Component
Myo-inositol
Myo-inositol. Species, exposure and limitations are retained in each linked claim.
28 recorded relationships. Experimental role, claim status and evidence remain attached to each record.
How nutrients influence it
Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
How nutrients reach it in more than one step
Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.
Tracing routes…
What it does
Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.
What it acts on
Added myo-inositol attenuated lithium-enhanced mutant-protein clearance in PC12 cells.
Experimental context and source evidence
- evidence_access
- Primary full text
- experimental_model
- Rat PC12; 1 mM myo-inositol with 10 mM LiCl.
- limitations
- Time-dependent and incomplete effects; not proof that oral inositol reverses mood stabilization.
- nutrient_topic
- Lithium collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Lithium
- plain_language
- A connected nutrient can counter an experimentally induced response.
- primary_references
- Lithium induces autophagy by inhibiting inositol monophosphatase. · 2005 · https://pubmed.ncbi.nlm.nih.gov/16186256/ · DOI 10.1083/jcb.200504035
Lithium: metal-sensitive enzymes, transport and cross-nutrient mechanisms (2026-09-19) · lines 104–110
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Rat PC12; 1 mM myo-inositol with 10 mM LiCl. · source_derived_draft · unverified_draft
## lithium-inositol-rescue A connected nutrient can counter an experimentally induced response. Added myo-inositol attenuated lithium-enhanced mutant-protein clearance in PC12 cells. Model: Rat PC12; 1 mM myo-inositol with 10 mM LiCl. Limitations: Time-dependent and incomplete effects; not proof that oral inositol reverses mood stabilization. Evidence access: Primary full text Lithium induces autophagy by inhibiting inositol monophosphatase. · 2005 · https://pubmed.ncbi.nlm.nih.gov/16186256/ · DOI 10.1083/jcb.200504035
Complete structured claim and evidenceIn the mouse tracer experiments, labeled D-chiro-inositol was not detected after heavy-water exposure or deuterated myo-inositol administration.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/inositol-research/19586572.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7c6e57e631fef5921afd04f75718024d5b14ca525460e2c96275a4fc320c3b26", "start_char": 0, "end_char": 1544, "text_sha256": "7c6e57e631fef5921afd04f75718024d5b14ca525460e2c96275a4fc320c3b26"}
- experimental_model
- Dietary balance, GC-MS and stable-isotope tracing
- exposure
- Defined diets, heavy water and deuterated myo-inositol/DCI
- limitations
- Failure to detect conversion in mice does not exclude all human or isolated-tissue activity. Isotope strategy, chemical identification, species and dietary DCI contamination may contribute to disagreement with earlier radiotracer reports.
- nutrient_topic
- Inositol research collection; topical membership is not evidence of a direct dietary effect. · Inositol (stereoisomer family)
- organism
- Rats and mice; conversion tracing in mice
- plain_language
- This study did not reproduce the proposed endogenous conversion route in its mouse experiments.
- primary_references
- [ino-p19586572] d- chiro-Inositol is absorbed but not synthesised in rodents. (2009). https://pubmed.ncbi.nlm.nih.gov/19586572/ DOI: 10.1017/s0007114509990456
- tissue_or_cell_type
- Gastrointestinal absorption, plasma and excreta
Inositol: synthesis, signaling, mineral interactions and conditional deficiency (2026-09-17) · lines 1224–1235
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Dietary balance, GC-MS and stable-isotope tracing · source_derived_draft · unverified_draft
### ino-dci-no-conversion In the mouse tracer experiments, labeled D-chiro-inositol was not detected after heavy-water exposure or deuterated myo-inositol administration. Condition category: normal nutrient_topic: Inositol research collection; topical membership is not evidence of a direct dietary effect. plain_language: This study did not reproduce the proposed endogenous conversion route in its mouse experiments. organism: Rats and mice; conversion tracing in mice tissue_or_cell_type: Gastrointestinal absorption, plasma and excreta experimental_model: Dietary balance, GC-MS and stable-isotope tracing limitations: Failure to detect conversion in mice does not exclude all human or isolated-tissue activity. Isotope strategy, chemical identification, species and dietary DCI contamination may contribute to disagreement with earlier radiotracer reports. exposure: Defined diets, heavy water and deuterated myo-inositol/DCI evidence_span: {"source_cache": "artifacts/inositol-research/19586572.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7c6e57e631fef5921afd04f75718024d5b14ca525460e2c96275a4fc320c3b26", "start_char": 0, "end_char": 1544, "text_sha256": "7c6e57e631fef5921afd04f75718024d5b14ca525460e2c96275a4fc320c3b26"} [ino-p19586572] d- chiro-Inositol is absorbed but not synthesised in rodents. (2009). https://pubmed.ncbi.nlm.nih.gov/19586572/ DOI: 10.1017/s0007114509990456
Complete structured claim and evidenceThe 2013 trial reported gestational diabetes in 6% of the myo-inositol-plus-folic-acid group versus 15.3% with folic acid alone.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/inositol-research/23340885.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "384eb5d40ed312af297e2ecdd98b1c3f804fda5555db8984de47dc08c3cdf336", "start_char": 0, "end_char": 1685, "text_sha256": "384eb5d40ed312af297e2ecdd98b1c3f804fda5555db8984de47dc08c3cdf336"}
- experimental_model
- Prospective randomized open-label pregnancy trial
- exposure
- Myo-inositol plus folic acid versus folic acid alone
- limitations
- Open-label design and selected risk group; this is neither an inositol-versus-folate comparison nor proof of a nutrient interaction.
- nutrient_topic
- Inositol research collection; topical membership is not evidence of a direct dietary effect. · Inositol (stereoisomer family)
- organism
- Homo sapiens
- plain_language
- An early trial suggested benefit in one risk group, with folic acid present in both groups.
- primary_references
- [ino-p23340885] myo-Inositol supplementation and onset of gestational diabetes mellitus in pregnant women with a family history of type 2 diabetes: a prospective, randomized, placebo-controlled study. (2013). https://pubmed.ncbi.nlm.nih.gov/23340885/ DOI: 10.2337/dc12-1371
- tissue_or_cell_type
- Pregnant women with a family history of type 2 diabetes
Inositol: synthesis, signaling, mineral interactions and conditional deficiency (2026-09-17) · lines 1328–1339
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Prospective randomized open-label pregnancy trial · source_derived_draft · unverified_draft
### ino-gdm-2013 The 2013 trial reported gestational diabetes in 6% of the myo-inositol-plus-folic-acid group versus 15.3% with folic acid alone. Condition category: normal nutrient_topic: Inositol research collection; topical membership is not evidence of a direct dietary effect. plain_language: An early trial suggested benefit in one risk group, with folic acid present in both groups. organism: Homo sapiens tissue_or_cell_type: Pregnant women with a family history of type 2 diabetes experimental_model: Prospective randomized open-label pregnancy trial limitations: Open-label design and selected risk group; this is neither an inositol-versus-folate comparison nor proof of a nutrient interaction. exposure: Myo-inositol plus folic acid versus folic acid alone evidence_span: {"source_cache": "artifacts/inositol-research/23340885.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "384eb5d40ed312af297e2ecdd98b1c3f804fda5555db8984de47dc08c3cdf336", "start_char": 0, "end_char": 1685, "text_sha256": "384eb5d40ed312af297e2ecdd98b1c3f804fda5555db8984de47dc08c3cdf336"} [ino-p23340885] myo-Inositol supplementation and onset of gestational diabetes mellitus in pregnant women with a family history of type 2 diabetes: a prospective, randomized, placebo-controlled study. (2013). https://pubmed.ncbi.nlm.nih.gov/23340885/ DOI: 10.2337/dc12-1371
Complete structured claim and evidenceIn MYPP, the gestational-diabetes/preeclampsia/preterm-birth composite occurred in 25.0% versus 26.8% (RR 0.93, 95% CI 0.68–1.28; P=0.67).
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/inositol-research/40920401.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f72221b219fbb1cae0af2c44b123ab1e95c74e0ba9c10f75ed601720b96248a0", "start_char": 0, "end_char": 1949, "text_sha256": "f72221b219fbb1cae0af2c44b123ab1e95c74e0ba9c10f75ed601720b96248a0"}
- experimental_model
- MYPP double-blind multicenter randomized trial
- exposure
- Myo-inositol 2 g plus folic acid 0.2 mg twice daily versus matching folic acid control until delivery
- limitations
- A larger null result for a prespecified composite in PCOS pregnancy; not the same population or endpoint as the 2013 trial. Confidence limits permit benefit or harm of varying sizes.
- nutrient_topic
- Inositol research collection; topical membership is not evidence of a direct dietary effect. · Inositol (stereoisomer family)
- organism
- Homo sapiens
- plain_language
- The larger blinded PCOS-pregnancy trial did not demonstrate a reduction in its main complication outcome.
