan: a meta-analysis of randomized controlled trials. (2014). https://pubmed.ncbi.nlm.nih.gov/25411276/ DOI: 10.3945/ajcn.114.086108
tissue_or_cell_type
Serum lipids
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 489–500
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Random-effects meta-analysis and meta-regression of 28 randomised controlled trials at or above 3 grams per day · source_derived_draft · unverified_draft
### bg-oat-glucan-lowers-ldl Oat beta-glucan in doses at or above 3 grams per day reduced low-density lipoprotein and total cholesterol relative to control by 0.25 mmol/L with 95% CI 0.20 to 0.30 and 0.30 mmol/L with 95% CI 0.24 to 0.35 respectively, there was no significant effect on high-density lipoprotein cholesterol or triglycerides and no evidence that dose across a range of 3.0 to 12.4 grams per day or duration of treatment from 2 to 12 weeks influenced the results, and LDL cholesterol lowering was significantly greater with higher baseline LDL cholesterol. 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: Three grams a day takes about a quarter of a millimole off the harmful cholesterol and leaves the other lipids alone. organism: Human tissue_or_cell_type: Serum lipids experimental_model: Random-effects meta-analysis and meta-regression of 28 randomised controlled trials at or above 3 grams per day limitations: A meta-analysis with some indication of heterogeneity. The diabetes subgroup rests on few studies, and in-house study reports from a commercial source were among those searched. exposure: Oat beta-glucan at 3.0 to 12.4 grams per day against an appropriate control for 2 to 12 weeks evidence_span: {"source_cache": "artifacts/glucan-research/25411276.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "33075c61a20f22975ba8719b6ef8834ce254f1d4e3ede6ca5d89cd4d81a82b28", "start_char": 0, "end_char": 2072, "text_sha256": "33075c61a20f22975ba8719b6ef8834ce254f1d4e3ede6ca5d89cd4d81a82b28"} [bg-p25411276] Cholesterol-lowering effects of oat β-glucan: a meta-analysis of randomized controlled trials. (2014). https://pubmed.ncbi.nlm.nih.gov/25411276/ DOI: 10.3945/ajcn.114.086108
Complete structured claim and evidence
A median dose of 3.5 grams per day of oat beta-glucan significantly lowered LDL-cholesterol by -0.19 with 95% CI -0.23 to -0.14 mmol/l, non-HDL-cholesterol by -0.20 with 95% CI -0.26 to -0.15 mmol/l and apoB by -0.03 with 95% CI -0.05 to -0.02 g/l compared with control interventions, and there was evidence for considerable unexplained heterogeneity in the analysis of LDL-cholesterol with I-squared of 79% and non-HDL-cholesterol with I-squared of 99%.
Oat mixed-linkage beta-(1->3)/(1->4)-glucan → Circulating apolipoprotein B concentration source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/glucan-research/27724985.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a764416442dac76f7e70e8b6a509b5913693d6a8f7b95cd03beb4567f5b5c9f3", "start_char": 0, "end_char": 1647, "text_sha256": "a764416442dac76f7e70e8b6a509b5913693d6a8f7b95cd03beb4567f5b5c9f3"}
experimental_model
Systematic review and random-effects meta-analysis of 58 randomised controlled trials in 3974 participants
exposure
Diets enriched with oat beta-glucan at a median 3.5 grams per day for at least three weeks
limitations
Considerable unexplained heterogeneity, with I-squared of 79 percent for LDL and 99 percent for non-HDL cholesterol. These are pooled estimates, not the expected effect of any particular product.
nutrient_topic
Beta-glucan research collection; topical membership is not evidence of a direct clinical effect, and each preparation is recorded as its own entity with no family link joining any pair. · Beta-glucan
organism
Human
plain_language
The particle count falls too, not just the cholesterol carried in it.
primary_references
[bg-p27724985] The effect of oat β-glucan on LDL-cholesterol, non-HDL-cholesterol and apoB for CVD risk reduction: a systematic review and meta-analysis of randomised-controlled trials. (2016). https://pubmed.ncbi.nlm.nih.gov/27724985/ DOI: 10.1017/s000711451600341x
tissue_or_cell_type
Serum lipoproteins
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 502–513
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Systematic review and random-effects meta-analysis of 58 randomised controlled trials in 3974 participants · source_derived_draft · unverified_draft
### bg-apob-and-non-hdl-move-too A median dose of 3.5 grams per day of oat beta-glucan significantly lowered LDL-cholesterol by -0.19 with 95% CI -0.23 to -0.14 mmol/l, non-HDL-cholesterol by -0.20 with 95% CI -0.26 to -0.15 mmol/l and apoB by -0.03 with 95% CI -0.05 to -0.02 g/l compared with control interventions, and there was evidence for considerable unexplained heterogeneity in the analysis of LDL-cholesterol with I-squared of 79% and non-HDL-cholesterol with I-squared of 99%. 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 particle count falls too, not just the cholesterol carried in it. organism: Human tissue_or_cell_type: Serum lipoproteins experimental_model: Systematic review and random-effects meta-analysis of 58 randomised controlled trials in 3974 participants limitations: Considerable unexplained heterogeneity, with I-squared of 79 percent for LDL and 99 percent for non-HDL cholesterol. These are pooled estimates, not the expected effect of any particular product. exposure: Diets enriched with oat beta-glucan at a median 3.5 grams per day for at least three weeks evidence_span: {"source_cache": "artifacts/glucan-research/27724985.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a764416442dac76f7e70e8b6a509b5913693d6a8f7b95cd03beb4567f5b5c9f3", "start_char": 0, "end_char": 1647, "text_sha256": "a764416442dac76f7e70e8b6a509b5913693d6a8f7b95cd03beb4567f5b5c9f3"} [bg-p27724985] The effect of oat β-glucan on LDL-cholesterol, non-HDL-cholesterol and apoB for CVD risk reduction: a systematic review and meta-analysis of randomised-controlled trials. (2016). https://pubmed.ncbi.nlm.nih.gov/27724985/ DOI: 10.1017/s000711451600341x
Complete structured claim and evidence
LDL cholesterol was significantly less with 3 g high molecular weight, 4 g medium molecular weight and 3 g medium molecular weight oat beta-glucan cereals than with the wheat-fiber cereal by 0.21 or 5.5%, 0.26 or 6.5% and 0.19 or 4.7% mmol/L respectively, however the effect of 4 g low molecular weight oat beta-glucan per day at 0.10 mmol/L was not significant, log of molecular weight times the amount solubilized was a significant determinant of LDL cholesterol, and efficacy was reduced by 50% when molecular weight was reduced to 210,000 g/mol.
Molecular weight of a glucan polymer → LDL cholesterol concentration source_derived_draftungraded
Experimental context and source evidence
availability_state
biomarker_context Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/glucan-research/20660224.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "dbd9787f6688f544bb47e44be561d20ec653daf5627f9022ac1302249924daf0", "start_char": 0, "end_char": 2139, "text_sha256": "dbd9787f6688f544bb47e44be561d20ec653daf5627f9022ac1302249924daf0"}
experimental_model
Double-blind parallel-design multicentre trial randomising 367 people across four molecular weights and two doses
exposure
Extruded cereal delivering 3 or 4 grams per day of oat beta-glucan at molecular weights of 2,210,000, 850,000, 530,000 or 210,000 grams per mole for four weeks
limitations
The comparator is a wheat-fibre cereal and 345 of 367 completed. A nonsignificant estimate in one arm is not a demonstration of no effect.
nutrient_topic
Beta-glucan research collection; topical membership is not evidence of a direct clinical effect, and each preparation is recorded as its own entity with no family link joining any pair. · Beta-glucan
organism
Human
plain_language
Cutting the polymer into shorter pieces halved what it did, even at a higher dose.
primary_references
[bg-p20660224] Physicochemical properties of oat β-glucan influence its ability to reduce serum LDL cholesterol in humans: a randomized clinical trial. (2010). https://pubmed.ncbi.nlm.nih.gov/20660224/ DOI: 10.3945/ajcn.2010.29174
tissue_or_cell_type
Serum LDL cholesterol
trigger_kind
biomarker_context Imported condition classification; unverified.
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 515–526
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Double-blind parallel-design multicentre trial randomising 367 people across four molecular weights and two doses · source_derived_draft · unverified_draft
### bg-depolymerising-halves-the-effect LDL cholesterol was significantly less with 3 g high molecular weight, 4 g medium molecular weight and 3 g medium molecular weight oat beta-glucan cereals than with the wheat-fiber cereal by 0.21 or 5.5%, 0.26 or 6.5% and 0.19 or 4.7% mmol/L respectively, however the effect of 4 g low molecular weight oat beta-glucan per day at 0.10 mmol/L was not significant, log of molecular weight times the amount solubilized was a significant determinant of LDL cholesterol, and efficacy was reduced by 50% when molecular weight was reduced to 210,000 g/mol. Condition category: biomarker_context 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: Cutting the polymer into shorter pieces halved what it did, even at a higher dose. organism: Human tissue_or_cell_type: Serum LDL cholesterol experimental_model: Double-blind parallel-design multicentre trial randomising 367 people across four molecular weights and two doses limitations: The comparator is a wheat-fibre cereal and 345 of 367 completed. A nonsignificant estimate in one arm is not a demonstration of no effect. exposure: Extruded cereal delivering 3 or 4 grams per day of oat beta-glucan at molecular weights of 2,210,000, 850,000, 530,000 or 210,000 grams per mole for four weeks evidence_span: {"source_cache": "artifacts/glucan-research/20660224.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "dbd9787f6688f544bb47e44be561d20ec653daf5627f9022ac1302249924daf0", "start_char": 0, "end_char": 2139, "text_sha256": "dbd9787f6688f544bb47e44be561d20ec653daf5627f9022ac1302249924daf0"} [bg-p20660224] Physicochemical properties of oat β-glucan influence its ability to reduce serum LDL cholesterol in humans: a randomized clinical trial. (2010). https://pubmed.ncbi.nlm.nih.gov/20660224/ DOI: 10.3945/ajcn.2010.29174
Complete structured claim and evidence
