Nutrient chapter

Sodium

Nutrient element sodium; dietary sodium restriction is distinct from distal luminal sodium delivery or serum sodium concentration.

107 recorded mechanisms · 14 availability situations · 12 preserved sources. Draft and verified records are labeled separately.

Read recorded mechanisms Open recursive mind map

The mechanisms

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

Serum-water sodium correlated strongly with (exchangeable sodium + exchangeable potassium)/total body water in the studied patients.
Exchangeable sodium plus potassium divided by total body water → Plasma or serum sodium concentration source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/sodium-research/13575523.fulltext.txt", "locator": "Exact primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ee58d9f6c640fec095876c15e7ddf6fe8bf539cb972c74841db02d2640eebbe2", "start_char": 54337, "end_char": 56036, "text_sha256": "29b3a155f7b33a8b86aa9e30182063d71f5af3c60910a237794c1310094a4c39"}
experimental_model
Simultaneous isotope-dilution and serum measurements, including serial observations
exposure
Observed variation in body composition
limitations
Historical observational regression; serum-water sodium and exchangeable pools are not interchangeable with current clinical plasma measurements or all body sodium. Not an individual correction calculator.
nutrient_topic
Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
organism
Human patients with chronic illnesses
plain_language
Blood sodium reflects a relationship between body cations and water, rather than a simple count of how much sodium was eaten.
primary_references
[sodium-p13575523] Interrelations between serum sodium concentration, serum osmolarity and total exchangeable sodium, total exchangeable potassium and total body water. (1958). https://pubmed.ncbi.nlm.nih.gov/13575523/ DOI: 10.1172/jci103712
tissue_or_cell_type
Whole-body water and exchangeable cations
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 265–276
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Simultaneous isotope-dilution and serum measurements, including serial observations · source_derived_draft · unverified_draft
### sodium-body-water-ratio Serum-water sodium correlated strongly with (exchangeable sodium + exchangeable potassium)/total body water in the studied patients. Condition category: normal nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Blood sodium reflects a relationship between body cations and water, rather than a simple count of how much sodium was eaten. organism: Human patients with chronic illnesses tissue_or_cell_type: Whole-body water and exchangeable cations experimental_model: Simultaneous isotope-dilution and serum measurements, including serial observations limitations: Historical observational regression; serum-water sodium and exchangeable pools are not interchangeable with current clinical plasma measurements or all body sodium. Not an individual correction calculator. exposure: Observed variation in body composition evidence_span: {"source_cache": "artifacts/sodium-research/13575523.fulltext.txt", "locator": "Exact primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ee58d9f6c640fec095876c15e7ddf6fe8bf539cb972c74841db02d2640eebbe2", "start_char": 54337, "end_char": 56036, "text_sha256": "29b3a155f7b33a8b86aa9e30182063d71f5af3c60910a237794c1310094a4c39"} [sodium-p13575523] Interrelations between serum sodium concentration, serum osmolarity and total exchangeable sodium, total exchangeable potassium and total body water. (1958). https://pubmed.ncbi.nlm.nih.gov/13575523/ DOI: 10.1172/jci103712
Complete structured claim and evidence
Normal intestinal SGLT1 couples glucose entry to the inward sodium electrochemical gradient.
Human sodium/glucose cotransporter SGLT1 / SLC5A1 → D-glucose source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/sodium-research/2008213.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ba4e32dc5111895acfe9e109cf57a7e07bc3c4e07e82ad3b4f7715cfaf10af74", "start_char": 0, "end_char": 1357, "text_sha256": "ba4e32dc5111895acfe9e109cf57a7e07bc3c4e07e82ad3b4f7715cfaf10af74"}
experimental_model
Family segregation and Xenopus oocyte transport assay
exposure
Disease-associated SGLT1 missense variant versus normal transporter
limitations
A genetic transporter defect is not sodium dietary deficiency; the sugar-malabsorption phenotype must not be presented as a reason to add salt.
nutrient_topic
Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
organism
Human SGLT1 expressed in frog oocytes
plain_language
A sodium gradient helps intestinal cells take up glucose.
primary_references
[sodium-p2008213] Glucose/galactose malabsorption caused by a defect in the Na+/glucose cotransporter. (1991). https://pubmed.ncbi.nlm.nih.gov/2008213/ DOI: 10.1038/350354a0
tissue_or_cell_type
Intestinal brush border
transport_effect
raises Couples glucose entry to the inward sodium electrochemical gradient.
transport_pool
the enterocyte interior Couples glucose entry to the inward sodium electrochemical gradient.
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 291–302
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Family segregation and Xenopus oocyte transport assay · source_derived_draft · unverified_draft
### sodium-sglt1-gradient Normal intestinal SGLT1 couples glucose entry to the inward sodium electrochemical gradient. Condition category: normal nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A sodium gradient helps intestinal cells take up glucose. organism: Human SGLT1 expressed in frog oocytes tissue_or_cell_type: Intestinal brush border experimental_model: Family segregation and Xenopus oocyte transport assay limitations: A genetic transporter defect is not sodium dietary deficiency; the sugar-malabsorption phenotype must not be presented as a reason to add salt. exposure: Disease-associated SGLT1 missense variant versus normal transporter evidence_span: {"source_cache": "artifacts/sodium-research/2008213.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ba4e32dc5111895acfe9e109cf57a7e07bc3c4e07e82ad3b4f7715cfaf10af74", "start_char": 0, "end_char": 1357, "text_sha256": "ba4e32dc5111895acfe9e109cf57a7e07bc3c4e07e82ad3b4f7715cfaf10af74"} [sodium-p2008213] Glucose/galactose malabsorption caused by a defect in the Na+/glucose cotransporter. (1991). https://pubmed.ncbi.nlm.nih.gov/2008213/ DOI: 10.1038/350354a0
Complete structured claim and evidence
Human OCTN2 expression increased sodium-dependent carnitine uptake with an apparent Km of 4.34 micromolar.
Human carnitine transporter OCTN2 / SLC22A5 → L-Carnitine source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/sodium-research/9685390.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "08cdedaad32299795a52b81183d565d2b476b7a190b2af7b950c829f8c11ddf6", "start_char": 0, "end_char": 1549, "text_sha256": "08cdedaad32299795a52b81183d565d2b476b7a190b2af7b950c829f8c11ddf6"}
experimental_model
Cloning and functional expression
exposure
Radiolabeled carnitine uptake and sodium dependence
limitations
Expression assay; dietary sodium intake, mitochondrial fatty-acid oxidation and clinical supplementation were not directly tested.
nutrient_topic
Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
organism
Human OCTN2 in HEK293 cells
plain_language
The sodium gradient helps bring carnitine into cells.
primary_references
[sodium-p9685390] Molecular and functional identification of sodium ion-dependent, high affinity human carnitine transporter OCTN2. (1998). https://pubmed.ncbi.nlm.nih.gov/9685390/ DOI: 10.1074/jbc.273.32.20378
tissue_or_cell_type
Cell plasma membrane
transport_effect
raises Expression increased sodium-dependent carnitine uptake.
transport_pool
the expressing cell Expression increased sodium-dependent carnitine uptake.
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 616–627
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cloning and functional expression · source_derived_draft · unverified_draft
### sodium-octn2-carnitine Human OCTN2 expression increased sodium-dependent carnitine uptake with an apparent Km of 4.34 micromolar. Condition category: normal nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The sodium gradient helps bring carnitine into cells. organism: Human OCTN2 in HEK293 cells tissue_or_cell_type: Cell plasma membrane experimental_model: Cloning and functional expression limitations: Expression assay; dietary sodium intake, mitochondrial fatty-acid oxidation and clinical supplementation were not directly tested. exposure: Radiolabeled carnitine uptake and sodium dependence evidence_span: {"source_cache": "artifacts/sodium-research/9685390.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "08cdedaad32299795a52b81183d565d2b476b7a190b2af7b950c829f8c11ddf6", "start_char": 0, "end_char": 1549, "text_sha256": "08cdedaad32299795a52b81183d565d2b476b7a190b2af7b950c829f8c11ddf6"} [sodium-p9685390] Molecular and functional identification of sodium ion-dependent, high affinity human carnitine transporter OCTN2. (1998). https://pubmed.ncbi.nlm.nih.gov/9685390/ DOI: 10.1074/jbc.273.32.20378
Complete structured claim and evidence
SLC34A3 mutations segregated with renal phosphate wasting and hypophosphatemic rickets in the studied families.
Sodium-phosphate cotransporter NaPi-IIc / SLC34A3 → Renal phosphate reabsorption source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/sodium-research/16358215.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "876374dd0624cf69b89f3f5b17e5be423d7d9a0358f135add88f2493314d2ceb", "start_char": 0, "end_char": 1515, "text_sha256": "876374dd0624cf69b89f3f5b17e5be423d7d9a0358f135add88f2493314d2ceb"}
experimental_model
Mapping and sequencing in families with hereditary hypophosphatemic rickets with hypercalciuria
exposure
SLC34A3 disease-associated mutations in five families
limitations
Genotype–phenotype evidence supports a primary renal defect; downstream calcitriol/calcium pattern is observed, not a dietary sodium intervention.
nutrient_topic
Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
organism
Human
plain_language
The kidney’s sodium/phosphate transporter is important for retaining phosphate.
primary_references
[sodium-p16358215] Hereditary hypophosphatemic rickets with hypercalciuria is caused by mutations in the sodium-phosphate cotransporter gene SLC34A3. (2006). https://pubmed.ncbi.nlm.nih.gov/16358215/ DOI: 10.1086/499410
tissue_or_cell_type
Renal proximal tubule and systemic mineral phenotype
trigger_kind
machinery_impairment Imported condition classification; unverified.
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 668–679
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mapping and sequencing in families with hereditary hypophosphatemic rickets with hypercalciuria · source_derived_draft · unverified_draft
### sodium-napi2c-phosphate SLC34A3 mutations segregated with renal phosphate wasting and hypophosphatemic rickets in the studied families. Condition category: machinery_impairment nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The kidney’s sodium/phosphate transporter is important for retaining phosphate. organism: Human tissue_or_cell_type: Renal proximal tubule and systemic mineral phenotype experimental_model: Mapping and sequencing in families with hereditary hypophosphatemic rickets with hypercalciuria limitations: Genotype–phenotype evidence supports a primary renal defect; downstream calcitriol/calcium pattern is observed, not a dietary sodium intervention. exposure: SLC34A3 disease-associated mutations in five families evidence_span: {"source_cache": "artifacts/sodium-research/16358215.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "876374dd0624cf69b89f3f5b17e5be423d7d9a0358f135add88f2493314d2ceb", "start_char": 0, "end_char": 1515, "text_sha256": "876374dd0624cf69b89f3f5b17e5be423d7d9a0358f135add88f2493314d2ceb"} [sodium-p16358215] Hereditary hypophosphatemic rickets with hypercalciuria is caused by mutations in the sodium-phosphate cotransporter gene SLC34A3. (2006). https://pubmed.ncbi.nlm.nih.gov/16358215/ DOI: 10.1086/499410
Complete structured claim and evidence
NCLX overexpression increased sodium-dependent mitochondrial calcium efflux; silencing reduced it and heterologous rescue restored it.