- primary_references
- [ino-p40920401] Myo-inositol Supplementation to Prevent Pregnancy Complications in Polycystic Ovary Syndrome: A Randomized Clinical Trial. (2025). https://pubmed.ncbi.nlm.nih.gov/40920401/ DOI: 10.1001/jama.2025.13668
- tissue_or_cell_type
- 464 pregnant individuals with PCOS at 13 Dutch hospitals
Inositol: synthesis, signaling, mineral interactions and conditional deficiency (2026-09-17) · lines 1341–1352
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · MYPP double-blind multicenter randomized trial · source_derived_draft · unverified_draft
### ino-gdm-2025 In MYPP, the gestational-diabetes/preeclampsia/preterm-birth composite occurred in 25.0% versus 26.8% (RR 0.93, 95% CI 0.68–1.28; P=0.67). Condition category: normal nutrient_topic: Inositol research collection; topical membership is not evidence of a direct dietary effect. plain_language: The larger blinded PCOS-pregnancy trial did not demonstrate a reduction in its main complication outcome. organism: Homo sapiens tissue_or_cell_type: 464 pregnant individuals with PCOS at 13 Dutch hospitals experimental_model: MYPP double-blind multicenter randomized trial limitations: A larger null result for a prespecified composite in PCOS pregnancy; not the same population or endpoint as the 2013 trial. Confidence limits permit benefit or harm of varying sizes. exposure: Myo-inositol 2 g plus folic acid 0.2 mg twice daily versus matching folic acid control until delivery evidence_span: {"source_cache": "artifacts/inositol-research/40920401.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f72221b219fbb1cae0af2c44b123ab1e95c74e0ba9c10f75ed601720b96248a0", "start_char": 0, "end_char": 1949, "text_sha256": "f72221b219fbb1cae0af2c44b123ab1e95c74e0ba9c10f75ed601720b96248a0"} [ino-p40920401] Myo-inositol Supplementation to Prevent Pregnancy Complications in Polycystic Ovary Syndrome: A Randomized Clinical Trial. (2025). https://pubmed.ncbi.nlm.nih.gov/40920401/ DOI: 10.1001/jama.2025.13668
Complete structured claim and evidenceMiGDM found no significant GDM difference among 43 completers, but early funding-related termination prevented a definitive efficacy test.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/inositol-research/41742988.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3b78fed7bce4eedabdbeae7d6e7e562bee8153fa1d0d805b5e96a52004344b29", "start_char": 0, "end_char": 3433, "text_sha256": "3b78fed7bce4eedabdbeae7d6e7e562bee8153fa1d0d805b5e96a52004344b29"}
- experimental_model
- MiGDM double-blind randomized pilot
- exposure
- Myo-inositol 2 g twice daily versus placebo; stopped early for funding
- limitations
- Only 67 enrolled and 43 completed versus 640 planned. Severe underpowering makes the result inconclusive, not proof of equivalence.
- nutrient_topic
- Inositol research collection; topical membership is not evidence of a direct dietary effect. · Inositol (stereoisomer family)
- organism
- Homo sapiens
- plain_language
- This small unfinished trial cannot settle whether the supplement works.
- primary_references
- [ino-p41742988] The Effect of Myo-Inositol Supplementation During Pregnancy on Fetal and Maternal Outcomes: Results of the Myo-Inositol for the Prevention of Gestational Diabetes Mellitus (MiGDM) Randomized Double-Blind, Placebo-Controlled Pilot Trial. (2026). https://pubmed.ncbi.nlm.nih.gov/41742988/ DOI: 10.7759/cureus.102259
- tissue_or_cell_type
- Pregnant women in Qatar
Inositol: synthesis, signaling, mineral interactions and conditional deficiency (2026-09-17) · lines 1354–1365
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · MiGDM double-blind randomized pilot · source_derived_draft · unverified_draft
### ino-gdm-2026 MiGDM found no significant GDM difference among 43 completers, but early funding-related termination prevented a definitive efficacy test. Condition category: normal nutrient_topic: Inositol research collection; topical membership is not evidence of a direct dietary effect. plain_language: This small unfinished trial cannot settle whether the supplement works. organism: Homo sapiens tissue_or_cell_type: Pregnant women in Qatar experimental_model: MiGDM double-blind randomized pilot limitations: Only 67 enrolled and 43 completed versus 640 planned. Severe underpowering makes the result inconclusive, not proof of equivalence. exposure: Myo-inositol 2 g twice daily versus placebo; stopped early for funding evidence_span: {"source_cache": "artifacts/inositol-research/41742988.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3b78fed7bce4eedabdbeae7d6e7e562bee8153fa1d0d805b5e96a52004344b29", "start_char": 0, "end_char": 3433, "text_sha256": "3b78fed7bce4eedabdbeae7d6e7e562bee8153fa1d0d805b5e96a52004344b29"} [ino-p41742988] The Effect of Myo-Inositol Supplementation During Pregnancy on Fetal and Maternal Outcomes: Results of the Myo-Inositol for the Prevention of Gestational Diabetes Mellitus (MiGDM) Randomized Double-Blind, Placebo-Controlled Pilot Trial. (2026). https://pubmed.ncbi.nlm.nih.gov/41742988/ DOI: 10.7759/cureus.102259
Complete structured claim and evidenceMyo-inositol supplementation of differentiation medium rescued the reported neuronal-progenitor phenotype in IMPA1-deficient patient-derived cultures.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_span
- {"source_cache": "artifacts/inositol-research/32839513.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5ca10517672cac78ad8cdb0c593f14f73f1989e55977432d979690eebc3eefed", "start_char": 0, "end_char": 1711, "text_sha256": "5ca10517672cac78ad8cdb0c593f14f73f1989e55977432d979690eebc3eefed"}
- experimental_model
- Patient-derived iPSC differentiation and rescue
- exposure
- Biallelic IMPA1 defect and myo-inositol-supplemented medium
- limitations
- Cellular rescue is not demonstrated neurological benefit in treated patients; effects were lineage-specific.
- nutrient_topic
- Inositol research collection; topical membership is not evidence of a direct dietary effect. · Inositol (stereoisomer family)
- organism
- Homo sapiens
- plain_language
- Providing the missing downstream molecule helped cells in culture; clinical benefit remains untested here.
- primary_references
- [ino-p32839513] Inositol monophosphatase 1 (IMPA1) mutation in intellectual disability patients impairs neurogenesis but not gliogenesis. (2021). https://pubmed.ncbi.nlm.nih.gov/32839513/ DOI: 10.1038/s41380-020-00862-9
- tissue_or_cell_type
- Hippocampal dentate-gyrus-like neuronal progenitors
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Inositol: synthesis, signaling, mineral interactions and conditional deficiency (2026-09-17) · lines 1276–1287
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Patient-derived iPSC differentiation and rescue · source_derived_draft · unverified_draft
### ino-impa1-myo-rescue Myo-inositol supplementation of differentiation medium rescued the reported neuronal-progenitor phenotype in IMPA1-deficient patient-derived cultures. Condition category: machinery_impairment nutrient_topic: Inositol research collection; topical membership is not evidence of a direct dietary effect. plain_language: Providing the missing downstream molecule helped cells in culture; clinical benefit remains untested here. organism: Homo sapiens tissue_or_cell_type: Hippocampal dentate-gyrus-like neuronal progenitors experimental_model: Patient-derived iPSC differentiation and rescue limitations: Cellular rescue is not demonstrated neurological benefit in treated patients; effects were lineage-specific. exposure: Biallelic IMPA1 defect and myo-inositol-supplemented medium evidence_span: {"source_cache": "artifacts/inositol-research/32839513.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5ca10517672cac78ad8cdb0c593f14f73f1989e55977432d979690eebc3eefed", "start_char": 0, "end_char": 1711, "text_sha256": "5ca10517672cac78ad8cdb0c593f14f73f1989e55977432d979690eebc3eefed"} [ino-p32839513] Inositol monophosphatase 1 (IMPA1) mutation in intellectual disability patients impairs neurogenesis but not gliogenesis. (2021). https://pubmed.ncbi.nlm.nih.gov/32839513/ DOI: 10.1038/s41380-020-00862-9
Complete structured claim and evidenceInositol stimulated hindgut-cell proliferation in curly-tail embryos, and this effect required PKC beta I.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/inositol-research/14613966.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "670b8f0a36bfbecfb417fe28f8748e65994ac47b153ffcf66c42c21e7489f9cc", "start_char": 0, "end_char": 1735, "text_sha256": "670b8f0a36bfbecfb417fe28f8748e65994ac47b153ffcf66c42c21e7489f9cc"}
- experimental_model
- Embryo culture with selective PKC inhibition
- exposure
- Inositol exposure in a folate-resistant neural-tube-defect model
- limitations
- Mechanistic mouse prevention does not establish human efficacy or permit replacing folic acid.
- nutrient_topic
- Inositol research collection; topical membership is not evidence of a direct dietary effect. · Inositol (stereoisomer family)
- organism
- Curly-tail mutant mice
- plain_language
- The rescue involved growth of a particular embryonic tissue, not just a general vitamin effect.