LDL cholesterol after 4 weeks was influenced by baseline LDL cholesterol and treatment but not ethnicity with p = 0.74, in all subjects compared to control the three bioactive arms reduced LDL cholesterol significantly by 4.8 to 6.5% while the 4 gram low molecular weight arm had no effect, and the bioactive oat beta-glucan treatments reduced LDL cholesterol by a combined mean of 0.18 mmol/L or 4.8% in Caucasians, a value not significantly different from the 0.37 mmol/L or 10.3% reduction in non-Caucasians, with insufficient power to determine if the magnitude differed by ethnicity.
Oat mixed-linkage beta-(1->3)/(1->4)-glucan → LDL cholesterol concentration source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/glucan-research/22118569.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e1f7121d5a128b1e43ab60ba66394c7ca094617309c976e0b4c8c92ac46b4f23", "start_char": 0, "end_char": 1812, "text_sha256": "e1f7121d5a128b1e43ab60ba66394c7ca094617309c976e0b4c8c92ac46b4f23"}
experimental_model
Post-hoc analysis of the same four-week multicentre trial by participant ethnicity
exposure
The same oat beta-glucan molecular weight and dose arms, analysed in Caucasian and non-Caucasian subgroups
limitations
A post-hoc subgroup analysis of a trial designed to answer a different question, and the authors state it was underpowered to detect a difference between the groups.
nutrient_topic
Beta-glucan research collection; topical membership is not evidence of a direct clinical effect, and each preparation is recorded as its own entity with no family link joining any pair. · Beta-glucan
organism
Human
plain_language
The effect showed up in both groups, and the trial was too small to say whether it is bigger in one.
primary_references
[bg-p22118569] Bioactive oat β-glucan reduces LDL cholesterol in Caucasians and non-Caucasians. (2011). https://pubmed.ncbi.nlm.nih.gov/22118569/ DOI: 10.1186/1475-2891-10-130
tissue_or_cell_type
Serum LDL cholesterol
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 528–539
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Post-hoc analysis of the same four-week multicentre trial by participant ethnicity · source_derived_draft · unverified_draft
### bg-the-effect-is-not-ethnicity-specific LDL cholesterol after 4 weeks was influenced by baseline LDL cholesterol and treatment but not ethnicity with p = 0.74, in all subjects compared to control the three bioactive arms reduced LDL cholesterol significantly by 4.8 to 6.5% while the 4 gram low molecular weight arm had no effect, and the bioactive oat beta-glucan treatments reduced LDL cholesterol by a combined mean of 0.18 mmol/L or 4.8% in Caucasians, a value not significantly different from the 0.37 mmol/L or 10.3% reduction in non-Caucasians, with insufficient power to determine if the magnitude differed by ethnicity. 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 effect showed up in both groups, and the trial was too small to say whether it is bigger in one. organism: Human tissue_or_cell_type: Serum LDL cholesterol experimental_model: Post-hoc analysis of the same four-week multicentre trial by participant ethnicity limitations: A post-hoc subgroup analysis of a trial designed to answer a different question, and the authors state it was underpowered to detect a difference between the groups. exposure: The same oat beta-glucan molecular weight and dose arms, analysed in Caucasian and non-Caucasian subgroups evidence_span: {"source_cache": "artifacts/glucan-research/22118569.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e1f7121d5a128b1e43ab60ba66394c7ca094617309c976e0b4c8c92ac46b4f23", "start_char": 0, "end_char": 1812, "text_sha256": "e1f7121d5a128b1e43ab60ba66394c7ca094617309c976e0b4c8c92ac46b4f23"} [bg-p22118569] Bioactive oat β-glucan reduces LDL cholesterol in Caucasians and non-Caucasians. (2011). https://pubmed.ncbi.nlm.nih.gov/22118569/ DOI: 10.1186/1475-2891-10-130
Complete structured claim and evidence
Native oat bran increased median excretion of bile acids by 144%, cholesterol excretion remained unchanged while cholesterol absorption decreased by 19% and the sum of bile acid and cholesterol excretion increased by 40% compared with hydrolysed oat bran, 7-alpha-hydroxy-4-cholesten-3-one reflecting bile acid synthesis increased by 57% within 24 hours of consumption while serum lathosterol concentration reflecting cholesterol synthesis increased by 12%, and these effects could possibly be explained by entrapment of whole micelles in the gut owing to higher viscosity.
Oat mixed-linkage beta-(1->3)/(1->4)-glucan → Faecal bile acid excretion source_derived_draftungraded
Experimental context and source evidence
availability_state
biomarker_context Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/glucan-research/17251929.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "96f0086004af03cea2b782fa14daef71ac29df5df3f790a2291fe375151c87b5", "start_char": 0, "end_char": 1618, "text_sha256": "96f0086004af03cea2b782fa14daef71ac29df5df3f790a2291fe375151c87b5"}
experimental_model
Crossover ileostomy study in nine volunteers with direct measurement of ileal output
exposure
Seventy-five grams of extruded oat bran cereal daily providing 11.6 grams of native or enzymatically hydrolysed beta-glucans over two 3-day periods
limitations
Nine ileostomy volunteers, which is what makes direct measurement of what leaves the small intestine possible. The comparator is the same material depolymerised, so the difference is attributable to the polymer rather than to the food.
nutrient_topic
Beta-glucan research collection; topical membership is not evidence of a direct clinical effect, and each preparation is recorded as its own entity with no family link joining any pair. · Beta-glucan
organism
Human
plain_language
The intact polymer swept bile acids out of the small intestine within a day, and the liver started making replacements.
primary_references
[bg-p17251929] Oat bran rapidly increases bile acid excretion and bile acid synthesis: an ileostomy study. (2007). https://pubmed.ncbi.nlm.nih.gov/17251929/ DOI: 10.1038/sj.ejcn.1602607
tissue_or_cell_type
Terminal ileum and serum
trigger_kind
biomarker_context Imported condition classification; unverified.
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 541–552
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Crossover ileostomy study in nine volunteers with direct measurement of ileal output · source_derived_draft · unverified_draft
### bg-viscosity-drives-out-bile-acids Native oat bran increased median excretion of bile acids by 144%, cholesterol excretion remained unchanged while cholesterol absorption decreased by 19% and the sum of bile acid and cholesterol excretion increased by 40% compared with hydrolysed oat bran, 7-alpha-hydroxy-4-cholesten-3-one reflecting bile acid synthesis increased by 57% within 24 hours of consumption while serum lathosterol concentration reflecting cholesterol synthesis increased by 12%, and these effects could possibly be explained by entrapment of whole micelles in the gut owing to higher viscosity. Condition category: biomarker_context 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 intact polymer swept bile acids out of the small intestine within a day, and the liver started making replacements. organism: Human tissue_or_cell_type: Terminal ileum and serum experimental_model: Crossover ileostomy study in nine volunteers with direct measurement of ileal output limitations: Nine ileostomy volunteers, which is what makes direct measurement of what leaves the small intestine possible. The comparator is the same material depolymerised, so the difference is attributable to the polymer rather than to the food. exposure: Seventy-five grams of extruded oat bran cereal daily providing 11.6 grams of native or enzymatically hydrolysed beta-glucans over two 3-day periods evidence_span: {"source_cache": "artifacts/glucan-research/17251929.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "96f0086004af03cea2b782fa14daef71ac29df5df3f790a2291fe375151c87b5", "start_char": 0, "end_char": 1618, "text_sha256": "96f0086004af03cea2b782fa14daef71ac29df5df3f790a2291fe375151c87b5"} [bg-p17251929] Oat bran rapidly increases bile acid excretion and bile acid synthesis: an ileostomy study. (2007). https://pubmed.ncbi.nlm.nih.gov/17251929/ DOI: 10.1038/sj.ejcn.1602607
Complete structured claim and evidence
A notable loss of beta-glucan of 0.7 to 2.4 g/d or 13 to 64% was found when intake was compared with excretion, in vitro a higher viscosity development with time for dispersions of oat bread compared with barley bread was noted which could be related to the higher molecular weight of the beta-glucan in this bread, and there seemed to be a depolymerization of the beta-glucan both during bread making and transit through the upper gastrointestinal tract.
Depolymerisation of a glucan polymer → Molecular weight of a glucan polymer source_derived_draftungraded
Experimental context and source evidence
availability_state
biomarker_context Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/glucan-research/8942412.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9d60ab74209102dfe9e61c4f1a0f45fdc2119c986e385b8174a101f9f98ae3e1", "start_char": 0, "end_char": 1172, "text_sha256": "9d60ab74209102dfe9e61c4f1a0f45fdc2119c986e385b8174a101f9f98ae3e1"}