Mammalian mitochondrial sodium/calcium exchanger NCLX / SLC8B1 → Mitochondrial calcium efflux source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/sodium-research/20018762.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8594465b44cbb04ed3a631d5dae19959e7c0494a86537d6a60d33d6db1821831", "start_char": 0, "end_char": 1085, "text_sha256": "8594465b44cbb04ed3a631d5dae19959e7c0494a86537d6a60d33d6db1821831"}
experimental_model
Overexpression, siRNA, rescue, mutant and fluorescent ion-imaging experiments
exposure
NCLX abundance, inactive mutant and ion substitutions
limitations
Supports molecular identification in these assays. Protein species and construct details must be taken from the original methods; not evidence for raising dietary sodium.
nutrient_topic
Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
organism
Mammalian cultured-cell preparations
plain_language
A mitochondrial exchanger connects sodium movement with calcium removal.
primary_references
[sodium-p20018762] NCLX is an essential component of mitochondrial Na+/Ca2+ exchange. (2010). https://pubmed.ncbi.nlm.nih.gov/20018762/ DOI: 10.1073/pnas.0908099107
tissue_or_cell_type
Mitochondrial cristae
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 733–744
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Overexpression, siRNA, rescue, mutant and fluorescent ion-imaging experiments · source_derived_draft · unverified_draft
### sodium-nclx-efflux NCLX overexpression increased sodium-dependent mitochondrial calcium efflux; silencing reduced it and heterologous rescue restored it. Condition category: normal nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A mitochondrial exchanger connects sodium movement with calcium removal. organism: Mammalian cultured-cell preparations tissue_or_cell_type: Mitochondrial cristae experimental_model: Overexpression, siRNA, rescue, mutant and fluorescent ion-imaging experiments limitations: Supports molecular identification in these assays. Protein species and construct details must be taken from the original methods; not evidence for raising dietary sodium. exposure: NCLX abundance, inactive mutant and ion substitutions evidence_span: {"source_cache": "artifacts/sodium-research/20018762.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8594465b44cbb04ed3a631d5dae19959e7c0494a86537d6a60d33d6db1821831", "start_char": 0, "end_char": 1085, "text_sha256": "8594465b44cbb04ed3a631d5dae19959e7c0494a86537d6a60d33d6db1821831"} [sodium-p20018762] NCLX is an essential component of mitochondrial Na+/Ca2+ exchange. (2010). https://pubmed.ncbi.nlm.nih.gov/20018762/ DOI: 10.1073/pnas.0908099107
Complete structured claim and evidence
Aldosterone increased collecting-duct sgk mRNA within 30 minutes through mineralocorticoid receptors without requiring new protein synthesis.
Aldosterone → SGK1 transcript and protein expression source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/sodium-research/10358046.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7d53e3e8ce41bb21d5cac2a5bfe6a6abdc702d0870add9c0a002e58ac374a97b", "start_char": 0, "end_char": 1343, "text_sha256": "7d53e3e8ce41bb21d5cac2a5bfe6a6abdc702d0870add9c0a002e58ac374a97b"}
experimental_model
Immediate-early gene induction and channel coexpression
exposure
Aldosterone exposure; receptor dependence and protein-synthesis tests
limitations
Cell and oocyte mechanism; the study does not imply that dietary sodium directly activates SGK1 in every tissue.
nutrient_topic
Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
organism
Rabbit/mouse collecting-duct preparations; mouse SGK in Xenopus oocytes
plain_language
A hormone can quickly increase the instructions for a kinase that regulates sodium transport.
primary_references
[sodium-p10358046] sgk is an aldosterone-induced kinase in the renal collecting duct. Effects on epithelial na+ channels. (1999). https://pubmed.ncbi.nlm.nih.gov/10358046/ DOI: 10.1074/jbc.274.24.16973
tissue_or_cell_type
Cortical collecting duct and expression system
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 395–406
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Immediate-early gene induction and channel coexpression · source_derived_draft · unverified_draft
### sodium-aldosterone-sgk Aldosterone increased collecting-duct sgk mRNA within 30 minutes through mineralocorticoid receptors without requiring new protein synthesis. Condition category: normal nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A hormone can quickly increase the instructions for a kinase that regulates sodium transport. organism: Rabbit/mouse collecting-duct preparations; mouse SGK in Xenopus oocytes tissue_or_cell_type: Cortical collecting duct and expression system experimental_model: Immediate-early gene induction and channel coexpression limitations: Cell and oocyte mechanism; the study does not imply that dietary sodium directly activates SGK1 in every tissue. exposure: Aldosterone exposure; receptor dependence and protein-synthesis tests evidence_span: {"source_cache": "artifacts/sodium-research/10358046.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7d53e3e8ce41bb21d5cac2a5bfe6a6abdc702d0870add9c0a002e58ac374a97b", "start_char": 0, "end_char": 1343, "text_sha256": "7d53e3e8ce41bb21d5cac2a5bfe6a6abdc702d0870add9c0a002e58ac374a97b"} [sodium-p10358046] sgk is an aldosterone-induced kinase in the renal collecting duct. Effects on epithelial na+ channels. (1999). https://pubmed.ncbi.nlm.nih.gov/10358046/ DOI: 10.1074/jbc.274.24.16973
Complete structured claim and evidence
Intestinal NHE3 deletion produced persistent watery, alkaline diarrhea.
Mouse sodium/hydrogen exchanger NHE3 / Slc9a3 → Intestinal fluid loss source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/sodium-research/32227118.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0a9c8f006f6b0b8ff35bd7e67c529c9c72e0cf3d3fd29cd46ec8c23942129b39", "start_char": 0, "end_char": 1643, "text_sha256": "0a9c8f006f6b0b8ff35bd7e67c529c9c72e0cf3d3fd29cd46ec8c23942129b39"}
experimental_model
Inducible intestinal epithelial Slc9a3 deletion
exposure
Tamoxifen-induced NHE3 loss
limitations
Genetic machinery failure, not isolated low sodium intake. Gut loss differs from proximal-tubule-specific deletion.
nutrient_topic
Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
organism
Mouse
plain_language
A transport defect can create ongoing intestinal fluid losses.
primary_references
[sodium-p32227118] An inducible intestinal epithelial cell-specific NHE3 knockout mouse model mimicking congenital sodium diarrhea. (2020). https://pubmed.ncbi.nlm.nih.gov/32227118/ DOI: 10.1042/cs20200065
tissue_or_cell_type
Intestine with systemic electrolyte measurements
trigger_kind
machinery_impairment Imported condition classification; unverified.
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 824–835
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Inducible intestinal epithelial Slc9a3 deletion · source_derived_draft · unverified_draft
### sodium-gut-loss Intestinal NHE3 deletion produced persistent watery, alkaline diarrhea. Condition category: machinery_impairment nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A transport defect can create ongoing intestinal fluid losses. organism: Mouse tissue_or_cell_type: Intestine with systemic electrolyte measurements experimental_model: Inducible intestinal epithelial Slc9a3 deletion limitations: Genetic machinery failure, not isolated low sodium intake. Gut loss differs from proximal-tubule-specific deletion. exposure: Tamoxifen-induced NHE3 loss evidence_span: {"source_cache": "artifacts/sodium-research/32227118.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0a9c8f006f6b0b8ff35bd7e67c529c9c72e0cf3d3fd29cd46ec8c23942129b39", "start_char": 0, "end_char": 1643, "text_sha256": "0a9c8f006f6b0b8ff35bd7e67c529c9c72e0cf3d3fd29cd46ec8c23942129b39"} [sodium-p32227118] An inducible intestinal epithelial cell-specific NHE3 knockout mouse model mimicking congenital sodium diarrhea. (2020). https://pubmed.ncbi.nlm.nih.gov/32227118/ DOI: 10.1042/cs20200065
Complete structured claim and evidence
The alpha- or beta-subunit variants identified in affected families caused loss of channel activity.
Epithelial sodium channel → ENaC-mediated sodium current source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/sodium-research/8589714.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c85f54f2086e1dc34cabaa8e4521a157bfeb5512b7882ca214ddfa2597b9bc4e", "start_char": 0, "end_char": 696, "text_sha256": "c85f54f2086e1dc34cabaa8e4521a157bfeb5512b7882ca214ddfa2597b9bc4e"}
experimental_model
Human family genetics and sodium-channel functional testing
exposure
Loss-of-function alpha- or beta-subunit variants in five kindreds
limitations
Autosomal recessive pseudohypoaldosteronism; not ordinary dietary sodium deficiency and not proof that additional aldosterone can repair the channel.
nutrient_topic
Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
organism
Human
plain_language
The sodium entry channel itself can fail.
primary_references
[sodium-p8589714] Mutations in subunits of the epithelial sodium channel cause salt wasting with hyperkalaemic acidosis, pseudohypoaldosteronism type 1. (1996). https://pubmed.ncbi.nlm.nih.gov/8589714/ DOI: 10.1038/ng0396-248
tissue_or_cell_type
ENaC-dependent epithelia and systemic electrolyte phenotype
trigger_kind
machinery_impairment Imported condition classification; unverified.
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 928–939
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human family genetics and sodium-channel functional testing · source_derived_draft · unverified_draft
### sodium-enac-loss-current The alpha- or beta-subunit variants identified in affected families caused loss of channel activity. Condition category: machinery_impairment nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The sodium entry channel itself can fail. organism: Human tissue_or_cell_type: ENaC-dependent epithelia and systemic electrolyte phenotype experimental_model: Human family genetics and sodium-channel functional testing limitations: Autosomal recessive pseudohypoaldosteronism; not ordinary dietary sodium deficiency and not proof that additional aldosterone can repair the channel. exposure: Loss-of-function alpha- or beta-subunit variants in five kindreds evidence_span: {"source_cache": "artifacts/sodium-research/8589714.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c85f54f2086e1dc34cabaa8e4521a157bfeb5512b7882ca214ddfa2597b9bc4e", "start_char": 0, "end_char": 696, "text_sha256": "c85f54f2086e1dc34cabaa8e4521a157bfeb5512b7882ca214ddfa2597b9bc4e"} [sodium-p8589714] Mutations in subunits of the epithelial sodium channel cause salt wasting with hyperkalaemic acidosis, pseudohypoaldosteronism type 1. (1996). https://pubmed.ncbi.nlm.nih.gov/8589714/ DOI: 10.1038/ng0396-248
Complete structured claim and evidence
Weight gain during the marathon was independently associated with hyponatremia, odds ratio 4.2 (95% CI 2.2–8.2).