- primary_references
- [ino-p14613966] Specific isoforms of protein kinase C are essential for prevention of folate-resistant neural tube defects by inositol. (2004). https://pubmed.ncbi.nlm.nih.gov/14613966/ DOI: 10.1093/hmg/ddh003
- tissue_or_cell_type
- Neurulation-stage embryos and hindgut
Inositol: synthesis, signaling, mineral interactions and conditional deficiency (2026-09-17) · lines 1393–1404
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Embryo culture with selective PKC inhibition · source_derived_draft · unverified_draft
### ino-ntd-hindgut Inositol stimulated hindgut-cell proliferation in curly-tail embryos, and this effect required PKC beta I. Condition category: normal nutrient_topic: Inositol research collection; topical membership is not evidence of a direct dietary effect. plain_language: The rescue involved growth of a particular embryonic tissue, not just a general vitamin effect. organism: Curly-tail mutant mice tissue_or_cell_type: Neurulation-stage embryos and hindgut experimental_model: Embryo culture with selective PKC inhibition limitations: Mechanistic mouse prevention does not establish human efficacy or permit replacing folic acid. exposure: Inositol exposure in a folate-resistant neural-tube-defect model evidence_span: {"source_cache": "artifacts/inositol-research/14613966.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "670b8f0a36bfbecfb417fe28f8748e65994ac47b153ffcf66c42c21e7489f9cc", "start_char": 0, "end_char": 1735, "text_sha256": "670b8f0a36bfbecfb417fe28f8748e65994ac47b153ffcf66c42c21e7489f9cc"} [ino-p14613966] Specific isoforms of protein kinase C are essential for prevention of folate-resistant neural tube defects by inositol. (2004). https://pubmed.ncbi.nlm.nih.gov/14613966/ DOI: 10.1093/hmg/ddh003
Complete structured claim and evidenceAmong randomized PONTI pregnancies, NTD recurrence occurred in 0/14 with inositol plus folic acid versus 1/19 with placebo plus folic acid.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/inositol-research/26847388.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a7617d160ca71553f41ce2a7346478950ed9580a4bc9cca9688d3b710ec0cf82", "start_char": 0, "end_char": 1680, "text_sha256": "a7617d160ca71553f41ce2a7346478950ed9580a4bc9cca9688d3b710ec0cf82"}
- experimental_model
- PONTI double-blind randomized pilot with separately described nonrandomized pregnancies
- exposure
- Periconceptional inositol plus folic acid versus folic acid plus placebo
- limitations
- 47 women randomized; only 33 randomized pregnancies. The pilot was not powered to establish prevention. Corrigendum PMID 26917444 corrects the separate nonrandomized pregnancy count from 22 to 24; randomized counts used here are unchanged. Nonrandomized outcomes must not be pooled as randomized evidence.
- nutrient_topic
- Inositol research collection; topical membership is not evidence of a direct dietary effect. · Inositol (stereoisomer family)
- organism
- Homo sapiens
- plain_language
- The pilot supported further study but was far too small to establish efficacy or replace folic acid.
- primary_references
- [ino-p26847388] Inositol for the prevention of neural tube defects: a pilot randomised controlled trial. (2016). https://pubmed.ncbi.nlm.nih.gov/26847388/ DOI: 10.1017/s0007114515005322
- tissue_or_cell_type
- Women with a prior neural-tube-defect pregnancy
Inositol: synthesis, signaling, mineral interactions and conditional deficiency (2026-09-17) · lines 1406–1417
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · PONTI double-blind randomized pilot with separately described nonrandomized pregnancies · source_derived_draft · unverified_draft
### ino-ponti Among randomized PONTI pregnancies, NTD recurrence occurred in 0/14 with inositol plus folic acid versus 1/19 with placebo plus folic acid. Condition category: normal nutrient_topic: Inositol research collection; topical membership is not evidence of a direct dietary effect. plain_language: The pilot supported further study but was far too small to establish efficacy or replace folic acid. organism: Homo sapiens tissue_or_cell_type: Women with a prior neural-tube-defect pregnancy experimental_model: PONTI double-blind randomized pilot with separately described nonrandomized pregnancies limitations: 47 women randomized; only 33 randomized pregnancies. The pilot was not powered to establish prevention. Corrigendum PMID 26917444 corrects the separate nonrandomized pregnancy count from 22 to 24; randomized counts used here are unchanged. Nonrandomized outcomes must not be pooled as randomized evidence. exposure: Periconceptional inositol plus folic acid versus folic acid plus placebo evidence_span: {"source_cache": "artifacts/inositol-research/26847388.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a7617d160ca71553f41ce2a7346478950ed9580a4bc9cca9688d3b710ec0cf82", "start_char": 0, "end_char": 1680, "text_sha256": "a7617d160ca71553f41ce2a7346478950ed9580a4bc9cca9688d3b710ec0cf82"} [ino-p26847388] Inositol for the prevention of neural tube defects: a pilot randomised controlled trial. (2016). https://pubmed.ncbi.nlm.nih.gov/26847388/ DOI: 10.1017/s0007114515005322
Complete structured claim and evidenceThe 1992 trial reported ROP in 13% of inositol-treated infants versus 26% of placebo recipients, and stage 4 ROP in 0% versus 9%.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/inositol-research/1560798.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6ece5de763b822dca6ca1a93b5f7a61a2d94be9af29755ffd9379f16a983027e", "start_char": 0, "end_char": 2123, "text_sha256": "6ece5de763b822dca6ca1a93b5f7a61a2d94be9af29755ffd9379f16a983027e"}
- experimental_model
- Randomized double-blind neonatal trial
- exposure
- Inositol 80 mg/kg/day for the first five days during parenteral nutrition
- limitations
- Early-era neonatal care and short exposure. The indexed abstract has inconsistent BPD count/percentage arithmetic; that endpoint is not numerically reproduced here. ROP findings are retained with the later adverse trial.
- nutrient_topic
- Inositol research collection; topical membership is not evidence of a direct dietary effect. · Inositol (stereoisomer family)
- organism
- Homo sapiens
- plain_language
- An early neonatal trial reported fewer severe eye complications.
- primary_references
- [ino-p1560798] Inositol supplementation in premature infants with respiratory distress syndrome. (1992). https://pubmed.ncbi.nlm.nih.gov/1560798/ DOI: 10.1056/nejm199205073261901
- tissue_or_cell_type
- 221 infants at 24–32 weeks gestation with respiratory distress
Inositol: synthesis, signaling, mineral interactions and conditional deficiency (2026-09-17) · lines 1432–1443
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized double-blind neonatal trial · source_derived_draft · unverified_draft
### ino-preterm-1992-rop The 1992 trial reported ROP in 13% of inositol-treated infants versus 26% of placebo recipients, and stage 4 ROP in 0% versus 9%. Condition category: normal nutrient_topic: Inositol research collection; topical membership is not evidence of a direct dietary effect. plain_language: An early neonatal trial reported fewer severe eye complications. organism: Homo sapiens tissue_or_cell_type: 221 infants at 24–32 weeks gestation with respiratory distress experimental_model: Randomized double-blind neonatal trial limitations: Early-era neonatal care and short exposure. The indexed abstract has inconsistent BPD count/percentage arithmetic; that endpoint is not numerically reproduced here. ROP findings are retained with the later adverse trial. exposure: Inositol 80 mg/kg/day for the first five days during parenteral nutrition evidence_span: {"source_cache": "artifacts/inositol-research/1560798.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6ece5de763b822dca6ca1a93b5f7a61a2d94be9af29755ffd9379f16a983027e", "start_char": 0, "end_char": 2123, "text_sha256": "6ece5de763b822dca6ca1a93b5f7a61a2d94be9af29755ffd9379f16a983027e"} [ino-p1560798] Inositol supplementation in premature infants with respiratory distress syndrome. (1992). https://pubmed.ncbi.nlm.nih.gov/1560798/ DOI: 10.1056/nejm199205073261901
Complete structured claim and evidenceDeath or type 1 ROP occurred in 29% with myo-inositol versus 21% with placebo (adjusted RR 1.41, 95% CI 1.08–1.83).
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/inositol-research/30357297.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "b3301c8c680b4b3c6424dfb6677ae55839221db1d3cd51d9df4724b9cf35d57f", "start_char": 0, "end_char": 2589, "text_sha256": "b3301c8c680b4b3c6424dfb6677ae55839221db1d3cd51d9df4724b9cf35d57f"}
- experimental_model
- Multicenter randomized neonatal trial stopped early
- exposure
- Myo-inositol 40 mg/kg every 12 hours, initially IV then enteral, for up to 10 weeks versus placebo
- limitations
- Early termination limits estimates but does not remove the mortality signal. Different era, gestational ages, treatment duration and endpoints may contribute to divergence from early trials; the explanation remains unresolved.
- nutrient_topic
- Inositol research collection; topical membership is not evidence of a direct dietary effect. · Inositol (stereoisomer family)
- organism
- Homo sapiens
- plain_language
- The later larger neonatal trial did not reproduce the expected overall benefit.
