Inorganic phosphate

availability_state

machinery_impairment Imported condition classification; unverified.

cross_nutrient

Vitamin D–calcium–phosphate regulation.

evidence_locator

Abstract: reported experimental results

evidence_scope

D3 active metabolite or VDR machinery experiment; not a direct D2-versus-D3 comparison.

experimental_model

VDR-ablated mice and control littermates receiving a mineral/lactose rescue diet

exposure

Combined mineral/lactose rescue diet; individual ingredient contributions and exact formulation are not resolved by the retrieved abstract.

limitations

This is a combined dietary rescue of receptor-deficient mice, not phosphate monotherapy, not a D2/D3 trial, and not evidence that VDR has no direct skeletal functions.

nutrient

Vitamin D2 and D3 · Vitamin D2 and D3

nutrient_topic

Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin D2 and D3

organism

Mus musculus

plain_language

Improving mineral delivery protected the skeleton even when the vitamin D receptor was missing.

primary_references

[vdm-li1998] Normalization of mineral ion homeostasis by dietary means prevents hyperparathyroidism, rickets, and osteomalacia, but not alopecia in vitamin D receptor-ablated mice. (1998). https://pubmed.ncbi.nlm.nih.gov/9751523/ DOI: 10.1210/endo.139.10.6262

tissue_or_cell_type

Skeleton

trigger_kind

machinery_impairment Imported condition classification; unverified.

Vitamin D2 and D3: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 761–775

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · VDR-ablated mice and control littermates receiving a mineral/lactose rescue diet · source_derived_draft · unverified_draft

### vdm-mineral-rescue-prevents-vdr-null-skeletal-defects The combined mineral/lactose rescue diet prevented rickets and osteomalacia in VDR-ablated mice. Condition category: machinery_impairment nutrient_topic: Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Improving mineral delivery protected the skeleton even when the vitamin D receptor was missing. organism: Mus musculus tissue_or_cell_type: Skeleton experimental_model: VDR-ablated mice and control littermates receiving a mineral/lactose rescue diet limitations: This is a combined dietary rescue of receptor-deficient mice, not phosphate monotherapy, not a D2/D3 trial, and not evidence that VDR has no direct skeletal functions. exposure: Combined mineral/lactose rescue diet; individual ingredient contributions and exact formulation are not resolved by the retrieved abstract. cross_nutrient: Vitamin D–calcium–phosphate regulation. evidence_locator: Abstract: reported experimental results nutrient: Vitamin D2 and D3 evidence_scope: D3 active metabolite or VDR machinery experiment; not a direct D2-versus-D3 comparison. [vdm-li1998] Normalization of mineral ion homeostasis by dietary means prevents hyperparathyroidism, rickets, and osteomalacia, but not alopecia in vitamin D receptor-ablated mice. (1998). https://pubmed.ncbi.nlm.nih.gov/9751523/ DOI: 10.1210/endo.139.10.6262

cross_nutrient

Vitamin D–calcium–phosphate regulation.

evidence_locator

Primary abstract and opening experimental-results summary; web-assay-excerpts.json

evidence_scope

D3 active metabolite or VDR machinery experiment; not a direct D2-versus-D3 comparison.

experimental_model

Primary mouse chondrocytes; caspase-9 pathway and apoptosis assays

exposure

Inorganic phosphate exposure in differentiated primary cultures; exact dose/time not recovered in the primary passages used.

limitations

Cell differentiation and exposure conditions matter; no nutrient dose recommendation, universal phosphate sensor or human serum threshold is established.

nutrient

Vitamin D2 and D3 · Vitamin D2 and D3

nutrient_topic

Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin D2 and D3

organism

Mus musculus

plain_language

Phosphate served as a signal for a cartilage-cell maturation pathway in this culture system.

primary_references

[vdm-sabbagh2005] Hypophosphatemia leads to rickets by impairing caspase-mediated apoptosis of hypertrophic chondrocytes. (2005). https://pubmed.ncbi.nlm.nih.gov/15976027/ DOI: 10.1073/pnas.0502249102

tissue_or_cell_type

Cultured hypertrophic chondrocytes

Vitamin D2 and D3: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 793–807

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Primary mouse chondrocytes; caspase-9 pathway and apoptosis assays · source_derived_draft · unverified_draft

### vdm-phosphate-activates-chondrocyte-caspase9 Phosphate exposure activated the caspase-9-dependent mitochondrial apoptotic pathway in cultured primary mouse hypertrophic chondrocytes. Condition category: normal nutrient_topic: Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Phosphate served as a signal for a cartilage-cell maturation pathway in this culture system. organism: Mus musculus tissue_or_cell_type: Cultured hypertrophic chondrocytes experimental_model: Primary mouse chondrocytes; caspase-9 pathway and apoptosis assays limitations: Cell differentiation and exposure conditions matter; no nutrient dose recommendation, universal phosphate sensor or human serum threshold is established. exposure: Inorganic phosphate exposure in differentiated primary cultures; exact dose/time not recovered in the primary passages used. cross_nutrient: Vitamin D–calcium–phosphate regulation. evidence_locator: Primary abstract and opening experimental-results summary; web-assay-excerpts.json nutrient: Vitamin D2 and D3 evidence_scope: D3 active metabolite or VDR machinery experiment; not a direct D2-versus-D3 comparison. [vdm-sabbagh2005] Hypophosphatemia leads to rickets by impairing caspase-mediated apoptosis of hypertrophic chondrocytes. (2005). https://pubmed.ncbi.nlm.nih.gov/15976027/ DOI: 10.1073/pnas.0502249102

availability_state

nutrient_deficiency Imported condition classification; unverified.

cross_nutrient

Vitamin D–calcium–phosphate regulation.

evidence_locator

Results: biochemical parameters, growth-plate histology and TUNEL; primary text excerpts cached in web-assay-excerpts.json

evidence_scope

D3 active metabolite or VDR machinery experiment; not a direct D2-versus-D3 comparison.

experimental_model

Wild-type mice fed high-calcium/low-phosphate diet; growth-plate histology and TUNEL assay

exposure

High-calcium/low-phosphate diet; biochemical comparisons at 24 days of age in Figure 2. Exact diet duration/formulation not resolved in retrieved passages.

limitations

The diet arm is separated from Vdr-null and Phex-mutant models. No single human serum threshold or claim that every rachitic disorder has one mechanism is inferred.

nutrient

Vitamin D2 and D3 · Vitamin D2 and D3

nutrient_topic

Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin D2 and D3

organism

Mus musculus

plain_language

Low phosphate disrupted maturation of growth-plate cartilage even when calcium was high.

primary_references

[vdm-sabbagh2005] Hypophosphatemia leads to rickets by impairing caspase-mediated apoptosis of hypertrophic chondrocytes. (2005). https://pubmed.ncbi.nlm.nih.gov/15976027/ DOI: 10.1073/pnas.0502249102

tissue_or_cell_type

Growth-plate hypertrophic chondrocytes

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Vitamin D2 and D3: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 777–791

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Wild-type mice fed high-calcium/low-phosphate diet; growth-plate histology and TUNEL assay · source_derived_draft · unverified_draft

### vdm-phosphate-restriction-reduces-growth-plate-apoptosis Diet-induced hypophosphatemic mice had impaired late hypertrophic-chondrocyte apoptosis and rachitic growth-plate expansion despite hypercalcemia and suppressed PTH. Condition category: nutrient_deficiency nutrient_topic: Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Low phosphate disrupted maturation of growth-plate cartilage even when calcium was high. organism: Mus musculus tissue_or_cell_type: Growth-plate hypertrophic chondrocytes experimental_model: Wild-type mice fed high-calcium/low-phosphate diet; growth-plate histology and TUNEL assay limitations: The diet arm is separated from Vdr-null and Phex-mutant models. No single human serum threshold or claim that every rachitic disorder has one mechanism is inferred. exposure: High-calcium/low-phosphate diet; biochemical comparisons at 24 days of age in Figure 2. Exact diet duration/formulation not resolved in retrieved passages. cross_nutrient: Vitamin D–calcium–phosphate regulation. evidence_locator: Results: biochemical parameters, growth-plate histology and TUNEL; primary text excerpts cached in web-assay-excerpts.json nutrient: Vitamin D2 and D3 evidence_scope: D3 active metabolite or VDR machinery experiment; not a direct D2-versus-D3 comparison. [vdm-sabbagh2005] Hypophosphatemia leads to rickets by impairing caspase-mediated apoptosis of hypertrophic chondrocytes. (2005). https://pubmed.ncbi.nlm.nih.gov/15976027/ DOI: 10.1073/pnas.0502249102

cross_nutrient

Phosphorus-containing inorganic phosphate alters a niacin precursor enzyme in vitro; no dietary phosphate deficiency was tested.

evidence_span

{"source_cache": "artifacts/niacin-precursors-sources/naprt2011.abstract.txt", "locator": "Indexed primary abstract; identified exact passage", "start_char": 815, "end_char": 876, "file_sha256": "c9f4959ad65f0b0621179b3ccf00c460f7f648293bf910209ecc6e7785417deb", "text_sha256": "53af728f32d65092c92246c77801e92e521892adac900df62bf3f8206129f714"}

experimental_model

Purified recombinant human NAPRT kinetic assays and site-directed mutagenesis

exposure

Biochemical or structural assay; no dietary intervention

limitations

Purified-enzyme evidence does not establish dietary intake requirements or clinical outcomes.

nutrient_topic

Niacin research collection; topical membership is not evidence of a direct dietary effect. · Niacin (vitamin B3)

organism

Homo sapiens

plain_language

Phosphate supported this isolated precursor enzyme.

primary_references

[b3-pre-naprt2011] Characterization of human nicotinate phosphoribosyltransferase: Kinetic studies, structure prediction and functional analysis by site-directed mutagenesis. (2012). https://pubmed.ncbi.nlm.nih.gov/21742010/ DOI: 10.1016/j.biochi.2011.06.033

tissue_or_cell_type

Purified recombinant protein; no intact tissue

Niacin: NAD metabolism, deficiency and nutrient interactions (2026-09-17) · lines 262–274