Weight gain during endurance exercise → Plasma or serum sodium concentration source_derived_draftungraded
Experimental context and source evidence
availability_state
biomarker_context Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/sodium-research/15829535.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9bf7f638ff3cfcad3d43536a75ffedf40a2ef726f783922f3169c9252c12a8e5", "start_char": 0, "end_char": 1893, "text_sha256": "9bf7f638ff3cfcad3d43536a75ffedf40a2ef726f783922f3169c9252c12a8e5"}
experimental_model
Prospective marathon cohort with prerace/postrace weights and blood sampling
exposure
2002 Boston Marathon; 488 usable finish-line blood samples
limitations
Observational associations and sampling limitations; fluid composition was not independently associated. Not a treatment protocol or pure dietary-depletion study.
nutrient_topic
Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
organism
Human runners
plain_language
A low sodium concentration can accompany gaining water rather than simply losing salt.
primary_references
[sodium-p15829535] Hyponatremia among runners in the Boston Marathon. (2005). https://pubmed.ncbi.nlm.nih.gov/15829535/ DOI: 10.1056/nejmoa043901
tissue_or_cell_type
Systemic water/sodium balance
trigger_kind
biomarker_context Imported condition classification; unverified.
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 1006–1017
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Prospective marathon cohort with prerace/postrace weights and blood sampling · source_derived_draft · unverified_draft
### sodium-marathon-weight Weight gain during the marathon was independently associated with hyponatremia, odds ratio 4.2 (95% CI 2.2–8.2). Condition category: biomarker_context nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A low sodium concentration can accompany gaining water rather than simply losing salt. organism: Human runners tissue_or_cell_type: Systemic water/sodium balance experimental_model: Prospective marathon cohort with prerace/postrace weights and blood sampling limitations: Observational associations and sampling limitations; fluid composition was not independently associated. Not a treatment protocol or pure dietary-depletion study. exposure: 2002 Boston Marathon; 488 usable finish-line blood samples evidence_span: {"source_cache": "artifacts/sodium-research/15829535.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9bf7f638ff3cfcad3d43536a75ffedf40a2ef726f783922f3169c9252c12a8e5", "start_char": 0, "end_char": 1893, "text_sha256": "9bf7f638ff3cfcad3d43536a75ffedf40a2ef726f783922f3169c9252c12a8e5"} [sodium-p15829535] Hyponatremia among runners in the Boston Marathon. (2005). https://pubmed.ncbi.nlm.nih.gov/15829535/ DOI: 10.1056/nejmoa043901
Complete structured claim and evidence
Mean weight-gain velocity was 26.9 versus 22.9 g/kg/day with supplementation versus placebo.
Sodium → Preterm infant weight-gain velocity source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/sodium-research/25406227.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a3c6cd28e4896dc8cdaeaacb7d524c55098b87dd5bf9d028ce49ba544832e339", "start_char": 0, "end_char": 1645, "text_sha256": "a3c6cd28e4896dc8cdaeaacb7d524c55098b87dd5bf9d028ce49ba544832e339"}
experimental_model
Randomized masked trial in 53 infants born before 32 weeks
exposure
4 mEq/kg/day supplemental sodium versus placebo, days 7–35
limitations
Study regimen, not a dosing recommendation. Small neonatal trial; improved weight gain is not proof that every blood sodium measurement diagnoses total-body depletion.
nutrient_topic
Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
organism
Human preterm infants
plain_language
The sodium intervention improved weight gain in this small preterm-infant trial.
primary_references
[sodium-p25406227] Impact of Early Sodium Supplementation on Hyponatremia and Growth in Premature Infants: A Randomized Controlled Trial. (2016). https://pubmed.ncbi.nlm.nih.gov/25406227/ DOI: 10.1177/0148607114558303
tissue_or_cell_type
Whole-body growth and serum sodium
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 980–991
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized masked trial in 53 infants born before 32 weeks · source_derived_draft · unverified_draft
### sodium-preterm-weight Mean weight-gain velocity was 26.9 versus 22.9 g/kg/day with supplementation versus placebo. Condition category: nutrient_deficiency nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The sodium intervention improved weight gain in this small preterm-infant trial. organism: Human preterm infants tissue_or_cell_type: Whole-body growth and serum sodium experimental_model: Randomized masked trial in 53 infants born before 32 weeks limitations: Study regimen, not a dosing recommendation. Small neonatal trial; improved weight gain is not proof that every blood sodium measurement diagnoses total-body depletion. exposure: 4 mEq/kg/day supplemental sodium versus placebo, days 7–35 evidence_span: {"source_cache": "artifacts/sodium-research/25406227.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a3c6cd28e4896dc8cdaeaacb7d524c55098b87dd5bf9d028ce49ba544832e339", "start_char": 0, "end_char": 1645, "text_sha256": "a3c6cd28e4896dc8cdaeaacb7d524c55098b87dd5bf9d028ce49ba544832e339"} [sodium-p25406227] Impact of Early Sodium Supplementation on Hyponatremia and Growth in Premature Infants: A Randomized Controlled Trial. (2016). https://pubmed.ncbi.nlm.nih.gov/25406227/ DOI: 10.1177/0148607114558303
Complete structured claim and evidence
The higher-salt diet increased urinary calcium excretion in the crossover trial (P=0.0008).
Sodium chloride → Urinary calcium excretion source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/sodium-research/18410231.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f831f038a6c4249510bbeeae68778a216f1c36aa440e33816072959d1a07fefa", "start_char": 0, "end_char": 1558, "text_sha256": "f831f038a6c4249510bbeeae68778a216f1c36aa440e33816072959d1a07fefa"}
experimental_model
Randomized crossover with stable-isotope calcium measures and compartmental modeling in 11 completers
exposure
Four five-week calcium/salt diet combinations: 518 or 1284 mg calcium; 3.9 or 11.2 g salt daily
limitations
Small study; bone balance was modeled, fractures were not measured. Salt means sodium chloride, not elemental sodium.
nutrient_topic
Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
organism
Human postmenopausal women
plain_language
More dietary salt increased measured urinary calcium loss in these women.
primary_references
[sodium-p18410231] Sodium and bone health: impact of moderately high and low salt intakes on calcium metabolism in postmenopausal women. (2008). https://pubmed.ncbi.nlm.nih.gov/18410231/ DOI: 10.1359/jbmr.080408
tissue_or_cell_type
Intestinal, renal and modeled skeletal calcium balance
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 1097–1108
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized crossover with stable-isotope calcium measures and compartmental modeling in 11 completers · source_derived_draft · unverified_draft
### sodium-salt-calciuria The higher-salt diet increased urinary calcium excretion in the crossover trial (P=0.0008). Condition category: normal nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: More dietary salt increased measured urinary calcium loss in these women. organism: Human postmenopausal women tissue_or_cell_type: Intestinal, renal and modeled skeletal calcium balance experimental_model: Randomized crossover with stable-isotope calcium measures and compartmental modeling in 11 completers limitations: Small study; bone balance was modeled, fractures were not measured. Salt means sodium chloride, not elemental sodium. exposure: Four five-week calcium/salt diet combinations: 518 or 1284 mg calcium; 3.9 or 11.2 g salt daily evidence_span: {"source_cache": "artifacts/sodium-research/18410231.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f831f038a6c4249510bbeeae68778a216f1c36aa440e33816072959d1a07fefa", "start_char": 0, "end_char": 1558, "text_sha256": "f831f038a6c4249510bbeeae68778a216f1c36aa440e33816072959d1a07fefa"} [sodium-p18410231] Sodium and bone health: impact of moderately high and low salt intakes on calcium metabolism in postmenopausal women. (2008). https://pubmed.ncbi.nlm.nih.gov/18410231/ DOI: 10.1359/jbmr.080408
Complete structured claim and evidence
High-to-intermediate sodium reduction lowered systolic pressure by 2.1 mmHg on the control diet and 1.3 mmHg on DASH; intermediate-to-low reduction lowered it by another 4.6 and 1.7 mmHg respectively.
Sodium → Arterial blood pressure source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/sodium-research/11136953.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7664fc223f123220dd64755a1e9bc4ee3e9942e09b5de444bd789f210f449133", "start_char": 0, "end_char": 1987, "text_sha256": "7664fc223f123220dd64755a1e9bc4ee3e9942e09b5de444bd789f210f449133"}
experimental_model
Randomized controlled feeding trial in 412 participants
exposure
Three sodium levels for 30 days each within assigned DASH or control diet
limitations
Blood-pressure trial, not a hard-outcome trial; DASH changes multiple nutrients and foods. Its combined effect cannot be assigned to one mineral.
nutrient_topic
Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
organism
Human adults with and without hypertension
plain_language
Reducing sodium lowered blood pressure under both tested dietary patterns.
primary_references
[sodium-p11136953] Effects on blood pressure of reduced dietary sodium and the Dietary Approaches to Stop Hypertension (DASH) diet. DASH-Sodium Collaborative Research Group. (2001). https://pubmed.ncbi.nlm.nih.gov/11136953/ DOI: 10.1056/nejm200101043440101
tissue_or_cell_type
Systemic blood pressure
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 1071–1082
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized controlled feeding trial in 412 participants · source_derived_draft · unverified_draft
### sodium-dash-sodium High-to-intermediate sodium reduction lowered systolic pressure by 2.1 mmHg on the control diet and 1.3 mmHg on DASH; intermediate-to-low reduction lowered it by another 4.6 and 1.7 mmHg respectively. Condition category: normal nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Reducing sodium lowered blood pressure under both tested dietary patterns. organism: Human adults with and without hypertension tissue_or_cell_type: Systemic blood pressure experimental_model: Randomized controlled feeding trial in 412 participants limitations: Blood-pressure trial, not a hard-outcome trial; DASH changes multiple nutrients and foods. Its combined effect cannot be assigned to one mineral. exposure: Three sodium levels for 30 days each within assigned DASH or control diet evidence_span: {"source_cache": "artifacts/sodium-research/11136953.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7664fc223f123220dd64755a1e9bc4ee3e9942e09b5de444bd789f210f449133", "start_char": 0, "end_char": 1987, "text_sha256": "7664fc223f123220dd64755a1e9bc4ee3e9942e09b5de444bd789f210f449133"} [sodium-p11136953] Effects on blood pressure of reduced dietary sodium and the Dietary Approaches to Stop Hypertension (DASH) diet. DASH-Sodium Collaborative Research Group. (2001). https://pubmed.ncbi.nlm.nih.gov/11136953/ DOI: 10.1056/nejm200101043440101
Complete structured claim and evidence
Serum sodium correlated only partly or poorly with the isolated body-composition ratios, including exchangeable sodium/body weight.