experimental_model
Ileostomy model comparing breads made from oat bran, a barley fraction and wheat flour
exposure
Diets based on oat bread, barley bread, wheat bread or oat bread with enzymatically degraded beta-glucan, providing 12.5, 12.9, 1.1 and 4.0 grams per day
limitations
Nine ileostomy subjects. The loss is inferred by comparing intake with excretion rather than measured directly as degradation.
nutrient_topic
Beta-glucan research collection; topical membership is not evidence of a direct clinical effect, and each preparation is recorded as its own entity with no family link joining any pair. · Beta-glucan
organism
Human
plain_language
A good deal of the polymer is already broken up by the time the bread is baked, let alone eaten.
primary_references
[bg-p8942412] Mixed-linked beta-glucan from breads of different cereals is partly degraded in the human ileostomy model. (1996). https://pubmed.ncbi.nlm.nih.gov/8942412/ DOI: 10.1093/ajcn/64.6.878
tissue_or_cell_type
Terminal ileum
trigger_kind
biomarker_context Imported condition classification; unverified.
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 554–565
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Ileostomy model comparing breads made from oat bran, a barley fraction and wheat flour · source_derived_draft · unverified_draft
### bg-bread-making-already-cuts-it A notable loss of beta-glucan of 0.7 to 2.4 g/d or 13 to 64% was found when intake was compared with excretion, in vitro a higher viscosity development with time for dispersions of oat bread compared with barley bread was noted which could be related to the higher molecular weight of the beta-glucan in this bread, and there seemed to be a depolymerization of the beta-glucan both during bread making and transit through the upper gastrointestinal tract. Condition category: biomarker_context 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: A good deal of the polymer is already broken up by the time the bread is baked, let alone eaten. organism: Human tissue_or_cell_type: Terminal ileum experimental_model: Ileostomy model comparing breads made from oat bran, a barley fraction and wheat flour limitations: Nine ileostomy subjects. The loss is inferred by comparing intake with excretion rather than measured directly as degradation. exposure: Diets based on oat bread, barley bread, wheat bread or oat bread with enzymatically degraded beta-glucan, providing 12.5, 12.9, 1.1 and 4.0 grams per day evidence_span: {"source_cache": "artifacts/glucan-research/8942412.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9d60ab74209102dfe9e61c4f1a0f45fdc2119c986e385b8174a101f9f98ae3e1", "start_char": 0, "end_char": 1172, "text_sha256": "9d60ab74209102dfe9e61c4f1a0f45fdc2119c986e385b8174a101f9f98ae3e1"} [bg-p8942412] Mixed-linked beta-glucan from breads of different cereals is partly degraded in the human ileostomy model. (1996). https://pubmed.ncbi.nlm.nih.gov/8942412/ DOI: 10.1093/ajcn/64.6.878
Complete structured claim and evidence
Oat beta-glucan reduced glucose incremental area under the curve and incremental peak rise by 23% and 28% and insulin by 22% and 24% respectively, dose, molecular weight and comparator were significant effect modifiers of glucose incremental area under the curve and peak, significant linear dose-response relationships were observed for all outcomes, oat beta-glucan molecular weight above 300 kg/mol significantly reduced glucose measures whereas molecular weight below 300 kg/mol did not, outcomes were similar in participants with and without diabetes, and all outcomes had high certainty of evidence.
Oat mixed-linkage beta-(1->3)/(1->4)-glucan → Postprandial glucose incremental area under the curve source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/glucan-research/33608654.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "676672cfbc790125f3f39b9afbaa9211422f6ba82c3dc394c816268de96002c7", "start_char": 0, "end_char": 1872, "text_sha256": "676672cfbc790125f3f39b9afbaa9211422f6ba82c3dc394c816268de96002c7"}
experimental_model
Systematic review and meta-analysis of 103 acute crossover trial comparisons in 538 participants
exposure
Oat beta-glucan concentrate or oat bran added to carbohydrate-containing test meals against carbohydrate-matched controls
limitations
Acute meal responses with high certainty of evidence by GRADE. The magnitude depends on dose, molecular weight and which control meal is used, so a pooled percentage is not a prediction for any particular food.
nutrient_topic
Beta-glucan research collection; topical membership is not evidence of a direct clinical effect, and each preparation is recorded as its own entity with no family link joining any pair. · Beta-glucan
organism
Human
plain_language
Adding it to a meal takes about a quarter off the glucose rise, but only if the polymer is long enough.
primary_references
[bg-p33608654] The effect of oat β-glucan on postprandial blood glucose and insulin responses: a systematic review and meta-analysis. (2021). https://pubmed.ncbi.nlm.nih.gov/33608654/ DOI: 10.1038/s41430-021-00875-9
tissue_or_cell_type
Postprandial glucose and insulin
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 567–578
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Systematic review and meta-analysis of 103 acute crossover trial comparisons in 538 participants · source_derived_draft · unverified_draft
### bg-acute-glycaemic-response-falls Oat beta-glucan reduced glucose incremental area under the curve and incremental peak rise by 23% and 28% and insulin by 22% and 24% respectively, dose, molecular weight and comparator were significant effect modifiers of glucose incremental area under the curve and peak, significant linear dose-response relationships were observed for all outcomes, oat beta-glucan molecular weight above 300 kg/mol significantly reduced glucose measures whereas molecular weight below 300 kg/mol did not, outcomes were similar in participants with and without diabetes, and all outcomes had high certainty of evidence. 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: Adding it to a meal takes about a quarter off the glucose rise, but only if the polymer is long enough. organism: Human tissue_or_cell_type: Postprandial glucose and insulin experimental_model: Systematic review and meta-analysis of 103 acute crossover trial comparisons in 538 participants limitations: Acute meal responses with high certainty of evidence by GRADE. The magnitude depends on dose, molecular weight and which control meal is used, so a pooled percentage is not a prediction for any particular food. exposure: Oat beta-glucan concentrate or oat bran added to carbohydrate-containing test meals against carbohydrate-matched controls evidence_span: {"source_cache": "artifacts/glucan-research/33608654.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "676672cfbc790125f3f39b9afbaa9211422f6ba82c3dc394c816268de96002c7", "start_char": 0, "end_char": 1872, "text_sha256": "676672cfbc790125f3f39b9afbaa9211422f6ba82c3dc394c816268de96002c7"} [bg-p33608654] The effect of oat β-glucan on postprandial blood glucose and insulin responses: a systematic review and meta-analysis. (2021). https://pubmed.ncbi.nlm.nih.gov/33608654/ DOI: 10.1038/s41430-021-00875-9
Complete structured claim and evidence
Compared with the control cereal, 4 grams of oat beta-glucan significantly reduced glucose incremental area under the curve at 78 compared with 135 mmol x min/L and insulin at 14.0 compared with 26.8 nmol x min/L and delayed gastric emptying half-time to a geometric mean of 285 minutes compared with 105 minutes, effects not seen after the beta-glucanase-treated arm of the same dose, while subjective appetite, PYY and ghrelin responses were similar to control and pizza intakes at a subsequent unrestricted meal were not significantly different.
Viscosity developed by a solubilised glucan → Human gastric emptying time source_derived_draftungraded
Experimental context and source evidence
availability_state
biomarker_context Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/glucan-research/31828287.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "983ae8675d933c4292f9f20059e93db94587b9a570fbfb602f5921f5bd7edd70", "start_char": 0, "end_char": 2204, "text_sha256": "983ae8675d933c4292f9f20059e93db94587b9a570fbfb602f5921f5bd7edd70"}
experimental_model
Double-blind randomised crossover trial in 28 participants with gastric emptying, appetite hormones and an unrestricted test lunch
exposure
Breakfast meals matched for weight, energy and macronutrients containing 2 or 4 grams of oat beta-glucan, or 4 grams treated with beta-glucanase to reduce molecular weight and viscosity
limitations
The beta-glucanase arm is the control that isolates viscosity. The trial was designed around food intake as the primary endpoint and found no effect on it.
nutrient_topic
Beta-glucan research collection; topical membership is not evidence of a direct clinical effect, and each preparation is recorded as its own entity with no family link joining any pair. · Beta-glucan
organism
Human
plain_language
The intact polymer held the meal in the stomach nearly three times longer; the same dose chopped up did nothing.
primary_references
[bg-p31828287] Increasing oat β-glucan viscosity in a breakfast meal slows gastric emptying and reduces glycemic and insulinemic responses but has no effect on appetite, food intake, or plasma ghrelin and PYY responses in healthy humans: a randomized, placebo-controlled, crossover trial. (2020). https://pubmed.ncbi.nlm.nih.gov/31828287/ DOI: 10.1093/ajcn/nqz285
tissue_or_cell_type
Stomach and postprandial circulation
trigger_kind
biomarker_context Imported condition classification; unverified.