- primary_references
- [ino-p30357297] Effects of Myo-inositol on Type 1 Retinopathy of Prematurity Among Preterm Infants <28 Weeks' Gestational Age: A Randomized Clinical Trial. (2018). https://pubmed.ncbi.nlm.nih.gov/30357297/ DOI: 10.1001/jama.2018.14996
- tissue_or_cell_type
- 638 infants born before 28 weeks at 18 US centers
Inositol: synthesis, signaling, mineral interactions and conditional deficiency (2026-09-17) · lines 1445–1456
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Multicenter randomized neonatal trial stopped early · source_derived_draft · unverified_draft
### ino-preterm-2018-composite Death or type 1 ROP occurred in 29% with myo-inositol versus 21% with placebo (adjusted RR 1.41, 95% CI 1.08–1.83). Condition category: normal nutrient_topic: Inositol research collection; topical membership is not evidence of a direct dietary effect. plain_language: The later larger neonatal trial did not reproduce the expected overall benefit. organism: Homo sapiens tissue_or_cell_type: 638 infants born before 28 weeks at 18 US centers experimental_model: Multicenter randomized neonatal trial stopped early limitations: Early termination limits estimates but does not remove the mortality signal. Different era, gestational ages, treatment duration and endpoints may contribute to divergence from early trials; the explanation remains unresolved. exposure: Myo-inositol 40 mg/kg every 12 hours, initially IV then enteral, for up to 10 weeks versus placebo evidence_span: {"source_cache": "artifacts/inositol-research/30357297.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "b3301c8c680b4b3c6424dfb6677ae55839221db1d3cd51d9df4724b9cf35d57f", "start_char": 0, "end_char": 2589, "text_sha256": "b3301c8c680b4b3c6424dfb6677ae55839221db1d3cd51d9df4724b9cf35d57f"} [ino-p30357297] Effects of Myo-inositol on Type 1 Retinopathy of Prematurity Among Preterm Infants <28 Weeks' Gestational Age: A Randomized Clinical Trial. (2018). https://pubmed.ncbi.nlm.nih.gov/30357297/ DOI: 10.1001/jama.2018.14996
Complete structured claim and evidenceMortality before 55 weeks postmenstrual age was 18% versus 11% (adjusted RR 1.66, 95% CI 1.14–2.43), prompting early trial termination.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/inositol-research/30357297.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "b3301c8c680b4b3c6424dfb6677ae55839221db1d3cd51d9df4724b9cf35d57f", "start_char": 0, "end_char": 2589, "text_sha256": "b3301c8c680b4b3c6424dfb6677ae55839221db1d3cd51d9df4724b9cf35d57f"}
- experimental_model
- Multicenter randomized neonatal trial stopped early
- exposure
- Myo-inositol 40 mg/kg every 12 hours, initially IV then enteral, for up to 10 weeks versus placebo
- limitations
- Early termination limits estimates but does not remove the mortality signal. Different era, gestational ages, treatment duration and endpoints may contribute to divergence from early trials; the explanation remains unresolved.
- nutrient_topic
- Inositol research collection; topical membership is not evidence of a direct dietary effect. · Inositol (stereoisomer family)
- organism
- Homo sapiens
- plain_language
- The increased deaths are essential evidence and cannot be hidden behind the earlier positive findings.
- primary_references
- [ino-p30357297] Effects of Myo-inositol on Type 1 Retinopathy of Prematurity Among Preterm Infants <28 Weeks' Gestational Age: A Randomized Clinical Trial. (2018). https://pubmed.ncbi.nlm.nih.gov/30357297/ DOI: 10.1001/jama.2018.14996
- tissue_or_cell_type
- 638 infants born before 28 weeks at 18 US centers
Inositol: synthesis, signaling, mineral interactions and conditional deficiency (2026-09-17) · lines 1458–1469
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Multicenter randomized neonatal trial stopped early · source_derived_draft · unverified_draft
### ino-preterm-2018-mortality Mortality before 55 weeks postmenstrual age was 18% versus 11% (adjusted RR 1.66, 95% CI 1.14–2.43), prompting early trial termination. Condition category: normal nutrient_topic: Inositol research collection; topical membership is not evidence of a direct dietary effect. plain_language: The increased deaths are essential evidence and cannot be hidden behind the earlier positive findings. organism: Homo sapiens tissue_or_cell_type: 638 infants born before 28 weeks at 18 US centers experimental_model: Multicenter randomized neonatal trial stopped early limitations: Early termination limits estimates but does not remove the mortality signal. Different era, gestational ages, treatment duration and endpoints may contribute to divergence from early trials; the explanation remains unresolved. exposure: Myo-inositol 40 mg/kg every 12 hours, initially IV then enteral, for up to 10 weeks versus placebo evidence_span: {"source_cache": "artifacts/inositol-research/30357297.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "b3301c8c680b4b3c6424dfb6677ae55839221db1d3cd51d9df4724b9cf35d57f", "start_char": 0, "end_char": 2589, "text_sha256": "b3301c8c680b4b3c6424dfb6677ae55839221db1d3cd51d9df4724b9cf35d57f"} [ino-p30357297] Effects of Myo-inositol on Type 1 Retinopathy of Prematurity Among Preterm Infants <28 Weeks' Gestational Age: A Randomized Clinical Trial. (2018). https://pubmed.ncbi.nlm.nih.gov/30357297/ DOI: 10.1001/jama.2018.14996
Complete structured claim and evidenceMyo-inositol plus raffinose reduced methoxamine-induced contraction in rat arteries; Kv7 inhibition or knockdown prevented the effect.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/inositol-research/32787517.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5581d37bc8ebfa221d5d351a107a7fa9a76a8b1e7476599e469648779622b3c3", "start_char": 0, "end_char": 1875, "text_sha256": "5581d37bc8ebfa221d5d351a107a7fa9a76a8b1e7476599e469648779622b3c3"}
- experimental_model
- Arterial physiology, protein interactions and knockdown
- exposure
- SMIT1 manipulation, myo-inositol/raffinose and Kv7 blockade
- limitations
- Rat ex vivo arteries; not proof of a blood-pressure benefit from human inositol supplements.
- nutrient_topic
- Inositol research collection; topical membership is not evidence of a direct dietary effect. · Inositol (stereoisomer family)
- organism
- Rattus norvegicus
- plain_language
- A combined experimental exposure changed contraction through a potassium-channel-dependent route.
- primary_references
- [ino-p32787517] SMIT (Sodium-Myo-Inositol Transporter) 1 Regulates Arterial Contractility Through the Modulation of Vascular Kv7 Channels. (2020). https://pubmed.ncbi.nlm.nih.gov/32787517/ DOI: 10.1161/atvbaha.120.315096
- tissue_or_cell_type
- Renal and mesenteric arteries
Inositol: synthesis, signaling, mineral interactions and conditional deficiency (2026-09-17) · lines 1055–1066
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Arterial physiology, protein interactions and knockdown · source_derived_draft · unverified_draft
### ino-smit1-artery Myo-inositol plus raffinose reduced methoxamine-induced contraction in rat arteries; Kv7 inhibition or knockdown prevented the effect. Condition category: normal nutrient_topic: Inositol research collection; topical membership is not evidence of a direct dietary effect. plain_language: A combined experimental exposure changed contraction through a potassium-channel-dependent route. organism: Rattus norvegicus tissue_or_cell_type: Renal and mesenteric arteries experimental_model: Arterial physiology, protein interactions and knockdown limitations: Rat ex vivo arteries; not proof of a blood-pressure benefit from human inositol supplements. exposure: SMIT1 manipulation, myo-inositol/raffinose and Kv7 blockade evidence_span: {"source_cache": "artifacts/inositol-research/32787517.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5581d37bc8ebfa221d5d351a107a7fa9a76a8b1e7476599e469648779622b3c3", "start_char": 0, "end_char": 1875, "text_sha256": "5581d37bc8ebfa221d5d351a107a7fa9a76a8b1e7476599e469648779622b3c3"} [ino-p32787517] SMIT (Sodium-Myo-Inositol Transporter) 1 Regulates Arterial Contractility Through the Modulation of Vascular Kv7 Channels. (2020). https://pubmed.ncbi.nlm.nih.gov/32787517/ DOI: 10.1161/atvbaha.120.315096
Complete structured claim and evidenceTSH fell from baseline in the myo-inositol-plus-selenomethionine arm, while no TSH change was reported in the selenomethionine-only arm; the reported TSH P value was a within-group comparison.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/inositol-research/24224112.fulltext.txt", "locator": "Exact primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "b9b55ed122a2f26149680eb0f4bfab9ea981927754bcbb40305d4697c5d32412", "start_char": 7984, "end_char": 8184, "text_sha256": "34e1c5b3fe451ea1278c2adfb27f4977a40d100b82946252ecad03a7879592dc"}
- experimental_model
- Double-blind randomized combination trial
- exposure
- Myo-inositol plus selenomethionine versus selenomethionine
- limitations
- Small combination trial without a myo-inositol-only arm. A significant within-group change versus a nonsignificant change in the other arm is not by itself a significant between-group difference or nutrient synergy.
- nutrient_topic
- Inositol research collection; topical membership is not evidence of a direct dietary effect. · Inositol (stereoisomer family)
- organism
- Homo sapiens
- plain_language
- A thyroid blood marker improved in the combined-treatment group, but these comparisons do not establish a statistical interaction between nutrients.