Total exchangeable body sodium → Plasma or serum sodium concentration source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/sodium-research/13575523.fulltext.txt", "locator": "Exact primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ee58d9f6c640fec095876c15e7ddf6fe8bf539cb972c74841db02d2640eebbe2", "start_char": 54337, "end_char": 56036, "text_sha256": "29b3a155f7b33a8b86aa9e30182063d71f5af3c60910a237794c1310094a4c39"}
experimental_model
Simultaneous isotope-dilution and serum measurements, including serial observations
exposure
Observed variation in body composition
limitations
Historical observational regression; serum-water sodium and exchangeable pools are not interchangeable with current clinical plasma measurements or all body sodium. Not an individual correction calculator.
nutrient_topic
Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
organism
Human patients with chronic illnesses
plain_language
A low blood sodium result does not, by itself, identify a dietary sodium shortage.
primary_references
[sodium-p13575523] Interrelations between serum sodium concentration, serum osmolarity and total exchangeable sodium, total exchangeable potassium and total body water. (1958). https://pubmed.ncbi.nlm.nih.gov/13575523/ DOI: 10.1172/jci103712
tissue_or_cell_type
Whole-body water and exchangeable cations
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 278–289
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Simultaneous isotope-dilution and serum measurements, including serial observations · source_derived_draft · unverified_draft
### sodium-body-sodium-marker-limit Serum sodium correlated only partly or poorly with the isolated body-composition ratios, including exchangeable sodium/body weight. Condition category: normal nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A low blood sodium result does not, by itself, identify a dietary sodium shortage. organism: Human patients with chronic illnesses tissue_or_cell_type: Whole-body water and exchangeable cations experimental_model: Simultaneous isotope-dilution and serum measurements, including serial observations limitations: Historical observational regression; serum-water sodium and exchangeable pools are not interchangeable with current clinical plasma measurements or all body sodium. Not an individual correction calculator. exposure: Observed variation in body composition evidence_span: {"source_cache": "artifacts/sodium-research/13575523.fulltext.txt", "locator": "Exact primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ee58d9f6c640fec095876c15e7ddf6fe8bf539cb972c74841db02d2640eebbe2", "start_char": 54337, "end_char": 56036, "text_sha256": "29b3a155f7b33a8b86aa9e30182063d71f5af3c60910a237794c1310094a4c39"} [sodium-p13575523] Interrelations between serum sodium concentration, serum osmolarity and total exchangeable sodium, total exchangeable potassium and total body water. (1958). https://pubmed.ncbi.nlm.nih.gov/13575523/ DOI: 10.1172/jci103712
Complete structured claim and evidence
The familial SGLT1 missense variant abolished sodium-dependent glucose transport in injected oocytes.
Human sodium/glucose cotransporter SGLT1 / SLC5A1 → Intestinal epithelial glucose uptake source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/sodium-research/2008213.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ba4e32dc5111895acfe9e109cf57a7e07bc3c4e07e82ad3b4f7715cfaf10af74", "start_char": 0, "end_char": 1357, "text_sha256": "ba4e32dc5111895acfe9e109cf57a7e07bc3c4e07e82ad3b4f7715cfaf10af74"}
experimental_model
Family segregation and Xenopus oocyte transport assay
exposure
Disease-associated SGLT1 missense variant versus normal transporter
limitations
A genetic transporter defect is not sodium dietary deficiency; the sugar-malabsorption phenotype must not be presented as a reason to add salt.
nutrient_topic
Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
organism
Human SGLT1 expressed in frog oocytes
plain_language
The transport protein itself can be the limiting step.
primary_references
[sodium-p2008213] Glucose/galactose malabsorption caused by a defect in the Na+/glucose cotransporter. (1991). https://pubmed.ncbi.nlm.nih.gov/2008213/ DOI: 10.1038/350354a0
tissue_or_cell_type
Intestinal brush border
trigger_kind
machinery_impairment Imported condition classification; unverified.
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 304–315
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Family segregation and Xenopus oocyte transport assay · source_derived_draft · unverified_draft
### sodium-sglt1-loss The familial SGLT1 missense variant abolished sodium-dependent glucose transport in injected oocytes. Condition category: machinery_impairment nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The transport protein itself can be the limiting step. organism: Human SGLT1 expressed in frog oocytes tissue_or_cell_type: Intestinal brush border experimental_model: Family segregation and Xenopus oocyte transport assay limitations: A genetic transporter defect is not sodium dietary deficiency; the sugar-malabsorption phenotype must not be presented as a reason to add salt. exposure: Disease-associated SGLT1 missense variant versus normal transporter evidence_span: {"source_cache": "artifacts/sodium-research/2008213.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ba4e32dc5111895acfe9e109cf57a7e07bc3c4e07e82ad3b4f7715cfaf10af74", "start_char": 0, "end_char": 1357, "text_sha256": "ba4e32dc5111895acfe9e109cf57a7e07bc3c4e07e82ad3b4f7715cfaf10af74"} [sodium-p2008213] Glucose/galactose malabsorption caused by a defect in the Na+/glucose cotransporter. (1991). https://pubmed.ncbi.nlm.nih.gov/2008213/ DOI: 10.1038/350354a0
Complete structured claim and evidence
Early proximal glucose reabsorption was 78 ± 6% in wild-type mice and absent in Sglt2-null mice.
Mouse sodium/glucose cotransporter SGLT2 / Slc5a2 → Renal glucose reabsorption source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/sodium-research/20616166.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0596ceea07c063931780bf6128a238c81622461ed65dd5b0d382f0202e1626f9", "start_char": 0, "end_char": 1704, "text_sha256": "0596ceea07c063931780bf6128a238c81622461ed65dd5b0d382f0202e1626f9"}
experimental_model
Sglt2-null mice, localization, clearance and micropuncture
exposure
Genetic Slc5a2 deletion
limitations
Renal glucose reabsorption and water output changed, but the knockout did not show the measured signs of volume depletion. Genetic deletion is not a dietary experiment.
nutrient_topic
Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
organism
Mouse
plain_language
The early kidney tubule uses a specific sodium/glucose transporter to reclaim filtered glucose.
primary_references
[sodium-p20616166] SGLT2 mediates glucose reabsorption in the early proximal tubule. (2011). https://pubmed.ncbi.nlm.nih.gov/20616166/ DOI: 10.1681/asn.2010030246
tissue_or_cell_type
Renal early proximal tubule
trigger_kind
machinery_impairment Imported condition classification; unverified.
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 317–328
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Sglt2-null mice, localization, clearance and micropuncture · source_derived_draft · unverified_draft
### sodium-sglt2-early Early proximal glucose reabsorption was 78 ± 6% in wild-type mice and absent in Sglt2-null mice. Condition category: machinery_impairment nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The early kidney tubule uses a specific sodium/glucose transporter to reclaim filtered glucose. organism: Mouse tissue_or_cell_type: Renal early proximal tubule experimental_model: Sglt2-null mice, localization, clearance and micropuncture limitations: Renal glucose reabsorption and water output changed, but the knockout did not show the measured signs of volume depletion. Genetic deletion is not a dietary experiment. exposure: Genetic Slc5a2 deletion evidence_span: {"source_cache": "artifacts/sodium-research/20616166.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0596ceea07c063931780bf6128a238c81622461ed65dd5b0d382f0202e1626f9", "start_char": 0, "end_char": 1704, "text_sha256": "0596ceea07c063931780bf6128a238c81622461ed65dd5b0d382f0202e1626f9"} [sodium-p20616166] SGLT2 mediates glucose reabsorption in the early proximal tubule. (2011). https://pubmed.ncbi.nlm.nih.gov/20616166/ DOI: 10.1681/asn.2010030246
Complete structured claim and evidence
Sglt2-null mice had glucosuria and polyuria without differences in plasma glucose or GFR versus controls.
Mouse sodium/glucose cotransporter SGLT2 / Slc5a2 → Urinary glucose excretion source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/sodium-research/20616166.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0596ceea07c063931780bf6128a238c81622461ed65dd5b0d382f0202e1626f9", "start_char": 0, "end_char": 1704, "text_sha256": "0596ceea07c063931780bf6128a238c81622461ed65dd5b0d382f0202e1626f9"}
experimental_model
Sglt2-null mice, localization, clearance and micropuncture
exposure
Genetic Slc5a2 deletion
limitations
Renal glucose reabsorption and water output changed, but the knockout did not show the measured signs of volume depletion. Genetic deletion is not a dietary experiment.
nutrient_topic
Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
organism
Mouse
plain_language
Losing this transporter sends glucose into urine; it does not mean the blood glucose must be high.
primary_references
[sodium-p20616166] SGLT2 mediates glucose reabsorption in the early proximal tubule. (2011). https://pubmed.ncbi.nlm.nih.gov/20616166/ DOI: 10.1681/asn.2010030246
tissue_or_cell_type
Renal early proximal tubule
trigger_kind
machinery_impairment Imported condition classification; unverified.
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 330–341
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Sglt2-null mice, localization, clearance and micropuncture · source_derived_draft · unverified_draft
### sodium-sglt2-urine Sglt2-null mice had glucosuria and polyuria without differences in plasma glucose or GFR versus controls. Condition category: machinery_impairment nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Losing this transporter sends glucose into urine; it does not mean the blood glucose must be high. organism: Mouse tissue_or_cell_type: Renal early proximal tubule experimental_model: Sglt2-null mice, localization, clearance and micropuncture limitations: Renal glucose reabsorption and water output changed, but the knockout did not show the measured signs of volume depletion. Genetic deletion is not a dietary experiment. exposure: Genetic Slc5a2 deletion evidence_span: {"source_cache": "artifacts/sodium-research/20616166.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0596ceea07c063931780bf6128a238c81622461ed65dd5b0d382f0202e1626f9", "start_char": 0, "end_char": 1704, "text_sha256": "0596ceea07c063931780bf6128a238c81622461ed65dd5b0d382f0202e1626f9"} [sodium-p20616166] SGLT2 mediates glucose reabsorption in the early proximal tubule. (2011). https://pubmed.ncbi.nlm.nih.gov/20616166/ DOI: 10.1681/asn.2010030246
Complete structured claim and evidence
The human Nav1.4–beta1 structure resolved its pore and voltage-sensing domains, supporting a molecular account of sodium permeation.
