D-glucose 6-phosphate

Where it participates (unsigned role)

1. SLC37A4 exchanges cytosolic glucose-6-phosphate for luminal inorganic phosphate.

   Human glucose-6-phosphate transporter / SLC37A4 → Glucose-6-phosphate import into the endoplasmic reticulum source_derived_draftungraded
   Experimental context and source evidence

   evidence_span

   {"source_cache": "artifacts/chlorogenic_acid-research/42520004.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c05de010432b8bfaee87bdbba5f9fe93e7a262d41a17d19ec6e0b7b480e35ee6", "start_char": 0, "end_char": 2009, "text_sha256": "c05de010432b8bfaee87bdbba5f9fe93e7a262d41a17d19ec6e0b7b480e35ee6"}

   experimental_model

   Cryo-EM with biochemical transport and thermostability assays

   exposure

   Apo, glucose-6-phosphate-bound and chlorogenic-acid-bound structures

   limitations

   Direct structural target evidence does not establish inhibition after ordinary food intake. Variant disease and compound exposure are different mechanisms; coffee does not thereby cause glycogen storage disease.

   nutrient_topic

   Chlorogenic acid research collection; topical membership is not evidence of a direct dietary effect. · Chlorogenic acid / 5-O-caffeoylquinic acid

   organism

   Human recombinant SLC37A4

   plain_language

   The transporter delivers substrate into the endoplasmic reticulum.

   primary_references

   [chlorogenic_acid-p42520004] Structural basis for substrate recognition and inhibition of human glucose-6-phosphate transporter SLC37A4. (2026). https://pubmed.ncbi.nlm.nih.gov/42520004/ DOI: 10.1371/journal.pbio.3003833

   tissue_or_cell_type

   HEK293-expressed transporter; purified membrane-protein preparation

   Chlorogenic acid: metabolism, signaling and nutrient connections (2026-09-17) · lines 334–345

   AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cryo-EM with biochemical transport and thermostability assays · source_derived_draft · unverified_draft

   ### chlorogenic_acid-g6p-import SLC37A4 exchanges cytosolic glucose-6-phosphate for luminal inorganic phosphate. Condition category: normal nutrient_topic: Chlorogenic acid research collection; topical membership is not evidence of a direct dietary effect. plain_language: The transporter delivers substrate into the endoplasmic reticulum. organism: Human recombinant SLC37A4 tissue_or_cell_type: HEK293-expressed transporter; purified membrane-protein preparation experimental_model: Cryo-EM with biochemical transport and thermostability assays limitations: Direct structural target evidence does not establish inhibition after ordinary food intake. Variant disease and compound exposure are different mechanisms; coffee does not thereby cause glycogen storage disease. exposure: Apo, glucose-6-phosphate-bound and chlorogenic-acid-bound structures evidence_span: {"source_cache": "artifacts/chlorogenic_acid-research/42520004.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c05de010432b8bfaee87bdbba5f9fe93e7a262d41a17d19ec6e0b7b480e35ee6", "start_char": 0, "end_char": 2009, "text_sha256": "c05de010432b8bfaee87bdbba5f9fe93e7a262d41a17d19ec6e0b7b480e35ee6"} [chlorogenic_acid-p42520004] Structural basis for substrate recognition and inhibition of human glucose-6-phosphate transporter SLC37A4. (2026). https://pubmed.ncbi.nlm.nih.gov/42520004/ DOI: 10.1371/journal.pbio.3003833

   Complete structured claim and evidence

2. The bound compound stabilizes an arrested state that prevents the transitions needed for G6P/Pi exchange.

   Chlorogenic acid / 5-O-caffeoylquinic acid → Human SLC37A4 conformational cycling for G6P/Pi exchange source_derived_draftungraded
   Experimental context and source evidence

   evidence_span

   {"source_cache": "artifacts/chlorogenic_acid-research/42520004.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c05de010432b8bfaee87bdbba5f9fe93e7a262d41a17d19ec6e0b7b480e35ee6", "start_char": 0, "end_char": 2009, "text_sha256": "c05de010432b8bfaee87bdbba5f9fe93e7a262d41a17d19ec6e0b7b480e35ee6"}

   experimental_model

   Cryo-EM with biochemical transport and thermostability assays

   exposure

   Apo, glucose-6-phosphate-bound and chlorogenic-acid-bound structures

   limitations

   Direct structural target evidence does not establish inhibition after ordinary food intake. Variant disease and compound exposure are different mechanisms; coffee does not thereby cause glycogen storage disease.

   nutrient_topic

   Chlorogenic acid research collection; topical membership is not evidence of a direct dietary effect. · Chlorogenic acid / 5-O-caffeoylquinic acid

   organism

   Human recombinant SLC37A4

   plain_language

   Holding the carrier in one state obstructs its transport cycle.