- primary_references
- [ino-p24224112] Combined treatment with Myo-inositol and selenium ensures euthyroidism in subclinical hypothyroidism patients with autoimmune thyroiditis. (2013). https://pubmed.ncbi.nlm.nih.gov/24224112/ DOI: 10.1155/2013/424163
- tissue_or_cell_type
- Women with autoimmune subclinical hypothyroidism
Inositol: synthesis, signaling, mineral interactions and conditional deficiency (2026-09-17) · lines 1419–1430
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Double-blind randomized combination trial · source_derived_draft · unverified_draft
### ino-thyroid-combination TSH fell from baseline in the myo-inositol-plus-selenomethionine arm, while no TSH change was reported in the selenomethionine-only arm; the reported TSH P value was a within-group comparison. Condition category: normal nutrient_topic: Inositol research collection; topical membership is not evidence of a direct dietary effect. plain_language: A thyroid blood marker improved in the combined-treatment group, but these comparisons do not establish a statistical interaction between nutrients. organism: Homo sapiens tissue_or_cell_type: Women with autoimmune subclinical hypothyroidism experimental_model: Double-blind randomized combination trial limitations: Small combination trial without a myo-inositol-only arm. A significant within-group change versus a nonsignificant change in the other arm is not by itself a significant between-group difference or nutrient synergy. exposure: Myo-inositol plus selenomethionine versus selenomethionine evidence_span: {"source_cache": "artifacts/inositol-research/24224112.fulltext.txt", "locator": "Exact primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "b9b55ed122a2f26149680eb0f4bfab9ea981927754bcbb40305d4697c5d32412", "start_char": 7984, "end_char": 8184, "text_sha256": "34e1c5b3fe451ea1278c2adfb27f4977a40d100b82946252ecad03a7879592dc"} [ino-p24224112] Combined treatment with Myo-inositol and selenium ensures euthyroidism in subclinical hypothyroidism patients with autoimmune thyroiditis. (2013). https://pubmed.ncbi.nlm.nih.gov/24224112/ DOI: 10.1155/2013/424163
Complete structured claim and evidence
What acts on it
Endogenous lithium depletion did not change brain inositol in the reported mouse comparison.
Experimental context and source evidence
- availability_state
- nutrient_deficiency Imported condition classification; unverified.
- evidence_access
- Primary full text
- experimental_model
- Mouse brain comparison with pharmacological IMPase rationale.
- limitations
- A scoped null measurement, not proof that inositol is irrelevant in every lithium setting.
- nutrient_topic
- Lithium collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Lithium
- plain_language
- Trace depletion did not reproduce every pharmacological pathway.
- primary_references
- Lithium deficiency and the onset of Alzheimer's disease. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40770094/ · DOI 10.1038/s41586-025-09335-x
- trigger_kind
- nutrient_deficiency Imported condition classification; unverified.
Lithium: metal-sensitive enzymes, transport and cross-nutrient mechanisms (2026-09-19) · lines 496–502
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse brain comparison with pharmacological IMPase rationale. · source_derived_draft · unverified_draft
## lithium-depletion-inositol-null Trace depletion did not reproduce every pharmacological pathway. Endogenous lithium depletion did not change brain inositol in the reported mouse comparison. Model: Mouse brain comparison with pharmacological IMPase rationale. Limitations: A scoped null measurement, not proof that inositol is irrelevant in every lithium setting. Evidence access: Primary full text Lithium deficiency and the onset of Alzheimer's disease. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40770094/ · DOI 10.1038/s41586-025-09335-x
Complete structured claim and evidenceHMIT expressed in Xenopus oocytes mediated electrogenic proton-coupled myo-inositol uptake that increased as pH fell, with maximal tested activity near pH 5.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/inositol-research/11500374.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "fb9efd53bbc0fae1bf1ada1525cdb7d10a4e700d3309bfba4e3a598c4a9c74b9", "start_char": 0, "end_char": 1270, "text_sha256": "fb9efd53bbc0fae1bf1ada1525cdb7d10a4e700d3309bfba4e3a598c4a9c74b9"}
- experimental_model
- Transporter expression and electrophysiology
- exposure
- Extracellular pH manipulation
- limitations
- Transport capacity after heterologous expression does not establish a neuronal plasma-membrane role in vivo.
- nutrient_topic
- Inositol research collection; topical membership is not evidence of a direct dietary effect. · Inositol (stereoisomer family)
- organism
- Rat brain transporter studied in Xenopus oocytes
- plain_language
- A different transporter can use a proton gradient, particularly in acidic experimental conditions.
- primary_references
- [ino-p11500374] Identification of a mammalian H(+)-myo-inositol symporter expressed predominantly in the brain. (2001). https://pubmed.ncbi.nlm.nih.gov/11500374/ DOI: 10.1093/emboj/20.16.4467
- tissue_or_cell_type
- Heterologous membranes and rat brain
- transport_effect
- raises Electrogenic proton-coupled myo-inositol uptake rising as pH fell.
- transport_pool
- the expressing cell Electrogenic proton-coupled myo-inositol uptake rising as pH fell.
Inositol: synthesis, signaling, mineral interactions and conditional deficiency (2026-09-17) · lines 366–377
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Transporter expression and electrophysiology · source_derived_draft · unverified_draft
### ino-hmit-acid HMIT expressed in Xenopus oocytes mediated electrogenic proton-coupled myo-inositol uptake that increased as pH fell, with maximal tested activity near pH 5. Condition category: normal nutrient_topic: Inositol research collection; topical membership is not evidence of a direct dietary effect. plain_language: A different transporter can use a proton gradient, particularly in acidic experimental conditions. organism: Rat brain transporter studied in Xenopus oocytes tissue_or_cell_type: Heterologous membranes and rat brain experimental_model: Transporter expression and electrophysiology limitations: Transport capacity after heterologous expression does not establish a neuronal plasma-membrane role in vivo. exposure: Extracellular pH manipulation evidence_span: {"source_cache": "artifacts/inositol-research/11500374.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "fb9efd53bbc0fae1bf1ada1525cdb7d10a4e700d3309bfba4e3a598c4a9c74b9", "start_char": 0, "end_char": 1270, "text_sha256": "fb9efd53bbc0fae1bf1ada1525cdb7d10a4e700d3309bfba4e3a598c4a9c74b9"} [ino-p11500374] Identification of a mammalian H(+)-myo-inositol symporter expressed predominantly in the brain. (2001). https://pubmed.ncbi.nlm.nih.gov/11500374/ DOI: 10.1093/emboj/20.16.4467
Complete structured claim and evidenceHuman MIOX catalyzes oxidative cleavage of myo-inositol to D-glucuronate.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/inositol-research/18364358.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9992644d489f26782d7ef0a70dc13ec5ca48e2b660a011173fba8e0d4e43ae19", "start_char": 0, "end_char": 1004, "text_sha256": "9992644d489f26782d7ef0a70dc13ec5ca48e2b660a011173fba8e0d4e43ae19"}
- experimental_model
- Human enzyme crystallography and catalytic analysis
- exposure
- Diiron center and inhibitor-bound structure
- limitations
- Catabolism of inositol is not evidence that humans synthesize vitamin C from it; the crystal ligand was an inhibitor.
- nutrient_topic
- Inositol research collection; topical membership is not evidence of a direct dietary effect. · Inositol (stereoisomer family)
- organism
- Homo sapiens
- plain_language
- MIOX opens the inositol ring, providing a route for its breakdown.
- primary_references
- [ino-p18364358] Structural and biophysical characterization of human myo-inositol oxygenase. (2008). https://pubmed.ncbi.nlm.nih.gov/18364358/ DOI: 10.1074/jbc.m800348200
- tissue_or_cell_type
- Purified MIOX
Inositol: synthesis, signaling, mineral interactions and conditional deficiency (2026-09-17) · lines 457–468
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human enzyme crystallography and catalytic analysis · source_derived_draft · unverified_draft
### ino-miox-cleavage Human MIOX catalyzes oxidative cleavage of myo-inositol to D-glucuronate. Condition category: normal nutrient_topic: Inositol research collection; topical membership is not evidence of a direct dietary effect. plain_language: MIOX opens the inositol ring, providing a route for its breakdown. organism: Homo sapiens tissue_or_cell_type: Purified MIOX experimental_model: Human enzyme crystallography and catalytic analysis limitations: Catabolism of inositol is not evidence that humans synthesize vitamin C from it; the crystal ligand was an inhibitor. exposure: Diiron center and inhibitor-bound structure evidence_span: {"source_cache": "artifacts/inositol-research/18364358.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9992644d489f26782d7ef0a70dc13ec5ca48e2b660a011173fba8e0d4e43ae19", "start_char": 0, "end_char": 1004, "text_sha256": "9992644d489f26782d7ef0a70dc13ec5ca48e2b660a011173fba8e0d4e43ae19"} [ino-p18364358] Structural and biophysical characterization of human myo-inositol oxygenase. (2008). https://pubmed.ncbi.nlm.nih.gov/18364358/ DOI: 10.1074/jbc.m800348200
Complete structured claim and evidenceRat liver cytosol contained activity converting myo-inositol to D-chiro-inositol.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/inositol-research/12051772.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "28ae1225b489898738997d2376ab09857f017314086979032d3ad907299a1154", "start_char": 0, "end_char": 2218, "text_sha256": "28ae1225b489898738997d2376ab09857f017314086979032d3ad907299a1154"}
- experimental_model
- Radiotracer conversion and cytosolic enzyme assays
- exposure
- Diabetic rat versus controls; reduced pyridine-nucleotide cofactors
- limitations
- The molecular identity of the activity was not established here. A later mouse stable-isotope study found no myo-to-D-chiro conversion; the research disagreement is recorded separately. Do not invent a human epimerase gene or infer a universal supplement ratio.
- nutrient_topic
- Inositol research collection; topical membership is not evidence of a direct dietary effect. · Inositol (stereoisomer family)
- organism
- Goto-Kakizaki and Wistar rats
- plain_language
- One stereoisomer can be converted into another in this rat tissue preparation.