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Purified recombinant human NAPRT kinetic assays and site-directed mutagenesis · source_derived_draft · unverified_draft

### b3-pre-naprt-phosphate Inorganic phosphate activated purified recombinant human NAPRT in the reported kinetic experiments. Condition category: normal nutrient_topic: Niacin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Phosphate supported this isolated precursor enzyme. organism: Homo sapiens tissue_or_cell_type: Purified recombinant protein; no intact tissue experimental_model: Purified recombinant human NAPRT kinetic assays and site-directed mutagenesis limitations: Purified-enzyme evidence does not establish dietary intake requirements or clinical outcomes. exposure: Biochemical or structural assay; no dietary intervention cross_nutrient: Phosphorus-containing inorganic phosphate alters a niacin precursor enzyme in vitro; no dietary phosphate deficiency was tested. evidence_span: {"source_cache": "artifacts/niacin-precursors-sources/naprt2011.abstract.txt", "locator": "Indexed primary abstract; identified exact passage", "start_char": 815, "end_char": 876, "file_sha256": "c9f4959ad65f0b0621179b3ccf00c460f7f648293bf910209ecc6e7785417deb", "text_sha256": "53af728f32d65092c92246c77801e92e521892adac900df62bf3f8206129f714"} [b3-pre-naprt2011] Characterization of human nicotinate phosphoribosyltransferase: Kinetic studies, structure prediction and functional analysis by site-directed mutagenesis. (2012). https://pubmed.ncbi.nlm.nih.gov/21742010/ DOI: 10.1016/j.biochi.2011.06.033

availability_state

nutrient_deficiency Imported condition classification; unverified.

evidence_span

{"source_cache": "artifacts/inositol-research/28126903.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6f5c96ed7d02591d5fe475d0e26aa2f21dc93f0c86c12998debb417f98254d2f", "start_char": 0, "end_char": 1981, "text_sha256": "6f5c96ed7d02591d5fe475d0e26aa2f21dc93f0c86c12998debb417f98254d2f"}

experimental_model

Cellular phosphate withdrawal/repletion and bifunctional enzyme kinetics

exposure

Phosphate availability and PPIP5K kinase/phosphatase assays

limitations

Cell-culture nutrient withdrawal is not a measured human dietary threshold; PPIP5K isoforms are not identical.

nutrient_topic

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

organism

Human HCT116 cells and human PPIP5K proteins

plain_language

The signaling network detects phosphate supply instead of depending only on the amount of free inositol.

primary_references

[ino-p28126903] The Significance of the Bifunctional Kinase/Phosphatase Activities of Diphosphoinositol Pentakisphosphate Kinases (PPIP5Ks) for Coupling Inositol Pyrophosphate Cell Signaling to Cellular Phosphate Homeostasis. (2017). https://pubmed.ncbi.nlm.nih.gov/28126903/ DOI: 10.1074/jbc.m116.765743

tissue_or_cell_type

Intestinal tumor-derived cell line; purified enzymes

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Inositol: synthesis, signaling, mineral interactions and conditional deficiency (2026-09-17) · lines 860–871

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cellular phosphate withdrawal/repletion and bifunctional enzyme kinetics · source_derived_draft · unverified_draft

### ino-phosphate-ip8 Phosphate starvation lowered ATP and 5-InsP7, while InsP8 showed a larger and more sensitive response; levels recovered with phosphate replenishment. Condition category: nutrient_deficiency nutrient_topic: Inositol research collection; topical membership is not evidence of a direct dietary effect. plain_language: The signaling network detects phosphate supply instead of depending only on the amount of free inositol. organism: Human HCT116 cells and human PPIP5K proteins tissue_or_cell_type: Intestinal tumor-derived cell line; purified enzymes experimental_model: Cellular phosphate withdrawal/repletion and bifunctional enzyme kinetics limitations: Cell-culture nutrient withdrawal is not a measured human dietary threshold; PPIP5K isoforms are not identical. exposure: Phosphate availability and PPIP5K kinase/phosphatase assays evidence_span: {"source_cache": "artifacts/inositol-research/28126903.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6f5c96ed7d02591d5fe475d0e26aa2f21dc93f0c86c12998debb417f98254d2f", "start_char": 0, "end_char": 1981, "text_sha256": "6f5c96ed7d02591d5fe475d0e26aa2f21dc93f0c86c12998debb417f98254d2f"} [ino-p28126903] The Significance of the Bifunctional Kinase/Phosphatase Activities of Diphosphoinositol Pentakisphosphate Kinases (PPIP5Ks) for Coupling Inositol Pyrophosphate Cell Signaling to Cellular Phosphate Homeostasis. (2017). https://pubmed.ncbi.nlm.nih.gov/28126903/ DOI: 10.1074/jbc.m116.765743

evidence_span

{"source_cache": "artifacts/inositol-research/28126903.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6f5c96ed7d02591d5fe475d0e26aa2f21dc93f0c86c12998debb417f98254d2f", "start_char": 0, "end_char": 1981, "text_sha256": "6f5c96ed7d02591d5fe475d0e26aa2f21dc93f0c86c12998debb417f98254d2f"}

experimental_model

Cellular phosphate withdrawal/repletion and bifunctional enzyme kinetics

exposure

Phosphate availability and PPIP5K kinase/phosphatase assays

limitations

Cell-culture nutrient withdrawal is not a measured human dietary threshold; PPIP5K isoforms are not identical.

nutrient_topic

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

organism

Human HCT116 cells and human PPIP5K proteins

plain_language

Phosphate availability can slow destruction of the inositol-pyrophosphate signal.

primary_references

[ino-p28126903] The Significance of the Bifunctional Kinase/Phosphatase Activities of Diphosphoinositol Pentakisphosphate Kinases (PPIP5Ks) for Coupling Inositol Pyrophosphate Cell Signaling to Cellular Phosphate Homeostasis. (2017). https://pubmed.ncbi.nlm.nih.gov/28126903/ DOI: 10.1074/jbc.m116.765743

tissue_or_cell_type

Intestinal tumor-derived cell line; purified enzymes

Inositol: synthesis, signaling, mineral interactions and conditional deficiency (2026-09-17) · lines 834–845

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cellular phosphate withdrawal/repletion and bifunctional enzyme kinetics · source_derived_draft · unverified_draft

### ino-pi-ppip-phosphatase Inorganic phosphate inhibited PPIP5K InsP8 phosphatase activities by approximately 40–90% across 0–1 mM in the reported assays. Condition category: normal nutrient_topic: Inositol research collection; topical membership is not evidence of a direct dietary effect. plain_language: Phosphate availability can slow destruction of the inositol-pyrophosphate signal. organism: Human HCT116 cells and human PPIP5K proteins tissue_or_cell_type: Intestinal tumor-derived cell line; purified enzymes experimental_model: Cellular phosphate withdrawal/repletion and bifunctional enzyme kinetics limitations: Cell-culture nutrient withdrawal is not a measured human dietary threshold; PPIP5K isoforms are not identical. exposure: Phosphate availability and PPIP5K kinase/phosphatase assays evidence_span: {"source_cache": "artifacts/inositol-research/28126903.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6f5c96ed7d02591d5fe475d0e26aa2f21dc93f0c86c12998debb417f98254d2f", "start_char": 0, "end_char": 1981, "text_sha256": "6f5c96ed7d02591d5fe475d0e26aa2f21dc93f0c86c12998debb417f98254d2f"} [ino-p28126903] The Significance of the Bifunctional Kinase/Phosphatase Activities of Diphosphoinositol Pentakisphosphate Kinases (PPIP5Ks) for Coupling Inositol Pyrophosphate Cell Signaling to Cellular Phosphate Homeostasis. (2017). https://pubmed.ncbi.nlm.nih.gov/28126903/ DOI: 10.1074/jbc.m116.765743

evidence_span

{"source_cache": "artifacts/inositol-research/28126903.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6f5c96ed7d02591d5fe475d0e26aa2f21dc93f0c86c12998debb417f98254d2f", "start_char": 0, "end_char": 1981, "text_sha256": "6f5c96ed7d02591d5fe475d0e26aa2f21dc93f0c86c12998debb417f98254d2f"}

experimental_model

Cellular phosphate withdrawal/repletion and bifunctional enzyme kinetics

exposure

Phosphate availability and PPIP5K kinase/phosphatase assays

limitations

Cell-culture nutrient withdrawal is not a measured human dietary threshold; PPIP5K isoforms are not identical.

nutrient_topic

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

organism

Human HCT116 cells and human PPIP5K proteins

plain_language

For this isoform, phosphate also increased the signal-building reaction.

primary_references

[ino-p28126903] The Significance of the Bifunctional Kinase/Phosphatase Activities of Diphosphoinositol Pentakisphosphate Kinases (PPIP5Ks) for Coupling Inositol Pyrophosphate Cell Signaling to Cellular Phosphate Homeostasis. (2017). https://pubmed.ncbi.nlm.nih.gov/28126903/ DOI: 10.1074/jbc.m116.765743

tissue_or_cell_type

Intestinal tumor-derived cell line; purified enzymes

Inositol: synthesis, signaling, mineral interactions and conditional deficiency (2026-09-17) · lines 847–858

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cellular phosphate withdrawal/repletion and bifunctional enzyme kinetics · source_derived_draft · unverified_draft