   primary_references

   [chlorogenic_acid-p42520004] Structural basis for substrate recognition and inhibition of human glucose-6-phosphate transporter SLC37A4. (2026). https://pubmed.ncbi.nlm.nih.gov/42520004/ DOI: 10.1371/journal.pbio.3003833

   tissue_or_cell_type

   HEK293-expressed transporter; purified membrane-protein preparation

   Chlorogenic acid: metabolism, signaling and nutrient connections (2026-09-17) · lines 360–371

   AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cryo-EM with biochemical transport and thermostability assays · source_derived_draft · unverified_draft

   ### chlorogenic_acid-slc37a4-arrest The bound compound stabilizes an arrested state that prevents the transitions needed for G6P/Pi exchange. Condition category: normal nutrient_topic: Chlorogenic acid research collection; topical membership is not evidence of a direct dietary effect. plain_language: Holding the carrier in one state obstructs its transport cycle. organism: Human recombinant SLC37A4 tissue_or_cell_type: HEK293-expressed transporter; purified membrane-protein preparation experimental_model: Cryo-EM with biochemical transport and thermostability assays limitations: Direct structural target evidence does not establish inhibition after ordinary food intake. Variant disease and compound exposure are different mechanisms; coffee does not thereby cause glycogen storage disease. exposure: Apo, glucose-6-phosphate-bound and chlorogenic-acid-bound structures evidence_span: {"source_cache": "artifacts/chlorogenic_acid-research/42520004.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c05de010432b8bfaee87bdbba5f9fe93e7a262d41a17d19ec6e0b7b480e35ee6", "start_char": 0, "end_char": 2009, "text_sha256": "c05de010432b8bfaee87bdbba5f9fe93e7a262d41a17d19ec6e0b7b480e35ee6"} [chlorogenic_acid-p42520004] Structural basis for substrate recognition and inhibition of human glucose-6-phosphate transporter SLC37A4. (2026). https://pubmed.ncbi.nlm.nih.gov/42520004/ DOI: 10.1371/journal.pbio.3003833

   Complete structured claim and evidence

3. Cryo-EM resolved chlorogenic acid at a cytosolic site in inward-facing human SLC37A4.

   Chlorogenic acid / 5-O-caffeoylquinic acid → Human glucose-6-phosphate transporter / SLC37A4 source_derived_draftungraded
   Experimental context and source evidence

   evidence_span

   {"source_cache": "artifacts/chlorogenic_acid-research/42520004.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c05de010432b8bfaee87bdbba5f9fe93e7a262d41a17d19ec6e0b7b480e35ee6", "start_char": 0, "end_char": 2009, "text_sha256": "c05de010432b8bfaee87bdbba5f9fe93e7a262d41a17d19ec6e0b7b480e35ee6"}

   experimental_model

   Cryo-EM with biochemical transport and thermostability assays

   exposure

   Apo, glucose-6-phosphate-bound and chlorogenic-acid-bound structures

   limitations

   Direct structural target evidence does not establish inhibition after ordinary food intake. Variant disease and compound exposure are different mechanisms; coffee does not thereby cause glycogen storage disease.

   nutrient_topic

   Chlorogenic acid research collection; topical membership is not evidence of a direct dietary effect. · Chlorogenic acid / 5-O-caffeoylquinic acid

   organism

   Human recombinant SLC37A4

   plain_language

   This is a measured protein complex, not only a docking prediction.

   primary_references

   [chlorogenic_acid-p42520004] Structural basis for substrate recognition and inhibition of human glucose-6-phosphate transporter SLC37A4. (2026). https://pubmed.ncbi.nlm.nih.gov/42520004/ DOI: 10.1371/journal.pbio.3003833

   tissue_or_cell_type

   HEK293-expressed transporter; purified membrane-protein preparation

   Chlorogenic acid: metabolism, signaling and nutrient connections (2026-09-17) · lines 347–358

   AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cryo-EM with biochemical transport and thermostability assays · source_derived_draft · unverified_draft

   ### chlorogenic_acid-slc37a4-binding Cryo-EM resolved chlorogenic acid at a cytosolic site in inward-facing human SLC37A4. Condition category: normal nutrient_topic: Chlorogenic acid research collection; topical membership is not evidence of a direct dietary effect. plain_language: This is a measured protein complex, not only a docking prediction. organism: Human recombinant SLC37A4 tissue_or_cell_type: HEK293-expressed transporter; purified membrane-protein preparation experimental_model: Cryo-EM with biochemical transport and thermostability assays limitations: Direct structural target evidence does not establish inhibition after ordinary food intake. Variant disease and compound exposure are different mechanisms; coffee does not thereby cause glycogen storage disease. exposure: Apo, glucose-6-phosphate-bound and chlorogenic-acid-bound structures evidence_span: {"source_cache": "artifacts/chlorogenic_acid-research/42520004.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c05de010432b8bfaee87bdbba5f9fe93e7a262d41a17d19ec6e0b7b480e35ee6", "start_char": 0, "end_char": 2009, "text_sha256": "c05de010432b8bfaee87bdbba5f9fe93e7a262d41a17d19ec6e0b7b480e35ee6"} [chlorogenic_acid-p42520004] Structural basis for substrate recognition and inhibition of human glucose-6-phosphate transporter SLC37A4. (2026). https://pubmed.ncbi.nlm.nih.gov/42520004/ DOI: 10.1371/journal.pbio.3003833