- primary_references
- [ino-p12051772] Both myo-inositol to chiro-inositol epimerase activities and chiro-inositol to myo-inositol ratios are decreased in tissues of GK type 2 diabetic rats compared to Wistar controls. (2002). https://pubmed.ncbi.nlm.nih.gov/12051772/ DOI: 10.1016/s0006-291x(02)00313-3
- tissue_or_cell_type
- Liver, muscle, kidney and adipose preparations
Inositol: synthesis, signaling, mineral interactions and conditional deficiency (2026-09-17) · lines 1172–1183
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Radiotracer conversion and cytosolic enzyme assays · source_derived_draft · unverified_draft
### ino-rat-epimerase Rat liver cytosol contained activity converting myo-inositol to D-chiro-inositol. Condition category: normal nutrient_topic: Inositol research collection; topical membership is not evidence of a direct dietary effect. plain_language: One stereoisomer can be converted into another in this rat tissue preparation. organism: Goto-Kakizaki and Wistar rats tissue_or_cell_type: Liver, muscle, kidney and adipose preparations experimental_model: Radiotracer conversion and cytosolic enzyme assays limitations: The molecular identity of the activity was not established here. A later mouse stable-isotope study found no myo-to-D-chiro conversion; the research disagreement is recorded separately. Do not invent a human epimerase gene or infer a universal supplement ratio. exposure: Diabetic rat versus controls; reduced pyridine-nucleotide cofactors evidence_span: {"source_cache": "artifacts/inositol-research/12051772.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "28ae1225b489898738997d2376ab09857f017314086979032d3ad907299a1154", "start_char": 0, "end_char": 2218, "text_sha256": "28ae1225b489898738997d2376ab09857f017314086979032d3ad907299a1154"} [ino-p12051772] Both myo-inositol to chiro-inositol epimerase activities and chiro-inositol to myo-inositol ratios are decreased in tissues of GK type 2 diabetic rats compared to Wistar controls. (2002). https://pubmed.ncbi.nlm.nih.gov/12051772/ DOI: 10.1016/s0006-291x(02)00313-3
Complete structured claim and evidenceHuman SMIT2 expression increased myo-inositol uptake 37-fold relative to vector control in rat L6 cells.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/inositol-research/19032932.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4fdc565b9aa26ef5f2d083c539a1b0367403b39f0c75d3ea1b194bf6fa525242", "start_char": 0, "end_char": 1164, "text_sha256": "4fdc565b9aa26ef5f2d083c539a1b0367403b39f0c75d3ea1b194bf6fa525242"}
- experimental_model
- Human SMIT2 overexpression and radiotracer uptake
- exposure
- Overexpression, glucose competition and insulin exposure
- limitations
- Overexpression is not normal transporter abundance. Insulin experiments used untransfected rat cells; changes in human diabetes are proposed, not demonstrated here.
- nutrient_topic
- Inositol research collection; topical membership is not evidence of a direct dietary effect. · Inositol (stereoisomer family)
- organism
- Human transporter in rat L6 myoblasts
- plain_language
- SMIT2 can bring free myo-inositol into cells.
- primary_references
- [ino-p19032932] Human sodium/inositol cotransporter 2 (SMIT2) transports inositols but not glucose in L6 cells. (2009). https://pubmed.ncbi.nlm.nih.gov/19032932/ DOI: 10.1016/j.abb.2008.11.008
- tissue_or_cell_type
- Skeletal-muscle cell model
- transport_effect
- raises Expression increased myo-inositol uptake 37-fold against vector control.
- transport_pool
- the expressing cell Expression increased myo-inositol uptake 37-fold against vector control.
Inositol: synthesis, signaling, mineral interactions and conditional deficiency (2026-09-17) · lines 288–299
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human SMIT2 overexpression and radiotracer uptake · source_derived_draft · unverified_draft
### ino-smit2-myo Human SMIT2 expression increased myo-inositol uptake 37-fold relative to vector control in rat L6 cells. Condition category: normal nutrient_topic: Inositol research collection; topical membership is not evidence of a direct dietary effect. plain_language: SMIT2 can bring free myo-inositol into cells. organism: Human transporter in rat L6 myoblasts tissue_or_cell_type: Skeletal-muscle cell model experimental_model: Human SMIT2 overexpression and radiotracer uptake limitations: Overexpression is not normal transporter abundance. Insulin experiments used untransfected rat cells; changes in human diabetes are proposed, not demonstrated here. exposure: Overexpression, glucose competition and insulin exposure evidence_span: {"source_cache": "artifacts/inositol-research/19032932.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4fdc565b9aa26ef5f2d083c539a1b0367403b39f0c75d3ea1b194bf6fa525242", "start_char": 0, "end_char": 1164, "text_sha256": "4fdc565b9aa26ef5f2d083c539a1b0367403b39f0c75d3ea1b194bf6fa525242"} [ino-p19032932] Human sodium/inositol cotransporter 2 (SMIT2) transports inositols but not glucose in L6 cells. (2009). https://pubmed.ncbi.nlm.nih.gov/19032932/ DOI: 10.1016/j.abb.2008.11.008
Complete structured claim and evidence
Where it participates (unsigned role)
Lrrc8d knockdown also reduced swelling-evoked myo-inositol efflux in the same rat astrocyte experiments.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Primary rat astrocytes and labeled myo-inositol.
- limitations
- Shared channel dependence does not prove competitive depletion or supplement synergy.
- nutrient_topic
- Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
- plain_language
- Taurine and inositol share part of the cell-volume release machinery.
- primary_references
- Molecular composition and heterogeneity of the LRRC8-containing swelling-activated osmolyte channels in primary rat astrocytes. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28833202/ · DOI 10.1113/JP275053
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 409–415
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Primary rat astrocytes and labeled myo-inositol. · source_derived_draft · unverified_draft
## taurine-vrac-inositol Taurine and inositol share part of the cell-volume release machinery. Lrrc8d knockdown also reduced swelling-evoked myo-inositol efflux in the same rat astrocyte experiments. Model: Primary rat astrocytes and labeled myo-inositol. Limitations: Shared channel dependence does not prove competitive depletion or supplement synergy. Evidence access: Primary abstract Molecular composition and heterogeneity of the LRRC8-containing swelling-activated osmolyte channels in primary rat astrocytes. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28833202/ · DOI 10.1113/JP275053
Complete structured claim and evidenceKinetics, modeling and mutagenesis supported a two-metal catalytic model for human inositol monophosphatase.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Human enzyme structural/kinetic study, including Mn, Zn and Mg titrations.
- limitations
- Historical mechanistic model; not a universal count for all conformations or family members.
- nutrient_topic
- Lithium collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Lithium
- plain_language
- Inositol recycling uses metal-dependent chemistry.
- primary_references
- Mechanism of inositol monophosphatase, the putative target of lithium therapy. · 1994 · https://pubmed.ncbi.nlm.nih.gov/8016062/ · DOI 10.1073/pnas.91.13.5766
Lithium: metal-sensitive enzymes, transport and cross-nutrient mechanisms (2026-09-19) · lines 32–38
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human enzyme structural/kinetic study, including Mn, Zn and Mg titrations. · source_derived_draft · unverified_draft
## lithium-impa-metal Inositol recycling uses metal-dependent chemistry. Kinetics, modeling and mutagenesis supported a two-metal catalytic model for human inositol monophosphatase. Model: Human enzyme structural/kinetic study, including Mn, Zn and Mg titrations. Limitations: Historical mechanistic model; not a universal count for all conformations or family members. Evidence access: Primary abstract Mechanism of inositol monophosphatase, the putative target of lithium therapy. · 1994 · https://pubmed.ncbi.nlm.nih.gov/8016062/ · DOI 10.1073/pnas.91.13.5766
Complete structured claim and evidenceLithium lowered IP3 in the COS-7 experiments; added myo-inositol raised it relative to lithium alone.
Experimental context and source evidence
- evidence_access
- Primary full text
- experimental_model
- Monkey COS-7; 10 mM LiCl, 1 mM myo-inositol rescue.
- limitations
- Cell-culture rescue is not a clinical supplement recommendation.
- nutrient_topic
- Lithium collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Lithium
- plain_language
- Availability of the precursor changes a signaling messenger.
- primary_references
- Lithium induces autophagy by inhibiting inositol monophosphatase. · 2005 · https://pubmed.ncbi.nlm.nih.gov/16186256/ · DOI 10.1083/jcb.200504035
Lithium: metal-sensitive enzymes, transport and cross-nutrient mechanisms (2026-09-19) · lines 80–86
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Monkey COS-7; 10 mM LiCl, 1 mM myo-inositol rescue. · source_derived_draft · unverified_draft
## lithium-ip3-decrease Availability of the precursor changes a signaling messenger. Lithium lowered IP3 in the COS-7 experiments; added myo-inositol raised it relative to lithium alone. Model: Monkey COS-7; 10 mM LiCl, 1 mM myo-inositol rescue. Limitations: Cell-culture rescue is not a clinical supplement recommendation. Evidence access: Primary full text Lithium induces autophagy by inhibiting inositol monophosphatase. · 2005 · https://pubmed.ncbi.nlm.nih.gov/16186256/ · DOI 10.1083/jcb.200504035
Complete structured claim and evidenceISYNA1 transcriptional silencing characterized SLC5A3-dependent AML lines and produced an inositol auxotrophy.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_span
- {"source_cache": "artifacts/inositol-research/34531253.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e709021b8916a9b38a3a52f092732c2b587c55247c0bd9bd3f96438e74ad4b27", "start_char": 0, "end_char": 1431, "text_sha256": "e709021b8916a9b38a3a52f092732c2b587c55247c0bd9bd3f96438e74ad4b27"}
- experimental_model
- Genetic screening, gain/loss of function and patient sample profiling
- exposure
- SLC5A3/ISYNA1 perturbation
- limitations
- Restricted to an epigenetically defined subset; no evidence that dietary inositol restriction treats leukemia.