### ino-pi-ppip5k2-kinase Phosphate increased PPIP5K2 5-InsP7 kinase activity approximately twofold across 0–5 mM. Condition category: normal nutrient_topic: Inositol research collection; topical membership is not evidence of a direct dietary effect. plain_language: For this isoform, phosphate also increased the signal-building reaction. organism: Human HCT116 cells and human PPIP5K proteins tissue_or_cell_type: Intestinal tumor-derived cell line; purified enzymes experimental_model: Cellular phosphate withdrawal/repletion and bifunctional enzyme kinetics limitations: Cell-culture nutrient withdrawal is not a measured human dietary threshold; PPIP5K isoforms are not identical. exposure: Phosphate availability and PPIP5K kinase/phosphatase assays evidence_span: {"source_cache": "artifacts/inositol-research/28126903.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6f5c96ed7d02591d5fe475d0e26aa2f21dc93f0c86c12998debb417f98254d2f", "start_char": 0, "end_char": 1981, "text_sha256": "6f5c96ed7d02591d5fe475d0e26aa2f21dc93f0c86c12998debb417f98254d2f"} [ino-p28126903] The Significance of the Bifunctional Kinase/Phosphatase Activities of Diphosphoinositol Pentakisphosphate Kinases (PPIP5Ks) for Coupling Inositol Pyrophosphate Cell Signaling to Cellular Phosphate Homeostasis. (2017). https://pubmed.ncbi.nlm.nih.gov/28126903/ DOI: 10.1074/jbc.m116.765743

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

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

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

evidence_location

Indexed abstract: intact/disrupted cells, PI-PLC and patient enzyme activity

experimental_model

Normal and hypophosphatasia human skin fibroblasts.

exposure

Extracellular PLP; intact versus disrupted cells; PI-PLC release.

limitations

Directly demonstrated in fibroblasts; does not itself measure brain entry.

nutrient_topic

Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B6

organism

Homo sapiens

plain_language

Cell-surface ALPL processes PLP outside the cell.

primary_references

[fedde1990] Alkaline phosphatase (tissue-nonspecific isoenzyme) is a phosphoethanolamine and pyridoxal-5'-phosphate ectophosphatase: normal and hypophosphatasia fibroblast study. (1990). https://pubmed.ncbi.nlm.nih.gov/2220817/

tissue_or_cell_type

Skin fibroblasts

Vitamin B6: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 309–320

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Normal and hypophosphatasia human skin fibroblasts. · source_derived_draft · unverified_draft

### b6-transport-alpl-ecto Human fibroblast ALPL hydrolyzed extracellular micromolar PLP at physiological pH; intact-cell and PI-PLC experiments supported lipid-anchored ecto-orientation. Condition category: normal nutrient_topic: Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Cell-surface ALPL processes PLP outside the cell. organism: Homo sapiens tissue_or_cell_type: Skin fibroblasts experimental_model: Normal and hypophosphatasia human skin fibroblasts. limitations: Directly demonstrated in fibroblasts; does not itself measure brain entry. exposure: Extracellular PLP; intact versus disrupted cells; PI-PLC release. evidence_location: Indexed abstract: intact/disrupted cells, PI-PLC and patient enzyme activity [fedde1990] Alkaline phosphatase (tissue-nonspecific isoenzyme) is a phosphoethanolamine and pyridoxal-5'-phosphate ectophosphatase: normal and hypophosphatasia fibroblast study. (1990). https://pubmed.ncbi.nlm.nih.gov/2220817/

evidence_location

Indexed abstract: cloning and substrate hydrolysis

experimental_model

Recombinant human pyridoxal phosphatase expressed in E. coli.

exposure

Recombinant-enzyme characterization.

limitations

Model-specific evidence; no dietary threshold or treatment benefit established.

nutrient_topic

Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B6

organism

Homo sapiens

plain_language

PDXP removes phosphate from a B6 vitamer.

primary_references

[jang2003] Human pyridoxal phosphatase. Molecular cloning, functional expression, and tissue distribution. (2003). https://pubmed.ncbi.nlm.nih.gov/14522954/ DOI: 10.1074/jbc.m309619200

tissue_or_cell_type

Purified recombinant human enzyme

Vitamin B6: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 256–267

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant human pyridoxal phosphatase expressed in E. coli. · source_derived_draft · unverified_draft

### b6-transport-pdxp-plp Catalytically active recombinant human pyridoxal phosphatase hydrolyzed pyridoxal-phosphate. Condition category: normal nutrient_topic: Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. plain_language: PDXP removes phosphate from a B6 vitamer. organism: Homo sapiens tissue_or_cell_type: Purified recombinant human enzyme experimental_model: Recombinant human pyridoxal phosphatase expressed in E. coli. limitations: Model-specific evidence; no dietary threshold or treatment benefit established. exposure: Recombinant-enzyme characterization. evidence_location: Indexed abstract: cloning and substrate hydrolysis [jang2003] Human pyridoxal phosphatase. Molecular cloning, functional expression, and tissue distribution. (2003). https://pubmed.ncbi.nlm.nih.gov/14522954/ DOI: 10.1074/jbc.m309619200

evidence_location

Indexed abstract: cloning and substrate hydrolysis

experimental_model

Recombinant human pyridoxal phosphatase expressed in E. coli.

exposure

Recombinant-enzyme characterization.

limitations

Model-specific evidence; no dietary threshold or treatment benefit established.

nutrient_topic

Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B6

organism

Homo sapiens

plain_language

PDXP removes phosphate from a B6 vitamer.

primary_references

[jang2003] Human pyridoxal phosphatase. Molecular cloning, functional expression, and tissue distribution. (2003). https://pubmed.ncbi.nlm.nih.gov/14522954/ DOI: 10.1074/jbc.m309619200

tissue_or_cell_type

Purified recombinant human enzyme

Vitamin B6: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 269–280

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant human pyridoxal phosphatase expressed in E. coli. · source_derived_draft · unverified_draft

### b6-transport-pdxp-pnp Catalytically active recombinant human pyridoxal phosphatase hydrolyzed pyridoxine-phosphate. Condition category: normal nutrient_topic: Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. plain_language: PDXP removes phosphate from a B6 vitamer. organism: Homo sapiens tissue_or_cell_type: Purified recombinant human enzyme experimental_model: Recombinant human pyridoxal phosphatase expressed in E. coli. limitations: Model-specific evidence; no dietary threshold or treatment benefit established. exposure: Recombinant-enzyme characterization. evidence_location: Indexed abstract: cloning and substrate hydrolysis [jang2003] Human pyridoxal phosphatase. Molecular cloning, functional expression, and tissue distribution. (2003). https://pubmed.ncbi.nlm.nih.gov/14522954/ DOI: 10.1074/jbc.m309619200

cross_nutrient

Vitamin D–calcium–phosphate regulation.

evidence_locator

Abstract: reported experimental results

evidence_scope

D3 active metabolite or VDR machinery experiment; not a direct D2-versus-D3 comparison.

experimental_model

Calcitriol-injected mice; bone Fgf23 transcript assay and circulating FGF23 measurement

exposure

Calcitriol administration; circulating FGF23 rose by 8 hours. Dose and transcript collection time not specified in the retrieved abstract.

limitations

The mRNA result is distinguished from circulating hormone and renal action; the separate cell reporter experiment supports receptor dependence but is not inferred to prove every bone enhancer.

nutrient

Vitamin D2 and D3 · Vitamin D2 and D3

nutrient_topic

Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin D2 and D3

organism

Mus musculus

plain_language

Active vitamin D induced a bone hormone that feeds back on vitamin D activation and phosphate handling.

primary_references

[vdm-liu2006] Fibroblast growth factor 23 is a counter-regulatory phosphaturic hormone for vitamin D. (2006). https://pubmed.ncbi.nlm.nih.gov/16597685/ DOI: 10.1681/asn.2005111185

tissue_or_cell_type

Bone

Vitamin D2 and D3: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 729–743

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Calcitriol-injected mice; bone Fgf23 transcript assay and circulating FGF23 measurement · source_derived_draft · unverified_draft

### vdm-calcitriol-increases-bone-fgf23-transcripts Calcitriol administration produced about a fourfold increase in bone Fgf23 transcripts in the Liu mouse study. Condition category: normal nutrient_topic: Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Active vitamin D induced a bone hormone that feeds back on vitamin D activation and phosphate handling. organism: Mus musculus tissue_or_cell_type: Bone experimental_model: Calcitriol-injected mice; bone Fgf23 transcript assay and circulating FGF23 measurement limitations: The mRNA result is distinguished from circulating hormone and renal action; the separate cell reporter experiment supports receptor dependence but is not inferred to prove every bone enhancer. exposure: Calcitriol administration; circulating FGF23 rose by 8 hours. Dose and transcript collection time not specified in the retrieved abstract. cross_nutrient: Vitamin D–calcium–phosphate regulation. evidence_locator: Abstract: reported experimental results nutrient: Vitamin D2 and D3 evidence_scope: D3 active metabolite or VDR machinery experiment; not a direct D2-versus-D3 comparison. [vdm-liu2006] Fibroblast growth factor 23 is a counter-regulatory phosphaturic hormone for vitamin D. (2006). https://pubmed.ncbi.nlm.nih.gov/16597685/ DOI: 10.1681/asn.2005111185

cross_nutrient

Vitamin D–calcium–phosphate regulation.

evidence_locator

Figure 6; Results: Increased circulating 1,25(OH)2D levels impair mineralization by upregulating mineralization inhibitors

evidence_scope

D3 active metabolite or VDR machinery experiment; not a direct D2-versus-D3 comparison.

experimental_model

Differentiated primary Vdr-intact mouse osteoblasts; conditioned-medium pyrophosphate normalized to DNA

exposure

10^-8 M calcitriol for 4 days after osteogenic differentiation.

limitations

Direct culture result does not imply that usual dietary vitamin D damages bone; physiological outcome also depends on intestinal mineral delivery.

nutrient

Vitamin D2 and D3 · Vitamin D2 and D3

nutrient_topic

Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin D2 and D3

organism

Mus musculus

plain_language

In this model, active vitamin D increased a molecule that restrains mineral deposition.