NaV1.4 / SCN4A → Sodium ion source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/sodium-research/30190309.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2c9e7fceab1407740b539362913e9f97227515a9a7d9439ce57113545d2f7436", "start_char": 0, "end_char": 876, "text_sha256": "2c9e7fceab1407740b539362913e9f97227515a9a7d9439ce57113545d2f7436"}
experimental_model
Cryo-EM reconstruction at 3.2 angstrom resolution
exposure
Purified Nav1.4–beta1 structure
limitations
Structural support for permeation and inactivation; this experiment did not test dietary sodium or clinical supplementation.
nutrient_topic
Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
organism
Human channel complex
plain_language
A dedicated sodium-channel protein helps electrically excitable cells generate signals.
primary_references
[sodium-p30190309] Structure of the human voltage-gated sodium channel Nav1.4 in complex with β1. (2018). https://pubmed.ncbi.nlm.nih.gov/30190309/ DOI: 10.1126/science.aau2486
tissue_or_cell_type
Skeletal-muscle Nav1.4 with beta1
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 343–354
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cryo-EM reconstruction at 3.2 angstrom resolution · source_derived_draft · unverified_draft
### sodium-nav14-pore The human Nav1.4–beta1 structure resolved its pore and voltage-sensing domains, supporting a molecular account of sodium permeation. Condition category: normal nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A dedicated sodium-channel protein helps electrically excitable cells generate signals. organism: Human channel complex tissue_or_cell_type: Skeletal-muscle Nav1.4 with beta1 experimental_model: Cryo-EM reconstruction at 3.2 angstrom resolution limitations: Structural support for permeation and inactivation; this experiment did not test dietary sodium or clinical supplementation. exposure: Purified Nav1.4–beta1 structure evidence_span: {"source_cache": "artifacts/sodium-research/30190309.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2c9e7fceab1407740b539362913e9f97227515a9a7d9439ce57113545d2f7436", "start_char": 0, "end_char": 876, "text_sha256": "2c9e7fceab1407740b539362913e9f97227515a9a7d9439ce57113545d2f7436"} [sodium-p30190309] Structure of the human voltage-gated sodium channel Nav1.4 in complex with β1. (2018). https://pubmed.ncbi.nlm.nih.gov/30190309/ DOI: 10.1126/science.aau2486
Complete structured claim and evidence
Analysis of the Nav1.4 structure and previously characterized residues supported an allosteric blocking mechanism of fast inactivation.
NaV1.4 / SCN4A → Nav1.4 fast inactivation source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/sodium-research/30190309.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2c9e7fceab1407740b539362913e9f97227515a9a7d9439ce57113545d2f7436", "start_char": 0, "end_char": 876, "text_sha256": "2c9e7fceab1407740b539362913e9f97227515a9a7d9439ce57113545d2f7436"}
experimental_model
Cryo-EM reconstruction at 3.2 angstrom resolution
exposure
Purified Nav1.4–beta1 structure
limitations
Structural support for permeation and inactivation; this experiment did not test dietary sodium or clinical supplementation.
nutrient_topic
Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
organism
Human channel complex
plain_language
The channel has a mechanism to stop sodium flow rapidly after activation.
primary_references
[sodium-p30190309] Structure of the human voltage-gated sodium channel Nav1.4 in complex with β1. (2018). https://pubmed.ncbi.nlm.nih.gov/30190309/ DOI: 10.1126/science.aau2486
tissue_or_cell_type
Skeletal-muscle Nav1.4 with beta1
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 356–367
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cryo-EM reconstruction at 3.2 angstrom resolution · source_derived_draft · unverified_draft
### sodium-nav14-inactivation Analysis of the Nav1.4 structure and previously characterized residues supported an allosteric blocking mechanism of fast inactivation. Condition category: normal nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The channel has a mechanism to stop sodium flow rapidly after activation. organism: Human channel complex tissue_or_cell_type: Skeletal-muscle Nav1.4 with beta1 experimental_model: Cryo-EM reconstruction at 3.2 angstrom resolution limitations: Structural support for permeation and inactivation; this experiment did not test dietary sodium or clinical supplementation. exposure: Purified Nav1.4–beta1 structure evidence_span: {"source_cache": "artifacts/sodium-research/30190309.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2c9e7fceab1407740b539362913e9f97227515a9a7d9439ce57113545d2f7436", "start_char": 0, "end_char": 876, "text_sha256": "2c9e7fceab1407740b539362913e9f97227515a9a7d9439ce57113545d2f7436"} [sodium-p30190309] Structure of the human voltage-gated sodium channel Nav1.4 in complex with β1. (2018). https://pubmed.ncbi.nlm.nih.gov/30190309/ DOI: 10.1126/science.aau2486
Complete structured claim and evidence
Current reversal measurements supported uptake of one glutamate anion with three sodium ions and one proton, coupled to outward movement of one potassium ion.
Mammalian glial glutamate transporter GLT-1 in the CHO assay → L-Glutamate source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/sodium-research/9822723.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7612750fb1528dcd6212222b248bc74a2ec7a3813f50cbe5cf8ccdadbe448064", "start_char": 0, "end_char": 1740, "text_sha256": "7612750fb1528dcd6212222b248bc74a2ec7a3813f50cbe5cf8ccdadbe448064"}
experimental_model
Whole-cell current reversal measurements
exposure
Ion substitution, intracellular sodium/glutamate and extracellular potassium
limitations
Stoichiometry inferred from reversal potentials; the predicted ischemic extracellular glutamate concentration is not an in-vivo result.
nutrient_topic
Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
organism
Mammalian GLT-1 expressed in Chinese hamster ovary cells
plain_language
Glutamate clearance uses sodium, potassium and proton gradients together.
primary_references
[sodium-p9822723] Stoichiometry of the glial glutamate transporter GLT-1 expressed inducibly in a Chinese hamster ovary cell line selected for low endogenous Na+-dependent glutamate uptake. (1998). https://pubmed.ncbi.nlm.nih.gov/9822723/ DOI: 10.1523/jneurosci.18-23-09620.1998
tissue_or_cell_type
Plasma membrane
transport_effect
raises Uptake of one glutamate anion with three sodium ions and one proton.
transport_pool
the expressing cell Uptake of one glutamate anion with three sodium ions and one proton.
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 369–380
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Whole-cell current reversal measurements · source_derived_draft · unverified_draft
### sodium-glt1-stoichiometry Current reversal measurements supported uptake of one glutamate anion with three sodium ions and one proton, coupled to outward movement of one potassium ion. Condition category: normal nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Glutamate clearance uses sodium, potassium and proton gradients together. organism: Mammalian GLT-1 expressed in Chinese hamster ovary cells tissue_or_cell_type: Plasma membrane experimental_model: Whole-cell current reversal measurements limitations: Stoichiometry inferred from reversal potentials; the predicted ischemic extracellular glutamate concentration is not an in-vivo result. exposure: Ion substitution, intracellular sodium/glutamate and extracellular potassium evidence_span: {"source_cache": "artifacts/sodium-research/9822723.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7612750fb1528dcd6212222b248bc74a2ec7a3813f50cbe5cf8ccdadbe448064", "start_char": 0, "end_char": 1740, "text_sha256": "7612750fb1528dcd6212222b248bc74a2ec7a3813f50cbe5cf8ccdadbe448064"} [sodium-p9822723] Stoichiometry of the glial glutamate transporter GLT-1 expressed inducibly in a Chinese hamster ovary cell line selected for low endogenous Na+-dependent glutamate uptake. (1998). https://pubmed.ncbi.nlm.nih.gov/9822723/ DOI: 10.1523/jneurosci.18-23-09620.1998
Complete structured claim and evidence
Increasing extracellular potassium around cells loaded with sodium and glutamate evoked an outward, blocker-sensitive reversed transport current.
Potassium ion → GLT-1-mediated reversed glutamate transport source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/sodium-research/9822723.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7612750fb1528dcd6212222b248bc74a2ec7a3813f50cbe5cf8ccdadbe448064", "start_char": 0, "end_char": 1740, "text_sha256": "7612750fb1528dcd6212222b248bc74a2ec7a3813f50cbe5cf8ccdadbe448064"}
experimental_model
Whole-cell current reversal measurements
exposure
Ion substitution, intracellular sodium/glutamate and extracellular potassium
limitations
Stoichiometry inferred from reversal potentials; the predicted ischemic extracellular glutamate concentration is not an in-vivo result.
nutrient_topic
Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
organism
Mammalian GLT-1 expressed in Chinese hamster ovary cells
plain_language
Changing the ion gradients can reverse a transporter that normally clears glutamate.
primary_references
[sodium-p9822723] Stoichiometry of the glial glutamate transporter GLT-1 expressed inducibly in a Chinese hamster ovary cell line selected for low endogenous Na+-dependent glutamate uptake. (1998). https://pubmed.ncbi.nlm.nih.gov/9822723/ DOI: 10.1523/jneurosci.18-23-09620.1998
tissue_or_cell_type
Plasma membrane
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 382–393
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Whole-cell current reversal measurements · source_derived_draft · unverified_draft
### sodium-glt1-reversal Increasing extracellular potassium around cells loaded with sodium and glutamate evoked an outward, blocker-sensitive reversed transport current. Condition category: normal nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Changing the ion gradients can reverse a transporter that normally clears glutamate. organism: Mammalian GLT-1 expressed in Chinese hamster ovary cells tissue_or_cell_type: Plasma membrane experimental_model: Whole-cell current reversal measurements limitations: Stoichiometry inferred from reversal potentials; the predicted ischemic extracellular glutamate concentration is not an in-vivo result. exposure: Ion substitution, intracellular sodium/glutamate and extracellular potassium evidence_span: {"source_cache": "artifacts/sodium-research/9822723.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7612750fb1528dcd6212222b248bc74a2ec7a3813f50cbe5cf8ccdadbe448064", "start_char": 0, "end_char": 1740, "text_sha256": "7612750fb1528dcd6212222b248bc74a2ec7a3813f50cbe5cf8ccdadbe448064"} [sodium-p9822723] Stoichiometry of the glial glutamate transporter GLT-1 expressed inducibly in a Chinese hamster ovary cell line selected for low endogenous Na+-dependent glutamate uptake. (1998). https://pubmed.ncbi.nlm.nih.gov/9822723/ DOI: 10.1523/jneurosci.18-23-09620.1998
Complete structured claim and evidence
Coexpression of mouse sgk with the three ENaC subunits increased sodium current in Xenopus oocytes.