- nutrient_topic
- Inositol research collection; topical membership is not evidence of a direct dietary effect. · Inositol (stereoisomer family)
- organism
- Human AML cells and in vivo leukemia models
- plain_language
- When a cell loses its synthesis route, the import route can become essential.
- primary_references
- [ino-p34531253] SLC5A3-Dependent Myo-inositol Auxotrophy in Acute Myeloid Leukemia. (2022). https://pubmed.ncbi.nlm.nih.gov/34531253/ DOI: 10.1158/2159-8290.cd-20-1849
- tissue_or_cell_type
- Acute myeloid leukemia
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Inositol: synthesis, signaling, mineral interactions and conditional deficiency (2026-09-17) · lines 405–416
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Genetic screening, gain/loss of function and patient sample profiling · source_derived_draft · unverified_draft
### ino-aml-silencing ISYNA1 transcriptional silencing characterized SLC5A3-dependent AML lines and produced an inositol auxotrophy. Condition category: machinery_impairment nutrient_topic: Inositol research collection; topical membership is not evidence of a direct dietary effect. plain_language: When a cell loses its synthesis route, the import route can become essential. organism: Human AML cells and in vivo leukemia models tissue_or_cell_type: Acute myeloid leukemia experimental_model: Genetic screening, gain/loss of function and patient sample profiling limitations: Restricted to an epigenetically defined subset; no evidence that dietary inositol restriction treats leukemia. exposure: SLC5A3/ISYNA1 perturbation evidence_span: {"source_cache": "artifacts/inositol-research/34531253.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e709021b8916a9b38a3a52f092732c2b587c55247c0bd9bd3f96438e74ad4b27", "start_char": 0, "end_char": 1431, "text_sha256": "e709021b8916a9b38a3a52f092732c2b587c55247c0bd9bd3f96438e74ad4b27"} [ino-p34531253] SLC5A3-Dependent Myo-inositol Auxotrophy in Acute Myeloid Leukemia. (2022). https://pubmed.ncbi.nlm.nih.gov/34531253/ DOI: 10.1158/2159-8290.cd-20-1849
Complete structured claim and evidenceHuman placental phosphatidylinositol synthase used myo-inositol and CDP-diacylglycerol to form phosphatidylinositol.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/inositol-research/8110188.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c05bb5272b443bde4f99d4af375d31988a4812150450d6c4462059a59aa8a09e", "start_char": 0, "end_char": 940, "text_sha256": "c05bb5272b443bde4f99d4af375d31988a4812150450d6c4462059a59aa8a09e"}
- experimental_model
- Purification and kinetics of placental PI synthase
- exposure
- Substrate and ion titrations
- limitations
- Assay optima and inhibitory concentrations are not dietary advice or proof of in vivo nutrient competition.
- nutrient_topic
- Inositol research collection; topical membership is not evidence of a direct dietary effect. · Inositol (stereoisomer family)
- organism
- Homo sapiens
- plain_language
- This step attaches the inositol head group to a membrane lipid.
- primary_references
- [ino-p8110188] Purification and characterization of phosphatidylinositol synthase from human placenta. (1994). https://pubmed.ncbi.nlm.nih.gov/8110188/ DOI: 10.1042/bj2970517
- tissue_or_cell_type
- Placental microsomal enzyme
Inositol: synthesis, signaling, mineral interactions and conditional deficiency (2026-09-17) · lines 496–507
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Purification and kinetics of placental PI synthase · source_derived_draft · unverified_draft
### ino-cdipt-synthesis Human placental phosphatidylinositol synthase used myo-inositol and CDP-diacylglycerol to form phosphatidylinositol. Condition category: normal nutrient_topic: Inositol research collection; topical membership is not evidence of a direct dietary effect. plain_language: This step attaches the inositol head group to a membrane lipid. organism: Homo sapiens tissue_or_cell_type: Placental microsomal enzyme experimental_model: Purification and kinetics of placental PI synthase limitations: Assay optima and inhibitory concentrations are not dietary advice or proof of in vivo nutrient competition. exposure: Substrate and ion titrations evidence_span: {"source_cache": "artifacts/inositol-research/8110188.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c05bb5272b443bde4f99d4af375d31988a4812150450d6c4462059a59aa8a09e", "start_char": 0, "end_char": 940, "text_sha256": "c05bb5272b443bde4f99d4af375d31988a4812150450d6c4462059a59aa8a09e"} [ino-p8110188] Purification and characterization of phosphatidylinositol synthase from human placenta. (1994). https://pubmed.ncbi.nlm.nih.gov/8110188/ DOI: 10.1042/bj2970517
Complete structured claim and evidenceHuman inositol monophosphatase hydrolyzes inositol monophosphates to regenerate free inositol.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/inositol-research/1332026.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "57cfa39b1fe68149ad3a1ea25ede4c979db0586ef14c905cbe402fe3f70ce9e5", "start_char": 0, "end_char": 1147, "text_sha256": "57cfa39b1fe68149ad3a1ea25ede4c979db0586ef14c905cbe402fe3f70ce9e5"}
- experimental_model
- Human enzyme crystallography and catalytic characterization
- exposure
- Structural analysis of the inositol recycling enzyme
- limitations
- Structure does not show that extra substrate bypasses a genetic enzyme defect in patients.
- nutrient_topic
- Inositol research collection; topical membership is not evidence of a direct dietary effect. · Inositol (stereoisomer family)
- organism
- Homo sapiens
- plain_language
- A recycling step removes the last phosphate so the inositol ring can be reused.
- primary_references
- [ino-p1332026] Structure of inositol monophosphatase, the putative target of lithium therapy. (1992). https://pubmed.ncbi.nlm.nih.gov/1332026/ DOI: 10.1073/pnas.89.21.10031
- tissue_or_cell_type
- Purified inositol monophosphatase
Inositol: synthesis, signaling, mineral interactions and conditional deficiency (2026-09-17) · lines 236–247
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human enzyme crystallography and catalytic characterization · source_derived_draft · unverified_draft
### ino-impa-recycling Human inositol monophosphatase hydrolyzes inositol monophosphates to regenerate free inositol. Condition category: normal nutrient_topic: Inositol research collection; topical membership is not evidence of a direct dietary effect. plain_language: A recycling step removes the last phosphate so the inositol ring can be reused. organism: Homo sapiens tissue_or_cell_type: Purified inositol monophosphatase experimental_model: Human enzyme crystallography and catalytic characterization limitations: Structure does not show that extra substrate bypasses a genetic enzyme defect in patients. exposure: Structural analysis of the inositol recycling enzyme evidence_span: {"source_cache": "artifacts/inositol-research/1332026.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "57cfa39b1fe68149ad3a1ea25ede4c979db0586ef14c905cbe402fe3f70ce9e5", "start_char": 0, "end_char": 1147, "text_sha256": "57cfa39b1fe68149ad3a1ea25ede4c979db0586ef14c905cbe402fe3f70ce9e5"} [ino-p1332026] Structure of inositol monophosphatase, the putative target of lithium therapy. (1992). https://pubmed.ncbi.nlm.nih.gov/1332026/ DOI: 10.1073/pnas.89.21.10031
Complete structured claim and evidenceHuman MIOX contains a diiron catalytic center involved in oxygen-dependent inositol cleavage.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/inositol-research/18364358.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9992644d489f26782d7ef0a70dc13ec5ca48e2b660a011173fba8e0d4e43ae19", "start_char": 0, "end_char": 1004, "text_sha256": "9992644d489f26782d7ef0a70dc13ec5ca48e2b660a011173fba8e0d4e43ae19"}
- experimental_model
- Human enzyme crystallography and catalytic analysis
- exposure
- Diiron center and inhibitor-bound structure
- limitations
- Catabolism of inositol is not evidence that humans synthesize vitamin C from it; the crystal ligand was an inhibitor.
- nutrient_topic
- Inositol research collection; topical membership is not evidence of a direct dietary effect. · Inositol (stereoisomer family)
- organism
- Homo sapiens
- plain_language
- Two iron atoms are part of this breakdown enzyme, linking inositol metabolism to iron chemistry.