primary_references

[vdm-lieben2012] Normocalcemia is maintained in mice under conditions of calcium malabsorption by vitamin D-induced inhibition of bone mineralization. (2012). https://pubmed.ncbi.nlm.nih.gov/22523068/ DOI: 10.1172/jci45890

tissue_or_cell_type

Osteoblast culture

Vitamin D2 and D3: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 809–823

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Differentiated primary Vdr-intact mouse osteoblasts; conditioned-medium pyrophosphate normalized to DNA · source_derived_draft · unverified_draft

### vdm-calcitriol-increases-extracellular-ppi Calcitriol treatment increased extracellular pyrophosphate in differentiated Vdr-intact mouse osteoblast cultures. Condition category: normal nutrient_topic: Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. plain_language: In this model, active vitamin D increased a molecule that restrains mineral deposition. organism: Mus musculus tissue_or_cell_type: Osteoblast culture experimental_model: Differentiated primary Vdr-intact mouse osteoblasts; conditioned-medium pyrophosphate normalized to DNA limitations: Direct culture result does not imply that usual dietary vitamin D damages bone; physiological outcome also depends on intestinal mineral delivery. exposure: 10^-8 M calcitriol for 4 days after osteogenic differentiation. cross_nutrient: Vitamin D–calcium–phosphate regulation. evidence_locator: Figure 6; Results: Increased circulating 1,25(OH)2D levels impair mineralization by upregulating mineralization inhibitors nutrient: Vitamin D2 and D3 evidence_scope: D3 active metabolite or VDR machinery experiment; not a direct D2-versus-D3 comparison. [vdm-lieben2012] Normocalcemia is maintained in mice under conditions of calcium malabsorption by vitamin D-induced inhibition of bone mineralization. (2012). https://pubmed.ncbi.nlm.nih.gov/22523068/ DOI: 10.1172/jci45890

cross_nutrient

Vitamin D–calcium–phosphate regulation.

evidence_locator

Abstract: reported experimental results

evidence_scope

D3 active metabolite or VDR machinery experiment; not a direct D2-versus-D3 comparison.

experimental_model

Wild-type and intestinal Slc34a2-deleted mice; active versus paracellular intestinal phosphate transport assays

exposure

Intraperitoneal calcitriol once daily for 2 days; dose not specified in the retrieved abstract.

limitations

Stimulation was segment-specific: increased transporter protein in ileum did not establish the same active-flux response there. No human dietary-dose inference.

nutrient

Vitamin D2 and D3 · Vitamin D2 and D3

nutrient_topic

Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin D2 and D3

organism

Mus musculus

plain_language

Active vitamin D increased the intestine’s sodium-coupled phosphate uptake in the responsive segment.

primary_references

[vdm-hernando2021] 1,25(OH)2 vitamin D3 stimulates active phosphate transport but not paracellular phosphate absorption in mouse intestine. (2021). https://pubmed.ncbi.nlm.nih.gov/33200827/ DOI: 10.1113/jp280345

tissue_or_cell_type

Jejunum

Vitamin D2 and D3: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 665–679

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Wild-type and intestinal Slc34a2-deleted mice; active versus paracellular intestinal phosphate transport assays · source_derived_draft · unverified_draft

### vdm-calcitriol-increases-jejunal-phosphate-transport Two daily calcitriol injections increased active phosphate transport in wild-type mouse jejunum. Condition category: normal nutrient_topic: Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Active vitamin D increased the intestine’s sodium-coupled phosphate uptake in the responsive segment. organism: Mus musculus tissue_or_cell_type: Jejunum experimental_model: Wild-type and intestinal Slc34a2-deleted mice; active versus paracellular intestinal phosphate transport assays limitations: Stimulation was segment-specific: increased transporter protein in ileum did not establish the same active-flux response there. No human dietary-dose inference. exposure: Intraperitoneal calcitriol once daily for 2 days; dose not specified in the retrieved abstract. cross_nutrient: Vitamin D–calcium–phosphate regulation. evidence_locator: Abstract: reported experimental results nutrient: Vitamin D2 and D3 evidence_scope: D3 active metabolite or VDR machinery experiment; not a direct D2-versus-D3 comparison. [vdm-hernando2021] 1,25(OH)2 vitamin D3 stimulates active phosphate transport but not paracellular phosphate absorption in mouse intestine. (2021). https://pubmed.ncbi.nlm.nih.gov/33200827/ DOI: 10.1113/jp280345

cross_nutrient

Vitamin D–calcium–phosphate regulation.

evidence_locator

Abstract: reported experimental results

evidence_scope

D3 active metabolite or VDR machinery experiment; not a direct D2-versus-D3 comparison.

experimental_model

Wild-type and intestinal Slc34a2-deleted mice; active versus paracellular intestinal phosphate transport assays

exposure

Intraperitoneal calcitriol once daily for 2 days; dose not specified in the retrieved abstract.

limitations

A negative result for this assay and regimen does not exclude other doses, durations, species or intestinal segments.

nutrient

Vitamin D2 and D3 · Vitamin D2 and D3

nutrient_topic

Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin D2 and D3

organism

Mus musculus

plain_language

The measured phosphate response involved transport through cells; the route between cells did not show the same increase.

primary_references

[vdm-hernando2021] 1,25(OH)2 vitamin D3 stimulates active phosphate transport but not paracellular phosphate absorption in mouse intestine. (2021). https://pubmed.ncbi.nlm.nih.gov/33200827/ DOI: 10.1113/jp280345

tissue_or_cell_type

Intestinal epithelium

Vitamin D2 and D3: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 681–695

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Wild-type and intestinal Slc34a2-deleted mice; active versus paracellular intestinal phosphate transport assays · source_derived_draft · unverified_draft

### vdm-calcitriol-no-detected-paracellular-phosphate-response The two-day calcitriol regimen did not detectably increase paracellular phosphate flux in the mouse intestine. Condition category: normal nutrient_topic: Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. plain_language: The measured phosphate response involved transport through cells; the route between cells did not show the same increase. organism: Mus musculus tissue_or_cell_type: Intestinal epithelium experimental_model: Wild-type and intestinal Slc34a2-deleted mice; active versus paracellular intestinal phosphate transport assays limitations: A negative result for this assay and regimen does not exclude other doses, durations, species or intestinal segments. exposure: Intraperitoneal calcitriol once daily for 2 days; dose not specified in the retrieved abstract. cross_nutrient: Vitamin D–calcium–phosphate regulation. evidence_locator: Abstract: reported experimental results nutrient: Vitamin D2 and D3 evidence_scope: D3 active metabolite or VDR machinery experiment; not a direct D2-versus-D3 comparison. [vdm-hernando2021] 1,25(OH)2 vitamin D3 stimulates active phosphate transport but not paracellular phosphate absorption in mouse intestine. (2021). https://pubmed.ncbi.nlm.nih.gov/33200827/ DOI: 10.1113/jp280345

cross_nutrient

Vitamin D–calcium–phosphate regulation.

evidence_locator

Abstract: reported experimental results

evidence_scope

D3 active metabolite or VDR machinery experiment; not a direct D2-versus-D3 comparison.

experimental_model

Single recombinant FGF23 injection in rodents; renal transcript/protein and serum phosphate measurements

exposure

Single recombinant FGF23 injection; serum phosphate reduction was first observed at 9 hours; dose not recovered in the primary abstract.

limitations

Transporter abundance is not itself a flux measurement. Lack of a PTH rise and parathyroidectomized-rat responses support a PTH-independent action in this experiment.

nutrient

Vitamin D2 and D3 · Vitamin D2 and D3

nutrient_topic

Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin D2 and D3

organism

Mus musculus; Rattus norvegicus

plain_language

FGF23 reduced a kidney transporter that normally helps retain phosphate.

primary_references

[vdm-shimada2004] FGF-23 is a potent regulator of vitamin D metabolism and phosphate homeostasis. (2004). https://pubmed.ncbi.nlm.nih.gov/15040831/ DOI: 10.1359/jbmr.0301264

tissue_or_cell_type

Kidney

Vitamin D2 and D3: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 745–759

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Single recombinant FGF23 injection in rodents; renal transcript/protein and serum phosphate measurements · source_derived_draft · unverified_draft

### vdm-fgf23-reduces-renal-napi2a Recombinant FGF23 reduced renal NaPi-IIa mRNA and protein abundance in the acute rodent injection study. Condition category: normal nutrient_topic: Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. plain_language: FGF23 reduced a kidney transporter that normally helps retain phosphate. organism: Mus musculus; Rattus norvegicus tissue_or_cell_type: Kidney experimental_model: Single recombinant FGF23 injection in rodents; renal transcript/protein and serum phosphate measurements limitations: Transporter abundance is not itself a flux measurement. Lack of a PTH rise and parathyroidectomized-rat responses support a PTH-independent action in this experiment. exposure: Single recombinant FGF23 injection; serum phosphate reduction was first observed at 9 hours; dose not recovered in the primary abstract. cross_nutrient: Vitamin D–calcium–phosphate regulation. evidence_locator: Abstract: reported experimental results nutrient: Vitamin D2 and D3 evidence_scope: D3 active metabolite or VDR machinery experiment; not a direct D2-versus-D3 comparison. [vdm-shimada2004] FGF-23 is a potent regulator of vitamin D metabolism and phosphate homeostasis. (2004). https://pubmed.ncbi.nlm.nih.gov/15040831/ DOI: 10.1359/jbmr.0301264

availability_state

machinery_impairment Imported condition classification; unverified.

cross_nutrient

Vitamin D–calcium–phosphate regulation.

evidence_locator

Abstract: reported experimental results

evidence_scope

D3 active metabolite or VDR machinery experiment; not a direct D2-versus-D3 comparison.

experimental_model

Vdr-null and wild-type mice; intestinal brush-border transporter immunodetection

exposure

Vdr deletion plus dietary phosphate restriction; exact dietary percentage and duration not given in the retrieved abstract.

limitations

Baseline NaPi-IIb protein and sodium-dependent phosphate transport were lower in knockout mice; preserved adaptation does not imply normal baseline transport.

nutrient

Vitamin D2 and D3 · Vitamin D2 and D3

nutrient_topic

Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin D2 and D3

organism

Mus musculus

plain_language

The intestine retained a phosphate-conservation response despite loss of vitamin D receptor signaling.

primary_references

[vdm-segawa2004] Intestinal Na-P(i) cotransporter adaptation to dietary P(i) content in vitamin D receptor null mice. (2004). https://pubmed.ncbi.nlm.nih.gov/14996670/ DOI: 10.1152/ajprenal.00375.2003

tissue_or_cell_type

Intestinal brush-border membrane

trigger_kind

machinery_impairment Imported condition classification; unverified.