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 580–591
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Double-blind randomised crossover trial in 28 participants with gastric emptying, appetite hormones and an unrestricted test lunch · source_derived_draft · unverified_draft
### bg-viscosity-slows-the-stomach Compared with the control cereal, 4 grams of oat beta-glucan significantly reduced glucose incremental area under the curve at 78 compared with 135 mmol x min/L and insulin at 14.0 compared with 26.8 nmol x min/L and delayed gastric emptying half-time to a geometric mean of 285 minutes compared with 105 minutes, effects not seen after the beta-glucanase-treated arm of the same dose, while subjective appetite, PYY and ghrelin responses were similar to control and pizza intakes at a subsequent unrestricted meal were not significantly different. Condition category: biomarker_context 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 intact polymer held the meal in the stomach nearly three times longer; the same dose chopped up did nothing. organism: Human tissue_or_cell_type: Stomach and postprandial circulation experimental_model: Double-blind randomised crossover trial in 28 participants with gastric emptying, appetite hormones and an unrestricted test lunch limitations: The beta-glucanase arm is the control that isolates viscosity. The trial was designed around food intake as the primary endpoint and found no effect on it. exposure: Breakfast meals matched for weight, energy and macronutrients containing 2 or 4 grams of oat beta-glucan, or 4 grams treated with beta-glucanase to reduce molecular weight and viscosity evidence_span: {"source_cache": "artifacts/glucan-research/31828287.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "983ae8675d933c4292f9f20059e93db94587b9a570fbfb602f5921f5bd7edd70", "start_char": 0, "end_char": 2204, "text_sha256": "983ae8675d933c4292f9f20059e93db94587b9a570fbfb602f5921f5bd7edd70"} [bg-p31828287] Increasing oat β-glucan viscosity in a breakfast meal slows gastric emptying and reduces glycemic and insulinemic responses but has no effect on appetite, food intake, or plasma ghrelin and PYY responses in healthy humans: a randomized, placebo-controlled, crossover trial. (2020). https://pubmed.ncbi.nlm.nih.gov/31828287/ DOI: 10.1093/ajcn/nqz285
Complete structured claim and evidence
Oat beta-glucan increased feelings of fullness and satiety but did not affect energy and amount eaten at the ad libitum test meal, and there was a treatment by time interaction for plasma GLP-1, plasma insulin and blood glucose, with GLP-1 significantly reduced at 90 minutes, blood glucose at 30 minutes and plasma insulin at 30 and 60 minutes following the oat beta-glucan breakfast compared with the control breakfast, so four grams of high molecular weight oat beta-glucan lowers appetite but not ad libitum eating and beneficially modulates postprandial glycaemia, it does however not increase plasma GLP-1 secretion.
Oat mixed-linkage beta-(1->3)/(1->4)-glucan → Glucagon-like peptide 1 / GLP-1 source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/glucan-research/29920323.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8038ec81d42b26e4b4892cd24cd0ce26597ba28ef57296a90062428f6ecbceb4", "start_char": 0, "end_char": 1413, "text_sha256": "8038ec81d42b26e4b4892cd24cd0ce26597ba28ef57296a90062428f6ecbceb4"}
experimental_model
Randomised double-blind crossover trial in 33 normal-weight subjects with an unrestricted test meal
exposure
A breakfast containing 4 grams of high molecular weight oat beta-glucan against a control breakfast
limitations
An acute crossover in normal-weight subjects. Fullness and satiety rose without any change in what was actually eaten afterwards.
nutrient_topic
Beta-glucan research collection; topical membership is not evidence of a direct clinical effect, and each preparation is recorded as its own entity with no family link joining any pair. · Beta-glucan
organism
Human
plain_language
People felt fuller and ate the same amount, and the gut hormone usually credited for fullness went down, not up.
primary_references
[bg-p29920323] Effects of oat β-glucan consumption at breakfast on ad libitum eating, appetite, glycemia, insulinemia and GLP-1 concentrations in healthy subjects. (2018). https://pubmed.ncbi.nlm.nih.gov/29920323/ DOI: 10.1016/j.appet.2018.06.019
tissue_or_cell_type
Postprandial circulation and appetite
Beta-glucan: a structural family rather than an agent, what decides whether a bound glucan actually signals, the complement route that a cereal and a yeast preparation share, and the unequal human evidence behind each (2026-09-22) · lines 593–604
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomised double-blind crossover trial in 33 normal-weight subjects with an unrestricted test meal · source_derived_draft · unverified_draft
### bg-satiety-rises-but-glp1-falls Oat beta-glucan increased feelings of fullness and satiety but did not affect energy and amount eaten at the ad libitum test meal, and there was a treatment by time interaction for plasma GLP-1, plasma insulin and blood glucose, with GLP-1 significantly reduced at 90 minutes, blood glucose at 30 minutes and plasma insulin at 30 and 60 minutes following the oat beta-glucan breakfast compared with the control breakfast, so four grams of high molecular weight oat beta-glucan lowers appetite but not ad libitum eating and beneficially modulates postprandial glycaemia, it does however not increase plasma GLP-1 secretion. Condition category: normal nutrient_topic: Beta-glucan research collection; topical membership is not evidence of a direct clinical effect, and each preparation is recorded as its own entity with no family link joining any pair. plain_language: People felt fuller and ate the same amount, and the gut hormone usually credited for fullness went down, not up. organism: Human tissue_or_cell_type: Postprandial circulation and appetite experimental_model: Randomised double-blind crossover trial in 33 normal-weight subjects with an unrestricted test meal limitations: An acute crossover in normal-weight subjects. Fullness and satiety rose without any change in what was actually eaten afterwards. exposure: A breakfast containing 4 grams of high molecular weight oat beta-glucan against a control breakfast evidence_span: {"source_cache": "artifacts/glucan-research/29920323.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8038ec81d42b26e4b4892cd24cd0ce26597ba28ef57296a90062428f6ecbceb4", "start_char": 0, "end_char": 1413, "text_sha256": "8038ec81d42b26e4b4892cd24cd0ce26597ba28ef57296a90062428f6ecbceb4"} [bg-p29920323] Effects of oat β-glucan consumption at breakfast on ad libitum eating, appetite, glycemia, insulinemia and GLP-1 concentrations in healthy subjects. (2018). https://pubmed.ncbi.nlm.nih.gov/29920323/ DOI: 10.1016/j.appet.2018.06.019
Complete structured claim and evidence
Most of the 16 human intervention studies considered pertinent for the scientific substantiation of the claim showed that oat beta-glucans reduce postprandial blood glucose peaks when consumed as part of foods or meals rich in available carbohydrates, the Panel also took into account that oat beta-glucans did not increase postprandial glycaemic or insulinaemic responses and that the mechanism by which consumption could exert the claimed effect is well established, and the Panel concludes that a cause-and-effect relationship has been established, with foods or meals required to contain at least 30 grams of available carbohydrates per portion and at least 3 grams of beta-glucans from oats for each 30 grams of available carbohydrates in order to bear the claim.
Oat mixed-linkage beta-(1->3)/(1->4)-glucan → Postprandial glucose incremental peak rise source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/glucan-research/41726114.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "22ad4a8c479116e3d7130ddcda6f561239dc9b2048d52e29279e48bac6799a3e", "start_char": 0, "end_char": 1617, "text_sha256": "22ad4a8c479116e3d7130ddcda6f561239dc9b2048d52e29279e48bac6799a3e"}
experimental_model
European Food Safety Authority assessment of 16 human intervention studies for a new health claim
exposure
Oat beta-glucans consumed as part of foods or meals rich in available carbohydrates
limitations
A regulatory opinion that weighs an evidence base and sets conditions of use. Authorisation is a separate legal step, and the claim applies only under the stated conditions.
nutrient_topic
Beta-glucan research collection; topical membership is not evidence of a direct clinical effect, and each preparation is recorded as its own entity with no family link joining any pair. · Beta-glucan
organism
Human
plain_language
A regulator accepted the effect on the glucose peak, and attached an exact amount and an exact kind of meal to it.
primary_references
[bg-p41726114] Oat beta-glucans and reduction of postprandial glucose peak: Evaluation of a health claim pursuant to Article 13(5) of Regulation (EC) No 1924/2006. (2026). https://pubmed.ncbi.nlm.nih.gov/41726114/ DOI: 10.2903/j.efsa.2026.9942
tissue_or_cell_type
Postprandial circulation
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 606–617
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · European Food Safety Authority assessment of 16 human intervention studies for a new health claim · source_derived_draft · unverified_draft