Serum and glucocorticoid-regulated kinase 1 → ENaC-mediated sodium current source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/sodium-research/10358046.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7d53e3e8ce41bb21d5cac2a5bfe6a6abdc702d0870add9c0a002e58ac374a97b", "start_char": 0, "end_char": 1343, "text_sha256": "7d53e3e8ce41bb21d5cac2a5bfe6a6abdc702d0870add9c0a002e58ac374a97b"}
experimental_model
Immediate-early gene induction and channel coexpression
exposure
Aldosterone exposure; receptor dependence and protein-synthesis tests
limitations
Cell and oocyte mechanism; the study does not imply that dietary sodium directly activates SGK1 in every tissue.
nutrient_topic
Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
organism
Rabbit/mouse collecting-duct preparations; mouse SGK in Xenopus oocytes
plain_language
The kinase can increase sodium flow through ENaC.
primary_references
[sodium-p10358046] sgk is an aldosterone-induced kinase in the renal collecting duct. Effects on epithelial na+ channels. (1999). https://pubmed.ncbi.nlm.nih.gov/10358046/ DOI: 10.1074/jbc.274.24.16973
tissue_or_cell_type
Cortical collecting duct and expression system
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 408–419
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Immediate-early gene induction and channel coexpression · source_derived_draft · unverified_draft
### sodium-sgk-enac Coexpression of mouse sgk with the three ENaC subunits increased sodium current in Xenopus oocytes. Condition category: normal nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The kinase can increase sodium flow through ENaC. organism: Rabbit/mouse collecting-duct preparations; mouse SGK in Xenopus oocytes tissue_or_cell_type: Cortical collecting duct and expression system experimental_model: Immediate-early gene induction and channel coexpression limitations: Cell and oocyte mechanism; the study does not imply that dietary sodium directly activates SGK1 in every tissue. exposure: Aldosterone exposure; receptor dependence and protein-synthesis tests evidence_span: {"source_cache": "artifacts/sodium-research/10358046.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7d53e3e8ce41bb21d5cac2a5bfe6a6abdc702d0870add9c0a002e58ac374a97b", "start_char": 0, "end_char": 1343, "text_sha256": "7d53e3e8ce41bb21d5cac2a5bfe6a6abdc702d0870add9c0a002e58ac374a97b"} [sodium-p10358046] sgk is an aldosterone-induced kinase in the renal collecting duct. Effects on epithelial na+ channels. (1999). https://pubmed.ncbi.nlm.nih.gov/10358046/ DOI: 10.1074/jbc.274.24.16973
Complete structured claim and evidence
Vasopressin increased apical AQP2 labeling and shifted AQP2 from intracellular vesicles toward the apical membrane.
Arginine vasopressin / antidiuretic hormone → Apical collecting-duct aquaporin-2 abundance source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/sodium-research/7532304.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "11ee4ffb0794466d6aaf66a0490324f1669a6082a647e8b185f7c5c47eec92c4", "start_char": 0, "end_char": 1588, "text_sha256": "11ee4ffb0794466d6aaf66a0490324f1669a6082a647e8b185f7c5c47eec92c4"}
experimental_model
Perfused collecting ducts with matched water-permeability measurement and immunoelectron microscopy
exposure
Vasopressin addition and withdrawal
limitations
Direct water-channel trafficking experiment; no claim that sodium dietary deficiency caused the response.
nutrient_topic
Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
organism
Rat
plain_language
The kidney can retain more water by moving water channels to the cell surface.
primary_references
[sodium-p7532304] Vasopressin increases water permeability of kidney collecting duct by inducing translocation of aquaporin-CD water channels to plasma membrane. (1995). https://pubmed.ncbi.nlm.nih.gov/7532304/ DOI: 10.1073/pnas.92.4.1013
tissue_or_cell_type
Inner medullary collecting duct
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 421–432
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Perfused collecting ducts with matched water-permeability measurement and immunoelectron microscopy · source_derived_draft · unverified_draft
### sodium-avp-aqp2 Vasopressin increased apical AQP2 labeling and shifted AQP2 from intracellular vesicles toward the apical membrane. Condition category: normal nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The kidney can retain more water by moving water channels to the cell surface. organism: Rat tissue_or_cell_type: Inner medullary collecting duct experimental_model: Perfused collecting ducts with matched water-permeability measurement and immunoelectron microscopy limitations: Direct water-channel trafficking experiment; no claim that sodium dietary deficiency caused the response. exposure: Vasopressin addition and withdrawal evidence_span: {"source_cache": "artifacts/sodium-research/7532304.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "11ee4ffb0794466d6aaf66a0490324f1669a6082a647e8b185f7c5c47eec92c4", "start_char": 0, "end_char": 1588, "text_sha256": "11ee4ffb0794466d6aaf66a0490324f1669a6082a647e8b185f7c5c47eec92c4"} [sodium-p7532304] Vasopressin increases water permeability of kidney collecting duct by inducing translocation of aquaporin-CD water channels to plasma membrane. (1995). https://pubmed.ncbi.nlm.nih.gov/7532304/ DOI: 10.1073/pnas.92.4.1013
Complete structured claim and evidence
Water permeability rose during vasopressin exposure and fell after withdrawal in parallel with AQP2 redistribution.
Arginine vasopressin / antidiuretic hormone → Collecting-duct osmotic water permeability source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/sodium-research/7532304.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "11ee4ffb0794466d6aaf66a0490324f1669a6082a647e8b185f7c5c47eec92c4", "start_char": 0, "end_char": 1588, "text_sha256": "11ee4ffb0794466d6aaf66a0490324f1669a6082a647e8b185f7c5c47eec92c4"}
experimental_model
Perfused collecting ducts with matched water-permeability measurement and immunoelectron microscopy
exposure
Vasopressin addition and withdrawal
limitations
Direct water-channel trafficking experiment; no claim that sodium dietary deficiency caused the response.
nutrient_topic
Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
organism
Rat
plain_language
This is a water-control mechanism that must be considered when interpreting blood sodium.
primary_references
[sodium-p7532304] Vasopressin increases water permeability of kidney collecting duct by inducing translocation of aquaporin-CD water channels to plasma membrane. (1995). https://pubmed.ncbi.nlm.nih.gov/7532304/ DOI: 10.1073/pnas.92.4.1013
tissue_or_cell_type
Inner medullary collecting duct
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 434–445
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Perfused collecting ducts with matched water-permeability measurement and immunoelectron microscopy · source_derived_draft · unverified_draft
### sodium-avp-water Water permeability rose during vasopressin exposure and fell after withdrawal in parallel with AQP2 redistribution. Condition category: normal nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: This is a water-control mechanism that must be considered when interpreting blood sodium. organism: Rat tissue_or_cell_type: Inner medullary collecting duct experimental_model: Perfused collecting ducts with matched water-permeability measurement and immunoelectron microscopy limitations: Direct water-channel trafficking experiment; no claim that sodium dietary deficiency caused the response. exposure: Vasopressin addition and withdrawal evidence_span: {"source_cache": "artifacts/sodium-research/7532304.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "11ee4ffb0794466d6aaf66a0490324f1669a6082a647e8b185f7c5c47eec92c4", "start_char": 0, "end_char": 1588, "text_sha256": "11ee4ffb0794466d6aaf66a0490324f1669a6082a647e8b185f7c5c47eec92c4"} [sodium-p7532304] Vasopressin increases water permeability of kidney collecting duct by inducing translocation of aquaporin-CD water channels to plasma membrane. (1995). https://pubmed.ncbi.nlm.nih.gov/7532304/ DOI: 10.1073/pnas.92.4.1013
Complete structured claim and evidence
Nax directly interacted with sodium/potassium-pump alpha subunits in the study.
Mouse sodium-sensing channel Nax / Scn7a → Sodium-potassium ATPase complexes source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/sodium-research/17408578.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5df7ccac391e94f2688ccacf287fda852b7a52e5279d1488ef48f0f52a3c6265", "start_char": 0, "end_char": 953, "text_sha256": "5df7ccac391e94f2688ccacf287fda852b7a52e5279d1488ef48f0f52a3c6265"}
experimental_model
Protein interaction, glial metabolism and SFO neuronal recordings
exposure
Elevated sodium; Nax knockout; lactate exposure
limitations
Brain salt-sensing pathway in experimental preparations; not a human sodium-intake threshold.
nutrient_topic
Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
organism
Mouse SFO and mammalian cell preparations
plain_language
A sodium-sensing channel can connect sodium detection to the cell’s energy use.
primary_references
[sodium-p17408578] Glial Nax channels control lactate signaling to neurons for brain [Na+] sensing. (2007). https://pubmed.ncbi.nlm.nih.gov/17408578/ DOI: 10.1016/j.neuron.2007.03.014
tissue_or_cell_type
Glial cells and GABAergic neurons of the subfornical organ
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 447–458
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Protein interaction, glial metabolism and SFO neuronal recordings · source_derived_draft · unverified_draft
### sodium-nax-pump Nax directly interacted with sodium/potassium-pump alpha subunits in the study. Condition category: normal nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A sodium-sensing channel can connect sodium detection to the cell’s energy use. organism: Mouse SFO and mammalian cell preparations tissue_or_cell_type: Glial cells and GABAergic neurons of the subfornical organ experimental_model: Protein interaction, glial metabolism and SFO neuronal recordings limitations: Brain salt-sensing pathway in experimental preparations; not a human sodium-intake threshold. exposure: Elevated sodium; Nax knockout; lactate exposure evidence_span: {"source_cache": "artifacts/sodium-research/17408578.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5df7ccac391e94f2688ccacf287fda852b7a52e5279d1488ef48f0f52a3c6265", "start_char": 0, "end_char": 953, "text_sha256": "5df7ccac391e94f2688ccacf287fda852b7a52e5279d1488ef48f0f52a3c6265"} [sodium-p17408578] Glial Nax channels control lactate signaling to neurons for brain [Na+] sensing. (2007). https://pubmed.ncbi.nlm.nih.gov/17408578/ DOI: 10.1016/j.neuron.2007.03.014
Complete structured claim and evidence
The sodium-associated increase in SFO lactate production occurred in wild-type but not Nax-knockout mice.
Mouse sodium-sensing channel Nax / Scn7a → Nax-dependent glial lactate production source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/sodium-research/17408578.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5df7ccac391e94f2688ccacf287fda852b7a52e5279d1488ef48f0f52a3c6265", "start_char": 0, "end_char": 953, "text_sha256": "5df7ccac391e94f2688ccacf287fda852b7a52e5279d1488ef48f0f52a3c6265"}
experimental_model
Protein interaction, glial metabolism and SFO neuronal recordings
exposure
Elevated sodium; Nax knockout; lactate exposure
limitations
Brain salt-sensing pathway in experimental preparations; not a human sodium-intake threshold.
nutrient_topic
Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
organism
Mouse SFO and mammalian cell preparations
plain_language
Glial cells turn a sodium signal into a metabolic signal carried by lactate.
primary_references
[sodium-p17408578] Glial Nax channels control lactate signaling to neurons for brain [Na+] sensing. (2007). https://pubmed.ncbi.nlm.nih.gov/17408578/ DOI: 10.1016/j.neuron.2007.03.014
tissue_or_cell_type
Glial cells and GABAergic neurons of the subfornical organ
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 460–471
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Protein interaction, glial metabolism and SFO neuronal recordings · source_derived_draft · unverified_draft
### sodium-nax-lactate The sodium-associated increase in SFO lactate production occurred in wild-type but not Nax-knockout mice. Condition category: normal nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Glial cells turn a sodium signal into a metabolic signal carried by lactate. organism: Mouse SFO and mammalian cell preparations tissue_or_cell_type: Glial cells and GABAergic neurons of the subfornical organ experimental_model: Protein interaction, glial metabolism and SFO neuronal recordings limitations: Brain salt-sensing pathway in experimental preparations; not a human sodium-intake threshold. exposure: Elevated sodium; Nax knockout; lactate exposure evidence_span: {"source_cache": "artifacts/sodium-research/17408578.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5df7ccac391e94f2688ccacf287fda852b7a52e5279d1488ef48f0f52a3c6265", "start_char": 0, "end_char": 953, "text_sha256": "5df7ccac391e94f2688ccacf287fda852b7a52e5279d1488ef48f0f52a3c6265"} [sodium-p17408578] Glial Nax channels control lactate signaling to neurons for brain [Na+] sensing. (2007). https://pubmed.ncbi.nlm.nih.gov/17408578/ DOI: 10.1016/j.neuron.2007.03.014
Complete structured claim and evidence
Lactate stimulated the activity of SFO GABAergic neurons.