Vitamin D2 and D3: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 713–727

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Vdr-null and wild-type mice; intestinal brush-border transporter immunodetection · source_derived_draft · unverified_draft

### vdm-low-phosphate-adaptation-persists-without-vdr A low-phosphate diet increased intestinal NaPi-IIb protein expression even in Vdr-null mice. Condition category: machinery_impairment nutrient_topic: Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. plain_language: The intestine retained a phosphate-conservation response despite loss of vitamin D receptor signaling. organism: Mus musculus tissue_or_cell_type: Intestinal brush-border membrane experimental_model: Vdr-null and wild-type mice; intestinal brush-border transporter immunodetection limitations: Baseline NaPi-IIb protein and sodium-dependent phosphate transport were lower in knockout mice; preserved adaptation does not imply normal baseline transport. exposure: Vdr deletion plus dietary phosphate restriction; exact dietary percentage and duration not given in the retrieved abstract. cross_nutrient: Vitamin D–calcium–phosphate regulation. evidence_locator: Abstract: reported experimental results nutrient: Vitamin D2 and D3 evidence_scope: D3 active metabolite or VDR machinery experiment; not a direct D2-versus-D3 comparison. [vdm-segawa2004] Intestinal Na-P(i) cotransporter adaptation to dietary P(i) content in vitamin D receptor null mice. (2004). https://pubmed.ncbi.nlm.nih.gov/14996670/ DOI: 10.1152/ajprenal.00375.2003

availability_state

machinery_impairment Imported condition classification; unverified.

cross_nutrient

Vitamin D–calcium–phosphate regulation.

evidence_locator

Abstract: reported experimental results

evidence_scope

D3 active metabolite or VDR machinery experiment; not a direct D2-versus-D3 comparison.

experimental_model

Wild-type and intestinal Slc34a2-deleted mice; active versus paracellular intestinal phosphate transport assays

exposure

Intraperitoneal calcitriol once daily for 2 days; dose not specified in the retrieved abstract.

limitations

Conditional transporter loss removes the measured hormonal increment; it does not prove that all baseline phosphate absorption is absent.

nutrient

Vitamin D2 and D3 · Vitamin D2 and D3

nutrient_topic

Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin D2 and D3

organism

Mus musculus

plain_language

Without this intestinal transporter, active vitamin D failed to produce its usual phosphate-uptake increment.

primary_references

[vdm-hernando2021] 1,25(OH)2 vitamin D3 stimulates active phosphate transport but not paracellular phosphate absorption in mouse intestine. (2021). https://pubmed.ncbi.nlm.nih.gov/33200827/ DOI: 10.1113/jp280345

tissue_or_cell_type

Intestinal epithelium

trigger_kind

machinery_impairment Imported condition classification; unverified.

Vitamin D2 and D3: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 697–711

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Wild-type and intestinal Slc34a2-deleted mice; active versus paracellular intestinal phosphate transport assays · source_derived_draft · unverified_draft

### vdm-slc34a2-deletion-removes-calcitriol-phosphate-increment Intestine-specific Slc34a2 deletion eliminated the phosphate-transport increase induced by the tested calcitriol regimen. Condition category: machinery_impairment nutrient_topic: Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Without this intestinal transporter, active vitamin D failed to produce its usual phosphate-uptake increment. organism: Mus musculus tissue_or_cell_type: Intestinal epithelium experimental_model: Wild-type and intestinal Slc34a2-deleted mice; active versus paracellular intestinal phosphate transport assays limitations: Conditional transporter loss removes the measured hormonal increment; it does not prove that all baseline phosphate absorption is absent. exposure: Intraperitoneal calcitriol once daily for 2 days; dose not specified in the retrieved abstract. cross_nutrient: Vitamin D–calcium–phosphate regulation. evidence_locator: Abstract: reported experimental results nutrient: Vitamin D2 and D3 evidence_scope: D3 active metabolite or VDR machinery experiment; not a direct D2-versus-D3 comparison. [vdm-hernando2021] 1,25(OH)2 vitamin D3 stimulates active phosphate transport but not paracellular phosphate absorption in mouse intestine. (2021). https://pubmed.ncbi.nlm.nih.gov/33200827/ DOI: 10.1113/jp280345

cross_nutrient

Vitamin D–calcium–phosphate regulation.

evidence_locator

Figure 6 and adjacent Results: mineralization restored by TNAP

evidence_scope

D3 active metabolite or VDR machinery experiment; not a direct D2-versus-D3 comparison.

experimental_model

Differentiated primary mouse osteoblasts; Alizarin red mineralization and conditioned-medium pyrophosphate assays

exposure

10^-8 M calcitriol and 1 U/mL added TNAP for 4 days; companion cultures tested 5 x 10^-6 M pyrophosphate.

limitations

Enzyme-addition culture rescue supports pyrophosphate involvement; it does not quantify human bone outcomes or establish the contribution of each calcitriol-regulated gene.

nutrient

Vitamin D2 and D3 · Vitamin D2 and D3

nutrient_topic

Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin D2 and D3

organism

Mus musculus

plain_language

Removing the pyrophosphate brake restored mineral deposition in the treated cultures.

primary_references

[vdm-lieben2012] Normocalcemia is maintained in mice under conditions of calcium malabsorption by vitamin D-induced inhibition of bone mineralization. (2012). https://pubmed.ncbi.nlm.nih.gov/22523068/ DOI: 10.1172/jci45890

tissue_or_cell_type

Osteoblast extracellular matrix

Vitamin D2 and D3: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 825–839

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Differentiated primary mouse osteoblasts; Alizarin red mineralization and conditioned-medium pyrophosphate assays · source_derived_draft · unverified_draft

### vdm-tnap-rescues-calcitriol-culture-mineralization Added TNAP restored mineralization in calcitriol-treated differentiated mouse osteoblast cultures while lowering extracellular pyrophosphate. Condition category: normal nutrient_topic: Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Removing the pyrophosphate brake restored mineral deposition in the treated cultures. organism: Mus musculus tissue_or_cell_type: Osteoblast extracellular matrix experimental_model: Differentiated primary mouse osteoblasts; Alizarin red mineralization and conditioned-medium pyrophosphate assays limitations: Enzyme-addition culture rescue supports pyrophosphate involvement; it does not quantify human bone outcomes or establish the contribution of each calcitriol-regulated gene. exposure: 10^-8 M calcitriol and 1 U/mL added TNAP for 4 days; companion cultures tested 5 x 10^-6 M pyrophosphate. cross_nutrient: Vitamin D–calcium–phosphate regulation. evidence_locator: Figure 6 and adjacent Results: mineralization restored by TNAP nutrient: Vitamin D2 and D3 evidence_scope: D3 active metabolite or VDR machinery experiment; not a direct D2-versus-D3 comparison. [vdm-lieben2012] Normocalcemia is maintained in mice under conditions of calcium malabsorption by vitamin D-induced inhibition of bone mineralization. (2012). https://pubmed.ncbi.nlm.nih.gov/22523068/ DOI: 10.1172/jci45890

evidence_access

Primary abstract

experimental_model

Isolated rat liver mitochondria; swelling and protein-release assays.

limitations

Numerical concentration ranges are not provided in the accessed abstract; no human protective threshold is inferred.

nutrient_topic

Agmatine Sulfate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Agmatine Sulfate

plain_language

A compound can change direction across concentrations and assay endpoints.

primary_references

Involvement of the biogenic active amine agmatine in mitochondrial membrane permeabilization and release of pro-apoptotic factors. · 2020 · https://pubmed.ncbi.nlm.nih.gov/31654209/ · DOI 10.1007/s00726-019-02791-6

Agmatine Sulfate: transport, guanidino metabolism, ion channels and cross-nutrient mechanisms (2026-09-20) · lines 388–394

AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Isolated rat liver mitochondria; swelling and protein-release assays. · source_derived_draft · unverified_draft

## agmatine-sulfate-mitochondrial-state A compound can change direction across concentrations and assay endpoints. Agmatine induced permeability transition at lower tested concentrations but inhibited calcium/phosphate-associated swelling at higher concentrations in isolated rat liver mitochondria. Model: Isolated rat liver mitochondria; swelling and protein-release assays. Limitations: Numerical concentration ranges are not provided in the accessed abstract; no human protective threshold is inferred. Evidence access: Primary abstract Involvement of the biogenic active amine agmatine in mitochondrial membrane permeabilization and release of pro-apoptotic factors. · 2020 · https://pubmed.ncbi.nlm.nih.gov/31654209/ · DOI 10.1007/s00726-019-02791-6

availability_state

machinery_impairment Imported condition classification; unverified.

evidence_access

Primary abstract

experimental_model

Human erythrocytes; DIDS pharmacological intervention.

limitations

DIDS is an inhibitor, not itself an exchanger; pharmacology does not establish a unique SLC4A1 transport substrate or route.

nutrient_topic

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

plain_language

Membrane transport can gate the redox response.

primary_references

Efflux of glutathione and glutathione complexes from human erythrocytes in response to vanadate. · 2013 · https://pubmed.ncbi.nlm.nih.gov/22824382/ · DOI 10.1016/j.bcmd.2012.07.001

trigger_kind

machinery_impairment Imported condition classification; unverified.