### bg-a-claim-with-conditions Most of the 16 human intervention studies considered pertinent for the scientific substantiation of the claim showed that oat beta-glucans reduce postprandial blood glucose peaks when consumed as part of foods or meals rich in available carbohydrates, the Panel also took into account that oat beta-glucans did not increase postprandial glycaemic or insulinaemic responses and that the mechanism by which consumption could exert the claimed effect is well established, and the Panel concludes that a cause-and-effect relationship has been established, with foods or meals required to contain at least 30 grams of available carbohydrates per portion and at least 3 grams of beta-glucans from oats for each 30 grams of available carbohydrates in order to bear the claim. 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: A regulator accepted the effect on the glucose peak, and attached an exact amount and an exact kind of meal to it. organism: Human tissue_or_cell_type: Postprandial circulation experimental_model: European Food Safety Authority assessment of 16 human intervention studies for a new health claim limitations: A regulatory opinion that weighs an evidence base and sets conditions of use. Authorisation is a separate legal step, and the claim applies only under the stated conditions. exposure: Oat beta-glucans consumed as part of foods or meals rich in available carbohydrates evidence_span: {"source_cache": "artifacts/glucan-research/41726114.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "22ad4a8c479116e3d7130ddcda6f561239dc9b2048d52e29279e48bac6799a3e", "start_char": 0, "end_char": 1617, "text_sha256": "22ad4a8c479116e3d7130ddcda6f561239dc9b2048d52e29279e48bac6799a3e"} [bg-p41726114] Oat beta-glucans and reduction of postprandial glucose peak: Evaluation of a health claim pursuant to Article 13(5) of Regulation (EC) No 1924/2006. (2026). https://pubmed.ncbi.nlm.nih.gov/41726114/ DOI: 10.2903/j.efsa.2026.9942
Complete structured claim and evidence
The applicant proposed a reduction of the lowest effective dose from 4 grams to 2 grams of beta-glucans per 30 grams of available carbohydrates and submitted 21 pertinent published human intervention studies with 59 trial comparisons plus four published systematic reviews and dose-response meta-regression analyses, and in weighing the evidence the Panel considered that the human intervention studies did not consistently show a significant effect of beta-glucans from oats or barley on postprandial glucose incremental area under the curve at doses between 2 and less than 4 grams per 30 grams of available carbohydrates, concluding that a consistent effect has not been demonstrated under the conditions of use proposed.
Oat mixed-linkage beta-(1->3)/(1->4)-glucan → Postprandial glucose incremental area under the curve source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/glucan-research/40980638.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ed76af02ac95b48fc5e1dd7e51a6ba51f54b5ba01a7daa7a01ce57bdd9d68bad", "start_char": 0, "end_char": 1864, "text_sha256": "ed76af02ac95b48fc5e1dd7e51a6ba51f54b5ba01a7daa7a01ce57bdd9d68bad"}
experimental_model
European Food Safety Authority assessment of a proposal to halve the dose condition on an existing claim
exposure
Beta-glucans from oat or barley at doses between 2 and less than 4 grams per 30 grams of available carbohydrates
limitations
An assessment of a proposed change to a condition of use, based on 21 studies with 59 trial comparisons plus four published dose-response analyses. A negative conclusion about a proposed lower dose is not a finding that lower doses never act.
nutrient_topic
Beta-glucan research collection; topical membership is not evidence of a direct clinical effect, and each preparation is recorded as its own entity with no family link joining any pair. · Beta-glucan
organism
Human
plain_language
Asked to halve the amount required, the regulator looked at the trials and said the evidence did not hold at that dose.
primary_references
[bg-p40980638] Beta-glucans from oats or barley and reduction of postprandial glycaemic responses: Modification of an authorised health claim pursuant to Article 13(1) of Regulation (EC) No 1924/2006 following a request in accordance with Article 19 of Regulation (EC) No 1924/2006. (2025). https://pubmed.ncbi.nlm.nih.gov/40980638/ DOI: 10.2903/j.efsa.2025.9630
tissue_or_cell_type
Postprandial circulation
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 619–630
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · European Food Safety Authority assessment of a proposal to halve the dose condition on an existing claim · source_derived_draft · unverified_draft
### bg-the-lower-dose-was-refused The applicant proposed a reduction of the lowest effective dose from 4 grams to 2 grams of beta-glucans per 30 grams of available carbohydrates and submitted 21 pertinent published human intervention studies with 59 trial comparisons plus four published systematic reviews and dose-response meta-regression analyses, and in weighing the evidence the Panel considered that the human intervention studies did not consistently show a significant effect of beta-glucans from oats or barley on postprandial glucose incremental area under the curve at doses between 2 and less than 4 grams per 30 grams of available carbohydrates, concluding that a consistent effect has not been demonstrated under the conditions of use proposed. 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: Asked to halve the amount required, the regulator looked at the trials and said the evidence did not hold at that dose. organism: Human tissue_or_cell_type: Postprandial circulation experimental_model: European Food Safety Authority assessment of a proposal to halve the dose condition on an existing claim limitations: An assessment of a proposed change to a condition of use, based on 21 studies with 59 trial comparisons plus four published dose-response analyses. A negative conclusion about a proposed lower dose is not a finding that lower doses never act. exposure: Beta-glucans from oat or barley at doses between 2 and less than 4 grams per 30 grams of available carbohydrates evidence_span: {"source_cache": "artifacts/glucan-research/40980638.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ed76af02ac95b48fc5e1dd7e51a6ba51f54b5ba01a7daa7a01ce57bdd9d68bad", "start_char": 0, "end_char": 1864, "text_sha256": "ed76af02ac95b48fc5e1dd7e51a6ba51f54b5ba01a7daa7a01ce57bdd9d68bad"} [bg-p40980638] Beta-glucans from oats or barley and reduction of postprandial glycaemic responses: Modification of an authorised health claim pursuant to Article 13(1) of Regulation (EC) No 1924/2006 following a request in accordance with Article 19 of Regulation (EC) No 1924/2006. (2025). https://pubmed.ncbi.nlm.nih.gov/40980638/ DOI: 10.2903/j.efsa.2025.9630
Complete structured claim and evidence
The applicant identified a total of 22 references which included three meta-analyses and 19 randomised controlled trials as being pertinent to the health claim, in weighing the evidence the Panel took into account that most of the trials investigating the effects of oat beta-glucan at doses of at least 3 grams per day have shown a statistically significant decrease in LDL-cholesterol concentrations and that there was strong evidence supporting the biological plausibility of the effect, and the Panel concludes that a cause and effect relationship has been established between the consumption of oat beta-glucan and lowering of blood LDL-cholesterol concentrations, considering that in order to bear the claim foods should provide at least 3 grams of oat beta-glucan per day.
Oat mixed-linkage beta-(1->3)/(1->4)-glucan → LDL cholesterol concentration source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/glucan-research/42004118.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "dcfcf120be06e5235e076afd33caa325371eea0a3c56b74b023ea34589e19717", "start_char": 0, "end_char": 1690, "text_sha256": "dcfcf120be06e5235e076afd33caa325371eea0a3c56b74b023ea34589e19717"}
experimental_model
European Food Safety Authority assessment of three meta-analyses and 19 randomised controlled trials
exposure
Oat beta-glucan at doses of at least 3 grams per day
limitations
A regulatory opinion on a disease-risk-reduction claim. It concerns lowering of LDL cholesterol; the cardiovascular part of the wording is an inference from the lipid change and not a measured event rate in these trials.
nutrient_topic
Beta-glucan research collection; topical membership is not evidence of a direct clinical effect, and each preparation is recorded as its own entity with no family link joining any pair. · Beta-glucan
organism
Human
plain_language
The cholesterol claim cleared the same regulator, at three grams a day.
primary_references
[bg-p42004118] Scientific Opinion on the substantiation of a health claim related to oat beta glucan and lowering blood cholesterol and reduced risk of (coronary) heart disease pursuant to Article 14 of Regulation (EC) No 1924/2006. (2010). https://pubmed.ncbi.nlm.nih.gov/42004118/ DOI: 10.2903/j.efsa.2010.1885
tissue_or_cell_type
Serum LDL cholesterol
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 632–643
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · European Food Safety Authority assessment of three meta-analyses and 19 randomised controlled trials · source_derived_draft · unverified_draft