L-Lactate → Subfornical-organ GABAergic neuron activity source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/sodium-research/17408578.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5df7ccac391e94f2688ccacf287fda852b7a52e5279d1488ef48f0f52a3c6265", "start_char": 0, "end_char": 953, "text_sha256": "5df7ccac391e94f2688ccacf287fda852b7a52e5279d1488ef48f0f52a3c6265"}
experimental_model
Protein interaction, glial metabolism and SFO neuronal recordings
exposure
Elevated sodium; Nax knockout; lactate exposure
limitations
Brain salt-sensing pathway in experimental preparations; not a human sodium-intake threshold.
nutrient_topic
Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
organism
Mouse SFO and mammalian cell preparations
plain_language
Lactate can pass information from sodium-sensing glia to nearby neurons.
primary_references
[sodium-p17408578] Glial Nax channels control lactate signaling to neurons for brain [Na+] sensing. (2007). https://pubmed.ncbi.nlm.nih.gov/17408578/ DOI: 10.1016/j.neuron.2007.03.014
tissue_or_cell_type
Glial cells and GABAergic neurons of the subfornical organ
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 473–484
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Protein interaction, glial metabolism and SFO neuronal recordings · source_derived_draft · unverified_draft
### sodium-lactate-neurons Lactate stimulated the activity of SFO GABAergic neurons. Condition category: normal nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Lactate can pass information from sodium-sensing glia to nearby neurons. organism: Mouse SFO and mammalian cell preparations tissue_or_cell_type: Glial cells and GABAergic neurons of the subfornical organ experimental_model: Protein interaction, glial metabolism and SFO neuronal recordings limitations: Brain salt-sensing pathway in experimental preparations; not a human sodium-intake threshold. exposure: Elevated sodium; Nax knockout; lactate exposure evidence_span: {"source_cache": "artifacts/sodium-research/17408578.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5df7ccac391e94f2688ccacf287fda852b7a52e5279d1488ef48f0f52a3c6265", "start_char": 0, "end_char": 953, "text_sha256": "5df7ccac391e94f2688ccacf287fda852b7a52e5279d1488ef48f0f52a3c6265"} [sodium-p17408578] Glial Nax channels control lactate signaling to neurons for brain [Na+] sensing. (2007). https://pubmed.ncbi.nlm.nih.gov/17408578/ DOI: 10.1016/j.neuron.2007.03.014
Complete structured claim and evidence
Increased NaCl enhanced cytokine-induced TH17 differentiation in human and mouse T-cell cultures.
Sodium chloride → Th17 differentiation source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/sodium-research/23467095.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d16bb4b4becde85238492e01054f360aeaf57ea90015cba99459cd155fa4251f", "start_char": 0, "end_char": 1913, "text_sha256": "d16bb4b4becde85238492e01054f360aeaf57ea90015cba99459cd155fa4251f"}
experimental_model
Cytokine-driven T-cell culture, gene silencing/inhibition and experimental autoimmune encephalomyelitis
exposure
Increased NaCl in culture or high-salt mouse diet
limitations
NaCl exposure includes both ions and osmotic context. Mouse EAE and cultured T cells do not establish that salt causes human multiple sclerosis.
nutrient_topic
Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
organism
Human and mouse T cells; mouse disease model
plain_language
Salt conditions can change immune-cell differentiation in an experimental setting.
primary_references
[sodium-p23467095] Sodium chloride drives autoimmune disease by the induction of pathogenic TH17 cells. (2013). https://pubmed.ncbi.nlm.nih.gov/23467095/ DOI: 10.1038/nature11868
tissue_or_cell_type
T-helper cells and experimental CNS autoimmunity
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 486–497
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cytokine-driven T-cell culture, gene silencing/inhibition and experimental autoimmune encephalomyelitis · source_derived_draft · unverified_draft
### sodium-salt-th17 Increased NaCl enhanced cytokine-induced TH17 differentiation in human and mouse T-cell cultures. Condition category: normal nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Salt conditions can change immune-cell differentiation in an experimental setting. organism: Human and mouse T cells; mouse disease model tissue_or_cell_type: T-helper cells and experimental CNS autoimmunity experimental_model: Cytokine-driven T-cell culture, gene silencing/inhibition and experimental autoimmune encephalomyelitis limitations: NaCl exposure includes both ions and osmotic context. Mouse EAE and cultured T cells do not establish that salt causes human multiple sclerosis. exposure: Increased NaCl in culture or high-salt mouse diet evidence_span: {"source_cache": "artifacts/sodium-research/23467095.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d16bb4b4becde85238492e01054f360aeaf57ea90015cba99459cd155fa4251f", "start_char": 0, "end_char": 1913, "text_sha256": "d16bb4b4becde85238492e01054f360aeaf57ea90015cba99459cd155fa4251f"} [sodium-p23467095] Sodium chloride drives autoimmune disease by the induction of pathogenic TH17 cells. (2013). https://pubmed.ncbi.nlm.nih.gov/23467095/ DOI: 10.1038/nature11868
Complete structured claim and evidence
Silencing or chemical inhibition of p38/MAPK blocked the high-salt enhancement of TH17 differentiation in the study.
p38 mitogen-activated protein kinase family → Th17 differentiation source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/sodium-research/23467095.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d16bb4b4becde85238492e01054f360aeaf57ea90015cba99459cd155fa4251f", "start_char": 0, "end_char": 1913, "text_sha256": "d16bb4b4becde85238492e01054f360aeaf57ea90015cba99459cd155fa4251f"}
experimental_model
Cytokine-driven T-cell culture, gene silencing/inhibition and experimental autoimmune encephalomyelitis
exposure
Increased NaCl in culture or high-salt mouse diet
limitations
NaCl exposure includes both ions and osmotic context. Mouse EAE and cultured T cells do not establish that salt causes human multiple sclerosis.
nutrient_topic
Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
organism
Human and mouse T cells; mouse disease model
plain_language
Blocking p38/MAPK interrupted this particular salt-sensitive immune response.
primary_references
[sodium-p23467095] Sodium chloride drives autoimmune disease by the induction of pathogenic TH17 cells. (2013). https://pubmed.ncbi.nlm.nih.gov/23467095/ DOI: 10.1038/nature11868
tissue_or_cell_type
T-helper cells and experimental CNS autoimmunity
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 499–510
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cytokine-driven T-cell culture, gene silencing/inhibition and experimental autoimmune encephalomyelitis · source_derived_draft · unverified_draft
### sodium-th17-p38 Silencing or chemical inhibition of p38/MAPK blocked the high-salt enhancement of TH17 differentiation in the study. Condition category: normal nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Blocking p38/MAPK interrupted this particular salt-sensitive immune response. organism: Human and mouse T cells; mouse disease model tissue_or_cell_type: T-helper cells and experimental CNS autoimmunity experimental_model: Cytokine-driven T-cell culture, gene silencing/inhibition and experimental autoimmune encephalomyelitis limitations: NaCl exposure includes both ions and osmotic context. Mouse EAE and cultured T cells do not establish that salt causes human multiple sclerosis. exposure: Increased NaCl in culture or high-salt mouse diet evidence_span: {"source_cache": "artifacts/sodium-research/23467095.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d16bb4b4becde85238492e01054f360aeaf57ea90015cba99459cd155fa4251f", "start_char": 0, "end_char": 1913, "text_sha256": "d16bb4b4becde85238492e01054f360aeaf57ea90015cba99459cd155fa4251f"} [sodium-p23467095] Sodium chloride drives autoimmune disease by the induction of pathogenic TH17 cells. (2013). https://pubmed.ncbi.nlm.nih.gov/23467095/ DOI: 10.1038/nature11868
Complete structured claim and evidence
Silencing or chemical inhibition of NFAT5 blocked the high-salt enhancement of TH17 differentiation in the study.
Nuclear factor of activated T cells 5 / NFAT5 → Th17 differentiation source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/sodium-research/23467095.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d16bb4b4becde85238492e01054f360aeaf57ea90015cba99459cd155fa4251f", "start_char": 0, "end_char": 1913, "text_sha256": "d16bb4b4becde85238492e01054f360aeaf57ea90015cba99459cd155fa4251f"}
experimental_model
Cytokine-driven T-cell culture, gene silencing/inhibition and experimental autoimmune encephalomyelitis
exposure
Increased NaCl in culture or high-salt mouse diet
limitations
NaCl exposure includes both ions and osmotic context. Mouse EAE and cultured T cells do not establish that salt causes human multiple sclerosis.
nutrient_topic
Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
organism
Human and mouse T cells; mouse disease model
plain_language
Blocking NFAT5 interrupted this particular salt-sensitive immune response.
primary_references
[sodium-p23467095] Sodium chloride drives autoimmune disease by the induction of pathogenic TH17 cells. (2013). https://pubmed.ncbi.nlm.nih.gov/23467095/ DOI: 10.1038/nature11868
tissue_or_cell_type
T-helper cells and experimental CNS autoimmunity
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 512–523
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cytokine-driven T-cell culture, gene silencing/inhibition and experimental autoimmune encephalomyelitis · source_derived_draft · unverified_draft
### sodium-th17-nfat5 Silencing or chemical inhibition of NFAT5 blocked the high-salt enhancement of TH17 differentiation in the study. Condition category: normal nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Blocking NFAT5 interrupted this particular salt-sensitive immune response. organism: Human and mouse T cells; mouse disease model tissue_or_cell_type: T-helper cells and experimental CNS autoimmunity experimental_model: Cytokine-driven T-cell culture, gene silencing/inhibition and experimental autoimmune encephalomyelitis limitations: NaCl exposure includes both ions and osmotic context. Mouse EAE and cultured T cells do not establish that salt causes human multiple sclerosis. exposure: Increased NaCl in culture or high-salt mouse diet evidence_span: {"source_cache": "artifacts/sodium-research/23467095.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d16bb4b4becde85238492e01054f360aeaf57ea90015cba99459cd155fa4251f", "start_char": 0, "end_char": 1913, "text_sha256": "d16bb4b4becde85238492e01054f360aeaf57ea90015cba99459cd155fa4251f"} [sodium-p23467095] Sodium chloride drives autoimmune disease by the induction of pathogenic TH17 cells. (2013). https://pubmed.ncbi.nlm.nih.gov/23467095/ DOI: 10.1038/nature11868
Complete structured claim and evidence
Silencing or chemical inhibition of SGK1 blocked the high-salt enhancement of TH17 differentiation in the study.