Vanadium: speciation, phosphate-sensitive enzymes and cross-nutrient mechanisms (2026-09-19) · lines 166–172

AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human erythrocytes; DIDS pharmacological intervention. · source_derived_draft · unverified_draft

## vanadium-anion-exchanger-block Membrane transport can gate the redox response. DIDS inhibited the intracellular thiol decrease and extracellular increase during vanadate exposure, supporting an anion-transport-dependent step. Model: Human erythrocytes; DIDS pharmacological intervention. Limitations: DIDS is an inhibitor, not itself an exchanger; pharmacology does not establish a unique SLC4A1 transport substrate or route. Evidence access: Primary abstract Efflux of glutathione and glutathione complexes from human erythrocytes in response to vanadate. · 2013 · https://pubmed.ncbi.nlm.nih.gov/22824382/ · DOI 10.1016/j.bcmd.2012.07.001

evidence_access

Primary abstract

experimental_model

Cell-free concentration-response experiments.

limitations

Not an established supplement dose-response in humans.

nutrient_topic

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

plain_language

The direction of an antioxidant’s effect can depend on concentration.

primary_references

Vanadate-mediated oxidation of NADH: description of an in vitro system requiring ascorbate and phosphate. · 1989 · https://pubmed.ncbi.nlm.nih.gov/2735768/ · DOI 10.1016/0003-9861(89)90196-3

Vanadium: speciation, phosphate-sensitive enzymes and cross-nutrient mechanisms (2026-09-19) · lines 134–140

AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Cell-free concentration-response experiments. · source_derived_draft · unverified_draft

## vanadium-ascorbate-concentration The direction of an antioxidant’s effect can depend on concentration. Ascorbate initiated NADH oxidation at lower concentrations but inhibited it at higher concentrations in the same chemical system. Model: Cell-free concentration-response experiments. Limitations: Not an established supplement dose-response in humans. Evidence access: Primary abstract Vanadate-mediated oxidation of NADH: description of an in vitro system requiring ascorbate and phosphate. · 1989 · https://pubmed.ncbi.nlm.nih.gov/2735768/ · DOI 10.1016/0003-9861(89)90196-3

evidence_access

Primary abstract

experimental_model

ESR and spin-trapping chemistry; cell-free solutions.

limitations

Buffer-dependent chemistry does not establish a human depletion rate or clinical interaction.

nutrient_topic

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

plain_language

Vitamin C and phosphate together changed vanadium’s oxidation state in this assay.

primary_references

One-electron reduction of vanadate by ascorbate and related free radical generation at physiological pH. · 1994 · https://pubmed.ncbi.nlm.nih.gov/8051539/ · DOI 10.1016/0162-0134(94)85032-1

Vanadium: speciation, phosphate-sensitive enzymes and cross-nutrient mechanisms (2026-09-19) · lines 94–100

AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · ESR and spin-trapping chemistry; cell-free solutions. · source_derived_draft · unverified_draft

## vanadium-ascorbate-reduction Vitamin C and phosphate together changed vanadium’s oxidation state in this assay. Ascorbate generated V(IV) from vanadate in phosphate buffer at pH 7.4, but not comparably in water or the tested cacodylate buffer. Model: ESR and spin-trapping chemistry; cell-free solutions. Limitations: Buffer-dependent chemistry does not establish a human depletion rate or clinical interaction. Evidence access: Primary abstract One-electron reduction of vanadate by ascorbate and related free radical generation at physiological pH. · 1994 · https://pubmed.ncbi.nlm.nih.gov/8051539/ · DOI 10.1016/0162-0134(94)85032-1

evidence_access

Primary abstract

experimental_model

Rat liver F1 crystallography.

limitations

A captured structure is not proof that a given oral dose suppresses mitochondrial ATP production.

nutrient_topic

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

plain_language

Another ATP-handling enzyme can bind the phosphate analogue.

primary_references

Mitochondrial ATP synthase. Crystal structure of the catalytic F1 unit in a vanadate-induced transition-like state and implications for mechanism. · 2006 · https://pubmed.ncbi.nlm.nih.gov/16531409/ · DOI 10.1074/jbc.M513369200

Vanadium: speciation, phosphate-sensitive enzymes and cross-nutrient mechanisms (2026-09-19) · lines 262–268

AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Rat liver F1 crystallography. · source_derived_draft · unverified_draft

## vanadium-f1-transition Another ATP-handling enzyme can bind the phosphate analogue. Vanadate crystallization of rat-liver F1 ATP synthase captured an ADP–vanadate–Mg transition-like state with remodeling of the catalytic P-loop region. Model: Rat liver F1 crystallography. Limitations: A captured structure is not proof that a given oral dose suppresses mitochondrial ATP production. Evidence access: Primary abstract Mitochondrial ATP synthase. Crystal structure of the catalytic F1 unit in a vanadate-induced transition-like state and implications for mechanism. · 2006 · https://pubmed.ncbi.nlm.nih.gov/16531409/ · DOI 10.1074/jbc.M513369200

evidence_access

Primary abstract

experimental_model

Cell-free model-hydroperoxide assay.

limitations

Cumene hydroperoxide is a model reagent, not direct measurement of membrane injury in humans.

nutrient_topic

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

plain_language

The same redox system can also react with a model lipid peroxide.

primary_references

One-electron reduction of vanadate by ascorbate and related free radical generation at physiological pH. · 1994 · https://pubmed.ncbi.nlm.nih.gov/8051539/ · DOI 10.1016/0162-0134(94)85032-1

Vanadium: speciation, phosphate-sensitive enzymes and cross-nutrient mechanisms (2026-09-19) · lines 110–116

AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Cell-free model-hydroperoxide assay. · source_derived_draft · unverified_draft

## vanadium-lipid-peroxide-radicals The same redox system can also react with a model lipid peroxide. V(IV) generated by ascorbate/vanadate chemistry produced hydroperoxide-derived radicals from cumene hydroperoxide. Model: Cell-free model-hydroperoxide assay. Limitations: Cumene hydroperoxide is a model reagent, not direct measurement of membrane injury in humans. Evidence access: Primary abstract One-electron reduction of vanadate by ascorbate and related free radical generation at physiological pH. · 1994 · https://pubmed.ncbi.nlm.nih.gov/8051539/ · DOI 10.1016/0162-0134(94)85032-1

evidence_access

Primary abstract

experimental_model

Cell-free NADH/NADPH oxidation experiments.

limitations

Not evidence of a measured whole-body NAD shortage.

nutrient_topic

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

plain_language

Reducing equivalents can be consumed by a metal-dependent reaction.

primary_references

Vanadate-mediated oxidation of NADH: description of an in vitro system requiring ascorbate and phosphate. · 1989 · https://pubmed.ncbi.nlm.nih.gov/2735768/ · DOI 10.1016/0003-9861(89)90196-3

Vanadium: speciation, phosphate-sensitive enzymes and cross-nutrient mechanisms (2026-09-19) · lines 118–124

AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Cell-free NADH/NADPH oxidation experiments. · source_derived_draft · unverified_draft

## vanadium-nadh-oxidation Reducing equivalents can be consumed by a metal-dependent reaction. A vanadate/ascorbate/phosphate system oxidized NADH, with similar results for NADPH, through a proposed superoxide-initiated chain reaction. Model: Cell-free NADH/NADPH oxidation experiments. Limitations: Not evidence of a measured whole-body NAD shortage. Evidence access: Primary abstract Vanadate-mediated oxidation of NADH: description of an in vitro system requiring ascorbate and phosphate. · 1989 · https://pubmed.ncbi.nlm.nih.gov/2735768/ · DOI 10.1016/0003-9861(89)90196-3

evidence_access

Primary abstract

experimental_model

Cell-free ESR spin trapping.

limitations

Chemical mechanism under specified reagents; not proof that vitamin C supplementation causes this injury in people.

nutrient_topic

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

plain_language

A reductant can enable pro-oxidant chemistry when peroxide is also present.

primary_references

One-electron reduction of vanadate by ascorbate and related free radical generation at physiological pH. · 1994 · https://pubmed.ncbi.nlm.nih.gov/8051539/ · DOI 10.1016/0162-0134(94)85032-1

Vanadium: speciation, phosphate-sensitive enzymes and cross-nutrient mechanisms (2026-09-19) · lines 102–108

AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Cell-free ESR spin trapping. · source_derived_draft · unverified_draft

## vanadium-peroxide-radicals A reductant can enable pro-oxidant chemistry when peroxide is also present. In phosphate/ascorbate mixtures with peroxide, reduced vanadium supported hydroxyl-radical generation; omitting phosphate sharply reduced the yield. Model: Cell-free ESR spin trapping. Limitations: Chemical mechanism under specified reagents; not proof that vitamin C supplementation causes this injury in people. Evidence access: Primary abstract One-electron reduction of vanadate by ascorbate and related free radical generation at physiological pH. · 1994 · https://pubmed.ncbi.nlm.nih.gov/8051539/ · DOI 10.1016/0162-0134(94)85032-1

evidence_access

Primary abstract

experimental_model

Recombinant-enzyme kinetic study; construct species not resolved from accessed primary abstract.

limitations

Assay affinity is not a dietary threshold, and PTP1B is not the only phosphatase inhibited.

nutrient_topic

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

plain_language

A phosphate-like inhibitor can occupy a phosphatase’s catalytic machinery.

primary_references

Mechanism of inhibition of protein-tyrosine phosphatases by vanadate and pervanadate. · 1997 · https://pubmed.ncbi.nlm.nih.gov/8995372/ · DOI 10.1074/jbc.272.2.843

Vanadium: speciation, phosphate-sensitive enzymes and cross-nutrient mechanisms (2026-09-19) · lines 14–20

AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Recombinant-enzyme kinetic study; construct species not resolved from accessed primary abstract. · source_derived_draft · unverified_draft