### bg-the-cholesterol-claim-was-accepted The applicant identified a total of 22 references which included three meta-analyses and 19 randomised controlled trials as being pertinent to the health claim, in weighing the evidence the Panel took into account that most of the trials investigating the effects of oat beta-glucan at doses of at least 3 grams per day have shown a statistically significant decrease in LDL-cholesterol concentrations and that there was strong evidence supporting the biological plausibility of the effect, and the Panel concludes that a cause and effect relationship has been established between the consumption of oat beta-glucan and lowering of blood LDL-cholesterol concentrations, considering that in order to bear the claim foods should provide at least 3 grams of oat beta-glucan per day. 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 cholesterol claim cleared the same regulator, at three grams a day. organism: Human tissue_or_cell_type: Serum LDL cholesterol experimental_model: European Food Safety Authority assessment of three meta-analyses and 19 randomised controlled trials limitations: A regulatory opinion on a disease-risk-reduction claim. It concerns lowering of LDL cholesterol; the cardiovascular part of the wording is an inference from the lipid change and not a measured event rate in these trials. exposure: Oat beta-glucan at doses of at least 3 grams per day evidence_span: {"source_cache": "artifacts/glucan-research/42004118.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "dcfcf120be06e5235e076afd33caa325371eea0a3c56b74b023ea34589e19717", "start_char": 0, "end_char": 1690, "text_sha256": "dcfcf120be06e5235e076afd33caa325371eea0a3c56b74b023ea34589e19717"} [bg-p42004118] Scientific Opinion on the substantiation of a health claim related to oat beta glucan and lowering blood cholesterol and reduced risk of (coronary) heart disease pursuant to Article 14 of Regulation (EC) No 1924/2006. (2010). https://pubmed.ncbi.nlm.nih.gov/42004118/ DOI: 10.2903/j.efsa.2010.1885
Complete structured claim and evidence
A three-day intervention with granola containing cereal beta-glucan improved the glycemic response and changed the gut microbiota, with circulating acetate and butyrate increasing while propionate did not, in a study in which participants consumed granolas of differing beta-glucan content in fixed sequence and in which the granolas also differed in other constituents.
Oat mixed-linkage beta-(1->3)/(1->4)-glucan → Circulating short-chain fatty acid concentrations source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/glucan-research/35578615.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "df79afd1ef3d79ffee2a9da5f5f7e487f296cca7e9ccfcda177266b08efed747", "start_char": 0, "end_char": 2197, "text_sha256": "df79afd1ef3d79ffee2a9da5f5f7e487f296cca7e9ccfcda177266b08efed747"}
experimental_model
Fixed-sequence crossover intervention with three granolas over three days each
exposure
Granola containing low, medium or high cereal beta-glucan, given in that order
limitations
Fourteen completers, a fixed sequence rather than randomised order, and granolas that differed in other constituents including inulin. Short-chain fatty acids were measured in blood while faecal samples were used for the microbiota.
nutrient_topic
Beta-glucan research collection; topical membership is not evidence of a direct clinical effect, and each preparation is recorded as its own entity with no family link joining any pair. · Beta-glucan
organism
Human
plain_language
Three days of a cereal glucan raised two of the three main fermentation acids in the blood.
primary_references
[bg-p35578615] A Three-Day Intervention With Granola Containing Cereal Beta-Glucan Improves Glycemic Response and Changes the Gut Microbiota in Healthy Individuals: A Crossover Study. (2022). https://pubmed.ncbi.nlm.nih.gov/35578615/ DOI: 10.3389/fnut.2022.796362
tissue_or_cell_type
Blood and faecal microbiota
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 645–656
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Fixed-sequence crossover intervention with three granolas over three days each · source_derived_draft · unverified_draft
### bg-circulating-scfa-rise-with-granola A three-day intervention with granola containing cereal beta-glucan improved the glycemic response and changed the gut microbiota, with circulating acetate and butyrate increasing while propionate did not, in a study in which participants consumed granolas of differing beta-glucan content in fixed sequence and in which the granolas also differed in other constituents. 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: Three days of a cereal glucan raised two of the three main fermentation acids in the blood. organism: Human tissue_or_cell_type: Blood and faecal microbiota experimental_model: Fixed-sequence crossover intervention with three granolas over three days each limitations: Fourteen completers, a fixed sequence rather than randomised order, and granolas that differed in other constituents including inulin. Short-chain fatty acids were measured in blood while faecal samples were used for the microbiota. exposure: Granola containing low, medium or high cereal beta-glucan, given in that order evidence_span: {"source_cache": "artifacts/glucan-research/35578615.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "df79afd1ef3d79ffee2a9da5f5f7e487f296cca7e9ccfcda177266b08efed747", "start_char": 0, "end_char": 2197, "text_sha256": "df79afd1ef3d79ffee2a9da5f5f7e487f296cca7e9ccfcda177266b08efed747"} [bg-p35578615] A Three-Day Intervention With Granola Containing Cereal Beta-Glucan Improves Glycemic Response and Changes the Gut Microbiota in Healthy Individuals: A Crossover Study. (2022). https://pubmed.ncbi.nlm.nih.gov/35578615/ DOI: 10.3389/fnut.2022.796362
Complete structured claim and evidence
Oat-beta-glucan enhances anti-PD-1 efficacy in murine models by selectively expanding Faecalibacterium prausnitzii, combining anti-PD-1 with either oat-beta-glucan or F. prausnitzii boosts intratumoral dendritic cell and CD8+ T cell infiltration and cytotoxic activation compared with anti-PD-1 monotherapy, metabolomics identifies F. prausnitzii-derived butyrate and indole-3-propionic acid as key mediators with butyrate activating dendritic cells via the HDAC8, H3K27ac and NF-kappa-B p65 pathway, in a colorectal cancer cohort undergoing anti-PD-1 treatment higher baseline F. prausnitzii abundance and elevated plasma butyrate and indole-3-propionic acid correlate with improved responses, and a human intervention study confirms oat-beta-glucan safety, its ability to increase butyrate and indole-3-propionic acid, and its capacity to modulate F. prausnitzii.
Oat mixed-linkage beta-(1->3)/(1->4)-glucan → Efficacy of anti-PD-1 checkpoint blockade source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/glucan-research/42214334.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1e145fb1c4163d9e0cd10a4055b68fa47de521dcf19d25253d42fc9c971d56ba", "start_char": 0, "end_char": 1310, "text_sha256": "1e145fb1c4163d9e0cd10a4055b68fa47de521dcf19d25253d42fc9c971d56ba"}
experimental_model
Murine tumour models with selective bacterial expansion and metabolomics, plus a human cohort and a human intervention study
exposure
Oat beta-glucan with anti-PD-1 checkpoint blockade in mice, and oat beta-glucan supplementation in people
limitations
The causal efficacy claim is demonstrated in mice. The human components are a correlation in a colorectal cancer cohort and an intervention study reporting safety and metabolite change, so no anticancer benefit in people is established here.
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 cereal glucan never touches the tumour; it feeds a gut bacterium whose products wake the cells that do.
primary_references
[bg-p42214334] Oat-β-glucan potentiates anti-PD-1 efficacy through Faecalibacterium prausnitzii-derived butyrate and indole-3-propionic acid. (2026). https://pubmed.ncbi.nlm.nih.gov/42214334/ DOI: 10.1016/j.chom.2026.05.002
tissue_or_cell_type
Gut microbiota and tumour microenvironment
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 658–669
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Murine tumour models with selective bacterial expansion and metabolomics, plus a human cohort and a human intervention study · source_derived_draft · unverified_draft
### bg-a-cereal-glucan-reaches-immunity Oat-beta-glucan enhances anti-PD-1 efficacy in murine models by selectively expanding Faecalibacterium prausnitzii, combining anti-PD-1 with either oat-beta-glucan or F. prausnitzii boosts intratumoral dendritic cell and CD8+ T cell infiltration and cytotoxic activation compared with anti-PD-1 monotherapy, metabolomics identifies F. prausnitzii-derived butyrate and indole-3-propionic acid as key mediators with butyrate activating dendritic cells via the HDAC8, H3K27ac and NF-kappa-B p65 pathway, in a colorectal cancer cohort undergoing anti-PD-1 treatment higher baseline F. prausnitzii abundance and elevated plasma butyrate and indole-3-propionic acid correlate with improved responses, and a human intervention study confirms oat-beta-glucan safety, its ability to increase butyrate and indole-3-propionic acid, and its capacity to modulate F. prausnitzii. 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 cereal glucan never touches the tumour; it feeds a gut bacterium whose products wake the cells that do. organism: Mouse tissue_or_cell_type: Gut microbiota and tumour microenvironment experimental_model: Murine tumour models with selective bacterial expansion and metabolomics, plus a human cohort and a human intervention study limitations: The causal efficacy claim is demonstrated in mice. The human components are a correlation in a colorectal cancer cohort and an intervention study reporting safety and metabolite change, so no anticancer benefit in people is established here. exposure: Oat beta-glucan with anti-PD-1 checkpoint blockade in mice, and oat beta-glucan supplementation in people evidence_span: {"source_cache": "artifacts/glucan-research/42214334.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1e145fb1c4163d9e0cd10a4055b68fa47de521dcf19d25253d42fc9c971d56ba", "start_char": 0, "end_char": 1310, "text_sha256": "1e145fb1c4163d9e0cd10a4055b68fa47de521dcf19d25253d42fc9c971d56ba"} [bg-p42214334] Oat-β-glucan potentiates anti-PD-1 efficacy through Faecalibacterium prausnitzii-derived butyrate and indole-3-propionic acid. (2026). https://pubmed.ncbi.nlm.nih.gov/42214334/ DOI: 10.1016/j.chom.2026.05.002
Complete structured claim and evidence