- primary_references
- [ino-p18364358] Structural and biophysical characterization of human myo-inositol oxygenase. (2008). https://pubmed.ncbi.nlm.nih.gov/18364358/ DOI: 10.1074/jbc.m800348200
- tissue_or_cell_type
- Purified MIOX
Inositol: synthesis, signaling, mineral interactions and conditional deficiency (2026-09-17) · lines 470–481
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human enzyme crystallography and catalytic analysis · source_derived_draft · unverified_draft
### ino-miox-iron Human MIOX contains a diiron catalytic center involved in oxygen-dependent inositol cleavage. Condition category: normal nutrient_topic: Inositol research collection; topical membership is not evidence of a direct dietary effect. plain_language: Two iron atoms are part of this breakdown enzyme, linking inositol metabolism to iron chemistry. organism: Homo sapiens tissue_or_cell_type: Purified MIOX experimental_model: Human enzyme crystallography and catalytic analysis limitations: Catabolism of inositol is not evidence that humans synthesize vitamin C from it; the crystal ligand was an inhibitor. exposure: Diiron center and inhibitor-bound structure evidence_span: {"source_cache": "artifacts/inositol-research/18364358.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9992644d489f26782d7ef0a70dc13ec5ca48e2b660a011173fba8e0d4e43ae19", "start_char": 0, "end_char": 1004, "text_sha256": "9992644d489f26782d7ef0a70dc13ec5ca48e2b660a011173fba8e0d4e43ae19"} [ino-p18364358] Structural and biophysical characterization of human myo-inositol oxygenase. (2008). https://pubmed.ncbi.nlm.nih.gov/18364358/ DOI: 10.1074/jbc.m800348200
Complete structured claim and evidenceBlocking PKC beta I prevented the inositol-mediated reduction of neural tube defects in curly-tail mouse embryos.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_span
- {"source_cache": "artifacts/inositol-research/14613966.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "670b8f0a36bfbecfb417fe28f8748e65994ac47b153ffcf66c42c21e7489f9cc", "start_char": 0, "end_char": 1735, "text_sha256": "670b8f0a36bfbecfb417fe28f8748e65994ac47b153ffcf66c42c21e7489f9cc"}
- experimental_model
- Embryo culture with selective PKC inhibition
- exposure
- Inositol exposure in a folate-resistant neural-tube-defect model
- limitations
- Mechanistic mouse prevention does not establish human efficacy or permit replacing folic acid.
- nutrient_topic
- Inositol research collection; topical membership is not evidence of a direct dietary effect. · Inositol (stereoisomer family)
- organism
- Curly-tail mutant mice
- plain_language
- Adding inositol could not overcome failure of this downstream signaling step.
- primary_references
- [ino-p14613966] Specific isoforms of protein kinase C are essential for prevention of folate-resistant neural tube defects by inositol. (2004). https://pubmed.ncbi.nlm.nih.gov/14613966/ DOI: 10.1093/hmg/ddh003
- tissue_or_cell_type
- Neurulation-stage embryos and hindgut
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Inositol: synthesis, signaling, mineral interactions and conditional deficiency (2026-09-17) · lines 1367–1378
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Embryo culture with selective PKC inhibition · source_derived_draft · unverified_draft
### ino-ntd-pkc-beta Blocking PKC beta I prevented the inositol-mediated reduction of neural tube defects in curly-tail mouse embryos. Condition category: machinery_impairment nutrient_topic: Inositol research collection; topical membership is not evidence of a direct dietary effect. plain_language: Adding inositol could not overcome failure of this downstream signaling step. organism: Curly-tail mutant mice tissue_or_cell_type: Neurulation-stage embryos and hindgut experimental_model: Embryo culture with selective PKC inhibition limitations: Mechanistic mouse prevention does not establish human efficacy or permit replacing folic acid. exposure: Inositol exposure in a folate-resistant neural-tube-defect model evidence_span: {"source_cache": "artifacts/inositol-research/14613966.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "670b8f0a36bfbecfb417fe28f8748e65994ac47b153ffcf66c42c21e7489f9cc", "start_char": 0, "end_char": 1735, "text_sha256": "670b8f0a36bfbecfb417fe28f8748e65994ac47b153ffcf66c42c21e7489f9cc"} [ino-p14613966] Specific isoforms of protein kinase C are essential for prevention of folate-resistant neural tube defects by inositol. (2004). https://pubmed.ncbi.nlm.nih.gov/14613966/ DOI: 10.1093/hmg/ddh003
Complete structured claim and evidencePKC gamma activity was also required for inositol prevention of neural tube defects in this mouse model.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_span
- {"source_cache": "artifacts/inositol-research/14613966.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "670b8f0a36bfbecfb417fe28f8748e65994ac47b153ffcf66c42c21e7489f9cc", "start_char": 0, "end_char": 1735, "text_sha256": "670b8f0a36bfbecfb417fe28f8748e65994ac47b153ffcf66c42c21e7489f9cc"}
- experimental_model
- Embryo culture with selective PKC inhibition
- exposure
- Inositol exposure in a folate-resistant neural-tube-defect model
- limitations
- Mechanistic mouse prevention does not establish human efficacy or permit replacing folic acid.
- nutrient_topic
- Inositol research collection; topical membership is not evidence of a direct dietary effect. · Inositol (stereoisomer family)
- organism
- Curly-tail mutant mice
- plain_language
- A second PKC isoform was separately required.
- primary_references
- [ino-p14613966] Specific isoforms of protein kinase C are essential for prevention of folate-resistant neural tube defects by inositol. (2004). https://pubmed.ncbi.nlm.nih.gov/14613966/ DOI: 10.1093/hmg/ddh003
- tissue_or_cell_type
- Neurulation-stage embryos and hindgut
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Inositol: synthesis, signaling, mineral interactions and conditional deficiency (2026-09-17) · lines 1380–1391
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Embryo culture with selective PKC inhibition · source_derived_draft · unverified_draft
### ino-ntd-pkc-gamma PKC gamma activity was also required for inositol prevention of neural tube defects in this mouse model. Condition category: machinery_impairment nutrient_topic: Inositol research collection; topical membership is not evidence of a direct dietary effect. plain_language: A second PKC isoform was separately required. organism: Curly-tail mutant mice tissue_or_cell_type: Neurulation-stage embryos and hindgut experimental_model: Embryo culture with selective PKC inhibition limitations: Mechanistic mouse prevention does not establish human efficacy or permit replacing folic acid. exposure: Inositol exposure in a folate-resistant neural-tube-defect model evidence_span: {"source_cache": "artifacts/inositol-research/14613966.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "670b8f0a36bfbecfb417fe28f8748e65994ac47b153ffcf66c42c21e7489f9cc", "start_char": 0, "end_char": 1735, "text_sha256": "670b8f0a36bfbecfb417fe28f8748e65994ac47b153ffcf66c42c21e7489f9cc"} [ino-p14613966] Specific isoforms of protein kinase C are essential for prevention of folate-resistant neural tube defects by inositol. (2004). https://pubmed.ncbi.nlm.nih.gov/14613966/ DOI: 10.1093/hmg/ddh003
Complete structured claim and evidenceHypertonic MDCK culture increased sodium/myo-inositol transporter transcription, mRNA and transport activity with different time courses.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/inositol-research/8430828.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0539c3e28460fcea154b9014b1d98f36bf5ee2b8b5a418f6951c9cf0ad92af8b", "start_char": 0, "end_char": 1156, "text_sha256": "0539c3e28460fcea154b9014b1d98f36bf5ee2b8b5a418f6951c9cf0ad92af8b"}
- experimental_model
- Hypertonic culture adaptation
- exposure
- Hypertonic exposure followed by isotonic recovery
- limitations
- Dog cell culture, not a human intake requirement.
- nutrient_topic
- Inositol research collection; topical membership is not evidence of a direct dietary effect. · Inositol (stereoisomer family)
- organism
- Canis familiaris
- plain_language
- Kidney-derived cells adjust inositol uptake as part of adaptation to concentrated surroundings.
- primary_references
- [ino-p8430828] Hypertonicity stimulates transcription of gene for Na(+)-myo-inositol cotransporter in MDCK cells. (1993). https://pubmed.ncbi.nlm.nih.gov/8430828/ DOI: 10.1152/ajprenal.1993.264.1.f20
- tissue_or_cell_type
- MDCK renal epithelial cells
Inositol: synthesis, signaling, mineral interactions and conditional deficiency (2026-09-17) · lines 353–364
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Hypertonic culture adaptation · source_derived_draft · unverified_draft
### ino-smit1-osmotic Hypertonic MDCK culture increased sodium/myo-inositol transporter transcription, mRNA and transport activity with different time courses. Condition category: normal nutrient_topic: Inositol research collection; topical membership is not evidence of a direct dietary effect. plain_language: Kidney-derived cells adjust inositol uptake as part of adaptation to concentrated surroundings. organism: Canis familiaris tissue_or_cell_type: MDCK renal epithelial cells experimental_model: Hypertonic culture adaptation limitations: Dog cell culture, not a human intake requirement. exposure: Hypertonic exposure followed by isotonic recovery evidence_span: {"source_cache": "artifacts/inositol-research/8430828.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0539c3e28460fcea154b9014b1d98f36bf5ee2b8b5a418f6951c9cf0ad92af8b", "start_char": 0, "end_char": 1156, "text_sha256": "0539c3e28460fcea154b9014b1d98f36bf5ee2b8b5a418f6951c9cf0ad92af8b"} [ino-p8430828] Hypertonicity stimulates transcription of gene for Na(+)-myo-inositol cotransporter in MDCK cells. (1993). https://pubmed.ncbi.nlm.nih.gov/8430828/ DOI: 10.1152/ajprenal.1993.264.1.f20
Complete structured claim and evidence
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.