## vanadium-ptp-competitive A phosphate-like inhibitor can occupy a phosphatase’s catalytic machinery. Vanadate competitively inhibited PTP1B with a reported Ki of 0.38 ± 0.02 micromolar. Model: Recombinant-enzyme kinetic study; construct species not resolved from accessed primary abstract. Limitations: Assay affinity is not a dietary threshold, and PTP1B is not the only phosphatase inhibited. Evidence access: Primary abstract Mechanism of inhibition of protein-tyrosine phosphatases by vanadate and pervanadate. · 1997 · https://pubmed.ncbi.nlm.nih.gov/8995372/ · DOI 10.1074/jbc.272.2.843

evidence_access

Primary abstract and RCSB PDB 5A3Q author deposition

experimental_model

Rabbit SERCA structure, deposition 5A3Q; primary abstract plus author-deposited structure identity.

limitations

Structure used nucleotide analogues and thapsigargin; not a measured human intracellular calcium effect.

nutrient_topic

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

plain_language

A phosphate analogue can trap a calcium pump in a catalytic state.

primary_references

Crystal Structure of the Vanadate-Inhibited Ca(2+)-ATPase. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27050689/ · DOI 10.1016/j.str.2016.02.018

Vanadium: speciation, phosphate-sensitive enzymes and cross-nutrient mechanisms (2026-09-19) · lines 254–260

AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Rabbit SERCA structure, deposition 5A3Q; primary abstract plus author-deposited structure identity. · source_derived_draft · unverified_draft

## vanadium-serca-transition A phosphate analogue can trap a calcium pump in a catalytic state. Vanadate occupied the catalytic site of calcium-free SERCA as planar VO3 with water and magnesium in a dephosphorylation-transition-like conformation. Model: Rabbit SERCA structure, deposition 5A3Q; primary abstract plus author-deposited structure identity. Limitations: Structure used nucleotide analogues and thapsigargin; not a measured human intracellular calcium effect. Evidence access: Primary abstract and RCSB PDB 5A3Q author deposition Crystal Structure of the Vanadate-Inhibited Ca(2+)-ATPase. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27050689/ · DOI 10.1016/j.str.2016.02.018

evidence_access

Primary abstract

experimental_model

Cell-free scavenger comparison.

limitations

Does not imply catalase is irrelevant to all vanadium toxicity.

nutrient_topic

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

plain_language

The scavenger comparison points to a superoxide-dependent step in this particular reaction.

primary_references

Vanadate-mediated oxidation of NADH: description of an in vitro system requiring ascorbate and phosphate. · 1989 · https://pubmed.ncbi.nlm.nih.gov/2735768/ · DOI 10.1016/0003-9861(89)90196-3

Vanadium: speciation, phosphate-sensitive enzymes and cross-nutrient mechanisms (2026-09-19) · lines 126–132

AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Cell-free scavenger comparison. · source_derived_draft · unverified_draft

## vanadium-sod-redox-rescue The scavenger comparison points to a superoxide-dependent step in this particular reaction. Superoxide dismutase inhibited NADH oxidation in the vanadate/ascorbate/phosphate system, whereas catalase and ethanol did not. Model: Cell-free scavenger comparison. Limitations: Does not imply catalase is irrelevant to all vanadium toxicity. Evidence access: Primary abstract Vanadate-mediated oxidation of NADH: description of an in vitro system requiring ascorbate and phosphate. · 1989 · https://pubmed.ncbi.nlm.nih.gov/2735768/ · DOI 10.1016/0003-9861(89)90196-3

evidence_span

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experimental_model

Phosphatase biochemistry, mitochondrial inhibition and adipocyte gene deletion

exposure

TNAP inhibition and adipocyte Alpl deletion

limitations

Mouse mechanism; it does not establish that creatine supplements cause weight loss in humans.

nutrient_topic

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

organism

Mouse thermogenic adipocytes and mice

plain_language

This phosphatase releases the stored phosphate without making ATP, allowing continued fuel use and heat production.

primary_references

[creatine-p33981039] Mitochondrial TNAP controls thermogenesis by hydrolysis of phosphocreatine. (2021). https://pubmed.ncbi.nlm.nih.gov/33981039/ DOI: 10.1038/s41586-021-03533-z

tissue_or_cell_type

Adipocyte mitochondria

Creatine: synthesis, transport, phosphocreatine energetics and nutrient interactions (2026-09-17) · lines 503–514

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Phosphatase biochemistry, mitochondrial inhibition and adipocyte gene deletion · source_derived_draft · unverified_draft

### creatine-tnap-pcr-hydrolysis TNAP localized to thermogenic adipocyte mitochondria and hydrolyzed phosphocreatine to support the futile creatine cycle. Condition category: normal nutrient_topic: Creatine research collection; topical membership is not evidence of a direct dietary effect. plain_language: This phosphatase releases the stored phosphate without making ATP, allowing continued fuel use and heat production. organism: Mouse thermogenic adipocytes and mice tissue_or_cell_type: Adipocyte mitochondria experimental_model: Phosphatase biochemistry, mitochondrial inhibition and adipocyte gene deletion limitations: Mouse mechanism; it does not establish that creatine supplements cause weight loss in humans. exposure: TNAP inhibition and adipocyte Alpl deletion evidence_span: {"source_cache": "artifacts/creatine-research/33981039.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "915403423e16b5e0e5db70e99ebc6518e612bc9ef69ceb1e25da3074a8410dca", "start_char": 0, "end_char": 1400, "text_sha256": "915403423e16b5e0e5db70e99ebc6518e612bc9ef69ceb1e25da3074a8410dca"} [creatine-p33981039] Mitochondrial TNAP controls thermogenesis by hydrolysis of phosphocreatine. (2021). https://pubmed.ncbi.nlm.nih.gov/33981039/ DOI: 10.1038/s41586-021-03533-z

evidence-scope

Brain mitochondria

evidence_locator

Results: ThTP synthesis in isolated mitochondria and energy coupling

evidence_spans

[{"source_document": "artifacts/thiamine_transport_sources/gangolf-2010-thtp-source-record.json", "source_field": "resultList.result[0].abstractText", "start_char": 0, "end_char": 1672}]

experimental_model

Isolated rat brain mitochondria; ThDP/Pi incubation, respiratory substrates and inhibitors.

limitations

Not a demonstrated human signaling function or a TPK1 reaction.

nutrient_topic

Thiamine research collection; topical membership is not evidence of a direct dietary effect. · Thiamine (vitamin B1)

organism

Rattus norvegicus

plain_language

A third phosphate can be added to B1 using respiratory energy in this preparation.

primary_references

[gangolf-2010-thtp] Thiamine Triphosphate Synthesis in Rat Brain Occurs in Mitochondria and Is Coupled to the Respiratory Chain (2010). https://pmc.ncbi.nlm.nih.gov/articles/PMC2804207/ DOI: 10.1074/jbc.M109.054379

reaction

ThDP + Pi <-> ThTP + water; coupled to respiratory energy

tissue_or_cell_type

Brain mitochondria

Thiamine: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 602–615

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Isolated rat brain mitochondria; ThDP/Pi incubation, respiratory substrates and inhibitors. · source_derived_draft · unverified_draft

### b1-brain-thtp-from-thdp-and-pi Rat brain mitochondria formed ThTP from ThDP and inorganic phosphate with respiratory substrates; ATP hydrolysis did not energize synthesis. Condition category: normal nutrient_topic: Thiamine research collection; topical membership is not evidence of a direct dietary effect. plain_language: A third phosphate can be added to B1 using respiratory energy in this preparation. organism: Rattus norvegicus tissue_or_cell_type: Brain mitochondria experimental_model: Isolated rat brain mitochondria; ThDP/Pi incubation, respiratory substrates and inhibitors. limitations: Not a demonstrated human signaling function or a TPK1 reaction. reaction: ThDP + Pi <-> ThTP + water; coupled to respiratory energy evidence_spans: [{"source_document": "artifacts/thiamine_transport_sources/gangolf-2010-thtp-source-record.json", "source_field": "resultList.result[0].abstractText", "start_char": 0, "end_char": 1672}] evidence_locator: Results: ThTP synthesis in isolated mitochondria and energy coupling evidence-scope: Brain mitochondria [gangolf-2010-thtp] Thiamine Triphosphate Synthesis in Rat Brain Occurs in Mitochondria and Is Coupled to the Respiratory Chain (2010). https://pmc.ncbi.nlm.nih.gov/articles/PMC2804207/ DOI: 10.1074/jbc.M109.054379

evidence_access

Primary abstract

experimental_model

Six water-loaded healthy subjects; 120-minute euglycemic insulin infusion, 98–193 microU/mL.

limitations

Insulin-clamp mechanism, not a fasting or refeeding-syndrome trial.

nutrient_topic

Fasting physiological-state collection; human protocols, cellular deprivation and refeeding are distinguished. · Fasting / abstention from energy intake

plain_language

Phosphate handling changed when insulin rose.

primary_references

The effect of insulin on renal handling of sodium, potassium, calcium, and phosphate in man. · 1975 · https://pubmed.ncbi.nlm.nih.gov/1120786/ · DOI 10.1172/JCI107996

Fasting: fuel switching, nutrient sensing, ketone signaling, nutrient dependencies and refeeding (2026-09-18) · lines 464–470

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Six water-loaded healthy subjects; 120-minute euglycemic insulin infusion, 98–193 microU/mL. · source_derived_draft · unverified_draft

## fast-insulin-phosphate Phosphate handling changed when insulin rose. Urinary phosphate excretion fell from 504 to 230 micrograms/min, with a small plasma phosphate decrease. Model: Six water-loaded healthy subjects; 120-minute euglycemic insulin infusion, 98–193 microU/mL. Limitations: Insulin-clamp mechanism, not a fasting or refeeding-syndrome trial. Evidence access: Primary abstract The effect of insulin on renal handling of sodium, potassium, calcium, and phosphate in man. · 1975 · https://pubmed.ncbi.nlm.nih.gov/1120786/ · DOI 10.1172/JCI107996

availability_state

nutrient_deficiency Imported condition classification; unverified.