   Complete structured claim and evidence

4. Fisetin inhibited glucose-6-phosphatase activity and increased glucose-6-phosphate content in the rat liver experiments.

   Fisetin → Rat liver glucose-6-phosphatase activity source_derived_draftungraded
   Experimental context and source evidence

   evidence_access

   Primary abstract

   experimental_model

   Rat liver biochemical activity measurements.

   limitations

   No isoform-specific binding site was established.

   nutrient_topic

   Fisetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Fisetin

   plain_language

   The final glucose-release step was affected.

   primary_references

   The actions of fisetin on glucose metabolism in the rat liver. · 2010 · https://pubmed.ncbi.nlm.nih.gov/20084677/ · DOI 10.1002/cbf.1635

   Fisetin: metabolism, cell-state responses and cross-nutrient mechanisms (2026-09-19) · lines 320–326

   AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Rat liver biochemical activity measurements. · source_derived_draft · unverified_draft

   ## fisetin-rat-g6pase The final glucose-release step was affected. Fisetin inhibited glucose-6-phosphatase activity and increased glucose-6-phosphate content in the rat liver experiments. Model: Rat liver biochemical activity measurements. Limitations: No isoform-specific binding site was established. Evidence access: Primary abstract The actions of fisetin on glucose metabolism in the rat liver. · 2010 · https://pubmed.ncbi.nlm.nih.gov/20084677/ · DOI 10.1002/cbf.1635

   Complete structured claim and evidence

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

   Acetic acid → Glycolysis source_derived_draftungraded
   Experimental context and source evidence

   evidence_span

   {"source_cache": "artifacts/acetate-research/11435516.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "130bbe406429175feedf86bcfa4597f8f7f81ac1d27a5d299efc545e3225175e", "start_char": 0, "end_char": 1638, "text_sha256": "130bbe406429175feedf86bcfa4597f8f7f81ac1d27a5d299efc545e3225175e"}

   experimental_model

   Food-deprived rats given graded dietary acetic acid for 2 hours

   exposure

   0, 0.1, 0.2 or 0.4 g acetic acid per 100 g diet for 2 hours after 15 hours of food deprivation

   limitations

   Only the 0.2 g dose reached significance for glycogen, so the dose-response is not monotonic. The glycolytic mechanism is the authors’ inference from metabolite ratios, not a direct enzyme measurement.

   nutrient_topic

   Acetic acid research collection; topical membership is not evidence of a direct clinical effect, and the ingested acid is recorded separately from the circulating acetate anion. · Acetic acid

   organism

   Rat

   plain_language

   The acid appears to slow the burning of glucose, which is why more of it ends up stored.

   primary_references

   [acetate-p11435516] Acetic acid feeding enhances glycogen repletion in liver and skeletal muscle of rats. (2001). https://pubmed.ncbi.nlm.nih.gov/11435516/ DOI: 10.1093/jn/131.7.1973

   tissue_or_cell_type

   Liver and skeletal muscle

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

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

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

   Complete structured claim and evidence

6. Human G6PD uses glucose-6-phosphate and catalytic NADP+ to generate NADPH.

   Glucose-6-phosphate dehydrogenase / G6PD → NADPH source_derived_draftungraded
   Experimental context and source evidence

   evidence_span

   {"source_cache": "artifacts/glutathione-research/35858355.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "02c2d0e880b17ab304fab0854064813ffec5fa9e647b978a083aa88fbf8a38f0", "start_char": 0, "end_char": 1328, "text_sha256": "02c2d0e880b17ab304fab0854064813ffec5fa9e647b978a083aa88fbf8a38f0"}

   experimental_model

   Cryo-EM and structural comparison

   exposure

   Ligand-free and NADP/G6P-bound states

   limitations

   Structural NADP and catalytic NADP are different sites; enzyme activity is not a niacin-treatment trial.

   nutrient_topic

   Glutathione research collection; topical membership is not evidence of a direct dietary effect. · GSH

   organism

   Human

   plain_language

   The reducing power used in glutathione recycling has to be replenished.