Availability and dependencies

Each situation shows the normal role first, then what the sources report under a specific condition. A shortfall in the diet, a fault in the machinery, and a low blood reading are kept separate because they are not the same thing.

When the preparation is not what the label implies

Condition: biomarker_context · Variation between commercial preparations in molecular weight, solution conformation, particle size and low molecular weight contaminants, none of which the product name records.

Normal role: A beta-glucan engages Dectin-1 through runs of beta-(1->3)-linked glucose presented in ordered, multivalent form, and the receptor clusters and signals inward.

Recorded consequence: Activity is not merely weaker but can reverse. Of five laminarin preparations from three suppliers, two were Dectin-1 agonists and two were antagonists, a fifth changed from antagonist to agonist once its low molecular weight material was dialysed away, and binding affinity predicted none of it. Denaturing a glucan removes its ability to signal while leaving its binding affinity unchanged.

Scope: Commercial preparations of a single named glucan, and defined fungal glucans of varied conformation

When complement or its receptor is missing

Condition: machinery_impairment · Absence of serum C3, absence of leukocyte CR3, or depletion of granulocytes.

Normal role: A beta-glucan primes CR3 on granulocytes and natural killer cells so that they will kill a target already coated with the complement fragment iC3b, which an antitumour antibody supplies by activating complement on the tumour surface.

Recorded consequence: The antitumour effect is abolished rather than reduced. Mice deficient in C3 or in CR3 showed therapeutic failure with both an oral barley mixed-linkage glucan and an oral yeast branched glucan, and no response occurred in granulocyte-depleted animals.

Scope: Mouse tumour models with genetic deficiency and cell depletion

When the receptor cannot signal inward

Condition: machinery_impairment · Inherited homozygous loss of CARD9, such as the Q295X premature termination variant.

Normal role: Recognition of fungal beta-glucan by Dectin-1 is relayed inward through a signalling module that includes CARD9, supporting antifungal defence and the development of interleukin-17-producing helper T cells.

Recorded consequence: Recognition is intact but the signal does not arrive. Affected people have low numbers of Th17 cells and persistent or recurrent candidal infection of mucosa and skin, and reconstitution experiments show the variant impairs innate signalling from Dectin-1 itself.

Scope: A consanguineous five-generation family with functional confirmation in reconstituted myeloid cells

When the polymer has been cut up

Condition: biomarker_context · Enzymatic hydrolysis, processing, or milling and baking, any of which shorten the chains. Bread-making alone accounts for a loss of 13 to 64 percent before the food is eaten.

Normal role: Cereal beta-glucan acts in the gut as a physical agent. Dissolved at high molecular weight it develops viscosity, which slows gastric emptying, impedes the reabsorption of bile acid micelles and blunts the rise in glucose after a meal.

Recorded consequence: The effects fall away with the viscosity. A four-gram dose at 210,000 g/mol lowered LDL cholesterol only half as much as three grams at high molecular weight and did not reach significance; a beta-glucanase-treated breakfast of the same dose neither delayed gastric emptying nor reduced the glucose response; and hydrolysed oat bran did not drive out bile acids the way the native polymer did.

Scope: Human trials and ileostomy studies of oat and barley preparations

The sources

Every document behind this chapter is preserved word for word. Open one to read it in full with its recorded conflicts marked in place.

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)AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · unverified_draftRead preserved source

Recorded disagreements

Where two sources say different things, both are kept and the difference is explained. You can discuss a disagreement or propose a mechanism that might account for it.