evidence_span

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experimental_model

Double-blind randomized comparison with physiological substudy

exposure

One treatment course of ferric carboxymaltose versus ferumoxytol; five-week follow-up

limitations

Formulation-specific pharmacological effect, not dietary iron or all intravenous iron. Trial funded by ferumoxytol manufacturer; mineral associations support but do not individually prove every causal arrow.

nutrient_topic

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

organism

1997 adults with iron-deficiency anemia; 185 in substudy

plain_language

The phosphate risk depended strongly on the iron formulation.

primary_references

[iron-p30518682] Randomized trial of intravenous iron-induced hypophosphatemia. (2018). https://pubmed.ncbi.nlm.nih.gov/30518682/ DOI: 10.1172/jci.insight.124486

tissue_or_cell_type

Blood and renal phosphate handling

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Iron: absorption, trafficking, iron-dependent enzymes and nutrient interactions (2026-09-17) · lines 940–951

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Double-blind randomized comparison with physiological substudy · source_derived_draft · unverified_draft

### iron-fcm-phosphate-frequency Phosphate below 2.0 mg/dL occurred in 50.8% with ferric carboxymaltose versus 0.9% with ferumoxytol; low phosphate persisted at five weeks in 29.1% versus none. Condition category: nutrient_deficiency nutrient_topic: Iron research collection; topical membership is not evidence of a direct dietary effect. plain_language: The phosphate risk depended strongly on the iron formulation. organism: 1997 adults with iron-deficiency anemia; 185 in substudy tissue_or_cell_type: Blood and renal phosphate handling experimental_model: Double-blind randomized comparison with physiological substudy limitations: Formulation-specific pharmacological effect, not dietary iron or all intravenous iron. Trial funded by ferumoxytol manufacturer; mineral associations support but do not individually prove every causal arrow. exposure: One treatment course of ferric carboxymaltose versus ferumoxytol; five-week follow-up evidence_span: {"source_cache": "artifacts/iron-research/30518682.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "489945718bb05c0630fd563dc5a6da0874e80685717ab06ceedfefc38d172257", "start_char": 0, "end_char": 2371, "text_sha256": "489945718bb05c0630fd563dc5a6da0874e80685717ab06ceedfefc38d172257"} [iron-p30518682] Randomized trial of intravenous iron-induced hypophosphatemia. (2018). https://pubmed.ncbi.nlm.nih.gov/30518682/ DOI: 10.1172/jci.insight.124486

availability_state

nutrient_deficiency Imported condition classification; unverified.

evidence_span

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experimental_model

Two open-label randomized trials

exposure

Ferric derisomaltose 1000 mg once versus ferric carboxymaltose 750 mg twice; 35 days

limitations

Formulation and total regimen differed; no fracture endpoint or identical risk in all populations is inferred.

nutrient_topic

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

organism

245 adults, predominantly women, without reduced kidney function

plain_language

A second pair of trials also found that iron formulations differed in their phosphate effects.

primary_references

[iron-p32016310] Effects of Iron Isomaltoside vs Ferric Carboxymaltose on Hypophosphatemia in Iron-Deficiency Anemia: Two Randomized Clinical Trials. (2020). https://pubmed.ncbi.nlm.nih.gov/32016310/ DOI: 10.1001/jama.2019.22450

tissue_or_cell_type

Serum phosphate

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Iron: absorption, trafficking, iron-dependent enzymes and nutrient interactions (2026-09-17) · lines 992–1003

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Two open-label randomized trials · source_derived_draft · unverified_draft

### iron-fdi-fcm-comparison Hypophosphatemia occurred in 7.9% versus 75.0% in trial A and 8.1% versus 73.7% in trial B with derisomaltose versus carboxymaltose. Condition category: nutrient_deficiency nutrient_topic: Iron research collection; topical membership is not evidence of a direct dietary effect. plain_language: A second pair of trials also found that iron formulations differed in their phosphate effects. organism: 245 adults, predominantly women, without reduced kidney function tissue_or_cell_type: Serum phosphate experimental_model: Two open-label randomized trials limitations: Formulation and total regimen differed; no fracture endpoint or identical risk in all populations is inferred. exposure: Ferric derisomaltose 1000 mg once versus ferric carboxymaltose 750 mg twice; 35 days evidence_span: {"source_cache": "artifacts/iron-research/32016310.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "883aac76c40012cb98ac88924e33b33f4985d356302929b8b26931c1869e2f0a", "start_char": 0, "end_char": 2731, "text_sha256": "883aac76c40012cb98ac88924e33b33f4985d356302929b8b26931c1869e2f0a"} [iron-p32016310] Effects of Iron Isomaltoside vs Ferric Carboxymaltose on Hypophosphatemia in Iron-Deficiency Anemia: Two Randomized Clinical Trials. (2020). https://pubmed.ncbi.nlm.nih.gov/32016310/ DOI: 10.1001/jama.2019.22450

availability_state

nutrient_deficiency Imported condition classification; unverified.

evidence_span

{"source_cache": "artifacts/iron-research/30518682.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "489945718bb05c0630fd563dc5a6da0874e80685717ab06ceedfefc38d172257", "start_char": 0, "end_char": 2371, "text_sha256": "489945718bb05c0630fd563dc5a6da0874e80685717ab06ceedfefc38d172257"}

experimental_model

Double-blind randomized comparison with physiological substudy

exposure

One treatment course of ferric carboxymaltose versus ferumoxytol; five-week follow-up

limitations

Formulation-specific pharmacological effect, not dietary iron or all intravenous iron. Trial funded by ferumoxytol manufacturer; mineral associations support but do not individually prove every causal arrow.

nutrient_topic

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

organism

1997 adults with iron-deficiency anemia; 185 in substudy

plain_language

More phosphate was being lost through the kidneys as the hormone rose.

primary_references

[iron-p30518682] Randomized trial of intravenous iron-induced hypophosphatemia. (2018). https://pubmed.ncbi.nlm.nih.gov/30518682/ DOI: 10.1172/jci.insight.124486

tissue_or_cell_type

Blood and renal phosphate handling

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Iron: absorption, trafficking, iron-dependent enzymes and nutrient interactions (2026-09-17) · lines 966–977

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Double-blind randomized comparison with physiological substudy · source_derived_draft · unverified_draft

### iron-fgf23-phosphate-loss The rise in active FGF23 was associated with increased renal phosphate wasting and hypophosphatemia. Condition category: nutrient_deficiency nutrient_topic: Iron research collection; topical membership is not evidence of a direct dietary effect. plain_language: More phosphate was being lost through the kidneys as the hormone rose. organism: 1997 adults with iron-deficiency anemia; 185 in substudy tissue_or_cell_type: Blood and renal phosphate handling experimental_model: Double-blind randomized comparison with physiological substudy limitations: Formulation-specific pharmacological effect, not dietary iron or all intravenous iron. Trial funded by ferumoxytol manufacturer; mineral associations support but do not individually prove every causal arrow. exposure: One treatment course of ferric carboxymaltose versus ferumoxytol; five-week follow-up evidence_span: {"source_cache": "artifacts/iron-research/30518682.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "489945718bb05c0630fd563dc5a6da0874e80685717ab06ceedfefc38d172257", "start_char": 0, "end_char": 2371, "text_sha256": "489945718bb05c0630fd563dc5a6da0874e80685717ab06ceedfefc38d172257"} [iron-p30518682] Randomized trial of intravenous iron-induced hypophosphatemia. (2018). https://pubmed.ncbi.nlm.nih.gov/30518682/ DOI: 10.1172/jci.insight.124486

evidence_span

{"source_cache": "artifacts/inositol-research/40128258.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4765253840f684d5dafa834980e3fea9edc5d7419379b4a27ccf1090f081ce00", "start_char": 0, "end_char": 1071, "text_sha256": "4765253840f684d5dafa834980e3fea9edc5d7419379b4a27ccf1090f081ce00"}

experimental_model

Cryo-EM and functional mutagenesis

exposure

InsP6 and phosphate binding

limitations

This paper tests InsP6 despite pyrophosphate wording in its title. It does not establish that dietary phytate reaches this intracellular site or overrides InsP8 selectivity in other assays.

nutrient_topic

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

organism

Human proteins

plain_language

An intracellular inositol phosphate helped stabilize an open exporter complex.

primary_references

[ino-p40128258] Synergistic activation of the human phosphate exporter XPR1 by KIDINS220 and inositol pyrophosphate. (2025). https://pubmed.ncbi.nlm.nih.gov/40128258/ DOI: 10.1038/s41467-025-58200-y

tissue_or_cell_type

XPR1-KIDINS220 transport complex

Inositol: synthesis, signaling, mineral interactions and conditional deficiency (2026-09-17) · lines 925–936

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

### ino-xpr1-ins-p6 In the presence of InsP6 and phosphate, human XPR1-KIDINS220 adopted an outward-open structure; InsP6 occupied SPX and juxtamembrane regions. Condition category: normal nutrient_topic: Inositol research collection; topical membership is not evidence of a direct dietary effect. plain_language: An intracellular inositol phosphate helped stabilize an open exporter complex. organism: Human proteins tissue_or_cell_type: XPR1-KIDINS220 transport complex experimental_model: Cryo-EM and functional mutagenesis limitations: This paper tests InsP6 despite pyrophosphate wording in its title. It does not establish that dietary phytate reaches this intracellular site or overrides InsP8 selectivity in other assays. exposure: InsP6 and phosphate binding evidence_span: {"source_cache": "artifacts/inositol-research/40128258.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4765253840f684d5dafa834980e3fea9edc5d7419379b4a27ccf1090f081ce00", "start_char": 0, "end_char": 1071, "text_sha256": "4765253840f684d5dafa834980e3fea9edc5d7419379b4a27ccf1090f081ce00"} [ino-p40128258] Synergistic activation of the human phosphate exporter XPR1 by KIDINS220 and inositol pyrophosphate. (2025). https://pubmed.ncbi.nlm.nih.gov/40128258/ DOI: 10.1038/s41467-025-58200-y