   primary_references

   [glutathione-p35858355] Allosteric role of a structural NADP+ molecule in glucose-6-phosphate dehydrogenase activity. (2022). https://pubmed.ncbi.nlm.nih.gov/35858355/ DOI: 10.1073/pnas.2119695119

   tissue_or_cell_type

   Purified wild-type G6PD and D200N

   Glutathione: metabolism, signaling and nutrient connections (2026-09-17) · lines 762–773

   AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cryo-EM and structural comparison · source_derived_draft · unverified_draft

   ### glutathione-g6pd-nadph Human G6PD uses glucose-6-phosphate and catalytic NADP+ to generate NADPH. Condition category: normal nutrient_topic: Glutathione research collection; topical membership is not evidence of a direct dietary effect. plain_language: The reducing power used in glutathione recycling has to be replenished. organism: Human tissue_or_cell_type: Purified wild-type G6PD and D200N experimental_model: Cryo-EM and structural comparison limitations: Structural NADP and catalytic NADP are different sites; enzyme activity is not a niacin-treatment trial. exposure: Ligand-free and NADP/G6P-bound states evidence_span: {"source_cache": "artifacts/glutathione-research/35858355.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "02c2d0e880b17ab304fab0854064813ffec5fa9e647b978a083aa88fbf8a38f0", "start_char": 0, "end_char": 1328, "text_sha256": "02c2d0e880b17ab304fab0854064813ffec5fa9e647b978a083aa88fbf8a38f0"} [glutathione-p35858355] Allosteric role of a structural NADP+ molecule in glucose-6-phosphate dehydrogenase activity. (2022). https://pubmed.ncbi.nlm.nih.gov/35858355/ DOI: 10.1073/pnas.2119695119

   Complete structured claim and evidence

7. Recombinant human ISYNA1 converted D-glucose 6-phosphate to 1D-myo-inositol 3-phosphate, an entry step in de novo inositol synthesis.

   ISYNA1 (human inositol-3-phosphate synthase 1) → 1D-myo-inositol 3-phosphate source_derived_draftungraded
   Experimental context and source evidence

   evidence_span

   {"source_cache": "artifacts/inositol-research/15024000.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5ab3a8eda77989c3e4a681b4a971fb7e969c285d3e5c8e41bc31713a7f88c9ac", "start_char": 0, "end_char": 1427, "text_sha256": "5ab3a8eda77989c3e4a681b4a971fb7e969c285d3e5c8e41bc31713a7f88c9ac"}

   experimental_model

   Recombinant human enzyme and complementation of yeast ino1 deletion

   exposure

   Substrate, NAD+, cation and valproate experiments

   limitations

   Purified-enzyme and yeast results do not establish supplement effects or a human dietary deficiency threshold.

   nutrient_topic

   Inositol research collection; topical membership is not evidence of a direct dietary effect. · Inositol (stereoisomer family)

   organism

   Human protein expressed in bacteria and yeast

   plain_language

   Cells have a route to build the inositol ring from a glucose-derived molecule.

   primary_references

   [ino-p15024000] Human 1-D-myo-inositol-3-phosphate synthase is functional in yeast. (2004). https://pubmed.ncbi.nlm.nih.gov/15024000/ DOI: 10.1074/jbc.m312078200

   tissue_or_cell_type

   Purified enzyme; yeast cultures

   Inositol: synthesis, signaling, mineral interactions and conditional deficiency (2026-09-17) · lines 171–182

   AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant human enzyme and complementation of yeast ino1 deletion · source_derived_draft · unverified_draft

   ### ino-isyna-synthesis Recombinant human ISYNA1 converted D-glucose 6-phosphate to 1D-myo-inositol 3-phosphate, an entry step in de novo inositol synthesis. Condition category: normal nutrient_topic: Inositol research collection; topical membership is not evidence of a direct dietary effect. plain_language: Cells have a route to build the inositol ring from a glucose-derived molecule. organism: Human protein expressed in bacteria and yeast tissue_or_cell_type: Purified enzyme; yeast cultures experimental_model: Recombinant human enzyme and complementation of yeast ino1 deletion limitations: Purified-enzyme and yeast results do not establish supplement effects or a human dietary deficiency threshold. exposure: Substrate, NAD+, cation and valproate experiments evidence_span: {"source_cache": "artifacts/inositol-research/15024000.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5ab3a8eda77989c3e4a681b4a971fb7e969c285d3e5c8e41bc31713a7f88c9ac", "start_char": 0, "end_char": 1427, "text_sha256": "5ab3a8eda77989c3e4a681b4a971fb7e969c285d3e5c8e41bc31713a7f88c9ac"} [ino-p15024000] Human 1-D-myo-inositol-3-phosphate synthase is functional in yeast. (2004). https://pubmed.ncbi.nlm.nih.gov/15024000/ DOI: 10.1074/jbc.m312078200

   Complete structured claim and evidence