Do cereal and fungal beta-glucans have separate mechanisms, one metabolic and one immune?The evidence bases do differ, and sharply. What cereal beta-glucan has in humans is modest LDL lowering and a reduced acute glycaemic response, both established across dozens of randomised trials and both accepted by a regulator with an exact dose attached. What the fungal and yeast preparations have is receptor pharmacology, trained immunity and oncology trials. That difference is real and it is what should govern any practical statement. It is not, however, a boundary between two kinds of molecule. One experiment gave mice oral barley mixed-linkage glucan and oral yeast branched glucan in the same protocol and found that both potentiated an antitumour antibody, with therapeutic failure in C3-deficient and CR3-deficient animals in each case, so the two converged on one complement-dependent route. A separate line reaches immunity from the other direction: oat beta-glucan improved anti-PD-1 efficacy in mice by expanding a gut bacterium whose butyrate and indole-3-propionic acid activated dendritic cells and CD8 T cells. The binding record points the same way, since pure beta-glucans from barley blocked the CR3 lectin site alongside those from yeast, mushroom and seaweed. The defensible statement is that the mechanisms overlap and the human evidence does not: a cereal glucan is not immunologically inert, and an immune effect in a mouse is not a treatment for a person.Read the recorded disagreement
Does an oral beta-glucan produce a systemic effect?In rodents it plainly does. Three water-soluble glucans given by mouth appeared in plasma with measurable peaks, were internalised by intestinal epithelium and gut-associated lymphoid tissue, raised gut-associated Dectin-1 and TLR2 expression, raised systemic interleukin-12 by 151% and improved survival against two organisms. A separate mouse study tracked labelled oral glucan through macrophages to the marrow and showed granulocytes acquiring the processed fragments. In the one human oral dosing study recorded here, a gram a day for seven days left beta-glucan barely detectable in serum and changed neither ex vivo cytokine production nor microbicidal activity. The human study is a fifteen-person open-label pilot of one product at one dose with ex vivo readouts, so it is not a refutation of every oral preparation; equally, the rodent work cannot be read across to people, and the two oncology trials here that used oral glucan measured clinical and antibody endpoints rather than systemic exposure. What the records jointly establish is that oral bioavailability and systemic effect are preparation-specific and species-specific questions that have to be measured rather than assumed.Read the recorded disagreement
Is it being particulate that lets a glucan signal through Dectin-1, or is it conformation?The phagocytic synapse study is unambiguous within its own design: Dectin-1 bound both soluble and particulate polymers but only particulate ones produced a signal, and the mechanism offered is that particles cluster the receptor into a contact that excludes the CD45 and CD148 phosphatases. A later study of defined fungal glucans reframes the variable. There, glucans of similar Dectin-1 affinity differed in agonistic potential according to how much helical structure they held in solution, denaturation removed the agonism without changing the affinity, and receptor aggregation tracked structure content rather than physical state. The two are reconcilable if what a particle supplies is one way of achieving ordered multivalent presentation and a highly structured soluble polymer is another. That reading is a synthesis rather than a measurement. Neither paper tested the preparations of the other, the later work followed a single receptor isoform, and the aggregates it recorded were small clusters of a few receptors rather than the synapse-scale structures of the earlier study.Read the recorded disagreement
Which receptor is the leukocyte beta-glucan receptor?Two papers a few years apart each announce that they have identified the long-sought leukocyte beta-glucan receptor, and they name different molecules. The earlier concludes that CR3 serves that role through a cation-independent lectin site C-terminal to the CD11b I-domain, with binding blocked by pure beta-glucans from four different sources. The later finds that non-opsonic zymosan binding is entirely unaffected by genetic CD11b deficiency or by a blocking anti-CR3 antibody, and that Dectin-1 is almost exclusively responsible, describing this as resolving the controversy. The records are not actually incompatible once the endpoints are separated: the first measured binding and inhibition, the second measured non-opsonic recognition of a particle, and a receptor can bind a ligand without being the one that mediates a given cellular response. Both receptors carry claims elsewhere in this collection, and the antitumour records depend on CR3 while the antifungal signalling records depend on Dectin-1. The highest-affinity ligand in the CR3 work was also not a pure beta-glucan but a mannose-rich zymosan polysaccharide, which weakens any reading of it as a pure glucan affinity.Read the recorded disagreement

Open questions in this collection

Questions the curators could not answer from the sources in front of them, kept here with the reason each one is still open. These are gaps in this collection, not findings or proof that no one has studied them.

What the 27 percent of glucan phosphate remaining in serum at 24 hours is a percentage of.The abstract states that 27 plus or minus 3 percent of the glucan phosphate and 20 plus or minus 7 percent of the laminarin remained in the serum at 24 hours without giving the denominator. A percentage of the peak plasma concentration and a percentage of the administered dose are very different pharmacokinetic statements, and the second would not be supportable for an oral polysaccharide. No claim here rests on either reading.
Whether the dectin-1 rs3901533 polymorphism is a predictive biomarker rather than an exploratory association.The same variant is associated with better overall survival in the phase I oral glucan trial and with antibody titre in the randomised phase 2 trial, which is more than a single-study finding. Neither trial was designed to test it, both analyses are secondary, and no trial in this collection prospectively selected patients by genotype.
Whether a pre-treatment anti-beta-glucan antibody level of 20 micrograms per millilitre should select patients for treatment.The threshold comes from a healthy volunteer pharmacodynamic study in which it separated subjects who did and did not respond immunologically, and it also separated those who did and did not have infusion reactions. No study here selected patients by that level and measured a tumour outcome.
Why premedication that reduced infusion reactions also inhibited the cytokine response, and whether that matters.The healthy volunteer study reports both effects together. Whether suppressing the cytokine response also suppresses antitumour activity is not tested by any record in this collection, and it cannot be inferred from a pharmacodynamic measurement.
Whether the short-chain fatty acids that rise after cereal glucan are what lowers glucose or cholesterol in people.The granola study measured circulating acetate and butyrate alongside an improved glycaemic response, but it was a fixed-sequence study of fourteen completers whose granolas differed in other constituents including inulin, and it measured association rather than mediation. The viscosity records in this collection offer a complete physical explanation for the acute glucose effect that does not require fermentation at all.
Whether the molecular weight threshold for the acute glycaemic effect is the same physical property as the one for LDL lowering.The postprandial meta-analysis found that oat beta-glucan above 300 kg/mol reduced glucose measures while below it did not, and the four-week lipid trial found efficacy halved at 210,000 g/mol with the product of molecular weight and solubilised amount as the significant determinant. Both point at viscosity, but the two thresholds come from different endpoints over different timescales and no record here measures viscosity as a common cause of both.
Whether an immobilised soluble glucan can signal through Dectin-1.This bears directly on the recorded disagreement about what makes the receptor fire, because immobilisation supplies ordered multivalent presentation without a particle. The abstracts preserved here do not report such an experiment, so the collection cannot settle it either way.
Whether orally administered beta-glucan reaches human marrow progenitors at all.The progenitor work is in mice given beta-glucan directly, and the trafficking record in this collection is also a mouse study. The one human oral dosing study here found beta-glucan barely detectable in serum and no change in leukocyte function, so the step from a swallowed dose to a marrow progenitor is not demonstrated in people by anything recorded here.
Whether the Raf-1 dependence of trained immunity generalises beyond the protocol that found it.Acute Dectin-1 signalling in this collection runs through Syk, and human CARD9 deficiency establishes the importance of that route in host defence, while the training protocol recorded here required the noncanonical Raf-1 pathway instead. No record here tests a second training protocol against both routes, so acute and trained programmes are recorded as interacting but distinguishable rather than as one pathway with a long tail.
Whether statin or metformin treatment measurably blunts trained immunity in people taking them.Both drugs inhibited the induction of trained immunity in the experimental systems recorded here, which establishes that the pathways interact. Neither record measured an outcome in treated patients, and nothing in this collection supports altering prescribed lipid-lowering or glucose-lowering treatment to preserve an immune response of unproven clinical value.

Chapters are assembled from supplied drafts and curated literature summaries. Statements remain unverified against the primary studies, and the ledger is not medical advice.

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