Serum and glucocorticoid-regulated kinase 1 → Th17 differentiation source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/sodium-research/23467095.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d16bb4b4becde85238492e01054f360aeaf57ea90015cba99459cd155fa4251f", "start_char": 0, "end_char": 1913, "text_sha256": "d16bb4b4becde85238492e01054f360aeaf57ea90015cba99459cd155fa4251f"}
experimental_model
Cytokine-driven T-cell culture, gene silencing/inhibition and experimental autoimmune encephalomyelitis
exposure
Increased NaCl in culture or high-salt mouse diet
limitations
NaCl exposure includes both ions and osmotic context. Mouse EAE and cultured T cells do not establish that salt causes human multiple sclerosis.
nutrient_topic
Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
organism
Human and mouse T cells; mouse disease model
plain_language
Blocking SGK1 interrupted this particular salt-sensitive immune response.
primary_references
[sodium-p23467095] Sodium chloride drives autoimmune disease by the induction of pathogenic TH17 cells. (2013). https://pubmed.ncbi.nlm.nih.gov/23467095/ DOI: 10.1038/nature11868
tissue_or_cell_type
T-helper cells and experimental CNS autoimmunity
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 525–536
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cytokine-driven T-cell culture, gene silencing/inhibition and experimental autoimmune encephalomyelitis · source_derived_draft · unverified_draft
### sodium-th17-sgk1 Silencing or chemical inhibition of SGK1 blocked the high-salt enhancement of TH17 differentiation in the study. Condition category: normal nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Blocking SGK1 interrupted this particular salt-sensitive immune response. organism: Human and mouse T cells; mouse disease model tissue_or_cell_type: T-helper cells and experimental CNS autoimmunity experimental_model: Cytokine-driven T-cell culture, gene silencing/inhibition and experimental autoimmune encephalomyelitis limitations: NaCl exposure includes both ions and osmotic context. Mouse EAE and cultured T cells do not establish that salt causes human multiple sclerosis. exposure: Increased NaCl in culture or high-salt mouse diet evidence_span: {"source_cache": "artifacts/sodium-research/23467095.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d16bb4b4becde85238492e01054f360aeaf57ea90015cba99459cd155fa4251f", "start_char": 0, "end_char": 1913, "text_sha256": "d16bb4b4becde85238492e01054f360aeaf57ea90015cba99459cd155fa4251f"} [sodium-p23467095] Sodium chloride drives autoimmune disease by the induction of pathogenic TH17 cells. (2013). https://pubmed.ncbi.nlm.nih.gov/23467095/ DOI: 10.1038/nature11868
Complete structured claim and evidence
Mice fed a high-salt diet developed more severe experimental autoimmune encephalomyelitis.
Sodium chloride → Experimental autoimmune encephalomyelitis severity in mice source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/sodium-research/23467095.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d16bb4b4becde85238492e01054f360aeaf57ea90015cba99459cd155fa4251f", "start_char": 0, "end_char": 1913, "text_sha256": "d16bb4b4becde85238492e01054f360aeaf57ea90015cba99459cd155fa4251f"}
experimental_model
Cytokine-driven T-cell culture, gene silencing/inhibition and experimental autoimmune encephalomyelitis
exposure
Increased NaCl in culture or high-salt mouse diet
limitations
NaCl exposure includes both ions and osmotic context. Mouse EAE and cultured T cells do not establish that salt causes human multiple sclerosis.
nutrient_topic
Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
organism
Human and mouse T cells; mouse disease model
plain_language
The cell findings had a disease-model counterpart in mice; human disease causation remains unproven.
primary_references
[sodium-p23467095] Sodium chloride drives autoimmune disease by the induction of pathogenic TH17 cells. (2013). https://pubmed.ncbi.nlm.nih.gov/23467095/ DOI: 10.1038/nature11868
tissue_or_cell_type
T-helper cells and experimental CNS autoimmunity
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 538–549
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cytokine-driven T-cell culture, gene silencing/inhibition and experimental autoimmune encephalomyelitis · source_derived_draft · unverified_draft
### sodium-salt-eae Mice fed a high-salt diet developed more severe experimental autoimmune encephalomyelitis. Condition category: normal nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The cell findings had a disease-model counterpart in mice; human disease causation remains unproven. organism: Human and mouse T cells; mouse disease model tissue_or_cell_type: T-helper cells and experimental CNS autoimmunity experimental_model: Cytokine-driven T-cell culture, gene silencing/inhibition and experimental autoimmune encephalomyelitis limitations: NaCl exposure includes both ions and osmotic context. Mouse EAE and cultured T cells do not establish that salt causes human multiple sclerosis. exposure: Increased NaCl in culture or high-salt mouse diet evidence_span: {"source_cache": "artifacts/sodium-research/23467095.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d16bb4b4becde85238492e01054f360aeaf57ea90015cba99459cd155fa4251f", "start_char": 0, "end_char": 1913, "text_sha256": "d16bb4b4becde85238492e01054f360aeaf57ea90015cba99459cd155fa4251f"} [sodium-p23467095] Sodium chloride drives autoimmune disease by the induction of pathogenic TH17 cells. (2013). https://pubmed.ncbi.nlm.nih.gov/23467095/ DOI: 10.1038/nature11868
Complete structured claim and evidence
The study identified SGK1-dependent deactivation of Foxo1 in the TH17 program.
Serum and glucocorticoid-regulated kinase 1 → Mouse forkhead transcription factor Foxo1 source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/sodium-research/23467085.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "25fdc34faa9d6f0b84dfc9daf98ecc8e09f2486853b9e99bdae552e5ca8c5b2e", "start_char": 0, "end_char": 1656, "text_sha256": "25fdc34faa9d6f0b84dfc9daf98ecc8e09f2486853b9e99bdae552e5ca8c5b2e"}
experimental_model
T-cell transcriptional profiling, kinase loss and experimental autoimmune assays
exposure
NaCl elevation and Sgk1 perturbation
limitations
The SGK1–Foxo1–IL23R pathway is scoped to this immune-cell program, not universal sodium action.
nutrient_topic
Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
organism
Mouse
plain_language
The same kinase family used in kidney salt handling has another role in immune cells.
primary_references
[sodium-p23467085] Induction of pathogenic TH17 cells by inducible salt-sensing kinase SGK1. (2013). https://pubmed.ncbi.nlm.nih.gov/23467085/ DOI: 10.1038/nature11984
tissue_or_cell_type
IL-23-responsive TH17 cells
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 551–562
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · T-cell transcriptional profiling, kinase loss and experimental autoimmune assays · source_derived_draft · unverified_draft
### sodium-sgk-foxo The study identified SGK1-dependent deactivation of Foxo1 in the TH17 program. Condition category: normal nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The same kinase family used in kidney salt handling has another role in immune cells. organism: Mouse tissue_or_cell_type: IL-23-responsive TH17 cells experimental_model: T-cell transcriptional profiling, kinase loss and experimental autoimmune assays limitations: The SGK1–Foxo1–IL23R pathway is scoped to this immune-cell program, not universal sodium action. exposure: NaCl elevation and Sgk1 perturbation evidence_span: {"source_cache": "artifacts/sodium-research/23467085.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "25fdc34faa9d6f0b84dfc9daf98ecc8e09f2486853b9e99bdae552e5ca8c5b2e", "start_char": 0, "end_char": 1656, "text_sha256": "25fdc34faa9d6f0b84dfc9daf98ecc8e09f2486853b9e99bdae552e5ca8c5b2e"} [sodium-p23467085] Induction of pathogenic TH17 cells by inducible salt-sensing kinase SGK1. (2013). https://pubmed.ncbi.nlm.nih.gov/23467085/ DOI: 10.1038/nature11984
Complete structured claim and evidence
Foxo1 acted as a direct repressor of IL-23 receptor expression in the study.
Mouse forkhead transcription factor Foxo1 → Mouse IL-23 receptor expression source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/sodium-research/23467085.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "25fdc34faa9d6f0b84dfc9daf98ecc8e09f2486853b9e99bdae552e5ca8c5b2e", "start_char": 0, "end_char": 1656, "text_sha256": "25fdc34faa9d6f0b84dfc9daf98ecc8e09f2486853b9e99bdae552e5ca8c5b2e"}
experimental_model
T-cell transcriptional profiling, kinase loss and experimental autoimmune assays
exposure
NaCl elevation and Sgk1 perturbation
limitations
The SGK1–Foxo1–IL23R pathway is scoped to this immune-cell program, not universal sodium action.
nutrient_topic
Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
organism
Mouse
plain_language
Turning down a repressor can let a receptor become more abundant.
primary_references
[sodium-p23467085] Induction of pathogenic TH17 cells by inducible salt-sensing kinase SGK1. (2013). https://pubmed.ncbi.nlm.nih.gov/23467085/ DOI: 10.1038/nature11984
tissue_or_cell_type
IL-23-responsive TH17 cells
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 564–575
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · T-cell transcriptional profiling, kinase loss and experimental autoimmune assays · source_derived_draft · unverified_draft
### sodium-foxo-il23r Foxo1 acted as a direct repressor of IL-23 receptor expression in the study. Condition category: normal nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Turning down a repressor can let a receptor become more abundant. organism: Mouse tissue_or_cell_type: IL-23-responsive TH17 cells experimental_model: T-cell transcriptional profiling, kinase loss and experimental autoimmune assays limitations: The SGK1–Foxo1–IL23R pathway is scoped to this immune-cell program, not universal sodium action. exposure: NaCl elevation and Sgk1 perturbation evidence_span: {"source_cache": "artifacts/sodium-research/23467085.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "25fdc34faa9d6f0b84dfc9daf98ecc8e09f2486853b9e99bdae552e5ca8c5b2e", "start_char": 0, "end_char": 1656, "text_sha256": "25fdc34faa9d6f0b84dfc9daf98ecc8e09f2486853b9e99bdae552e5ca8c5b2e"} [sodium-p23467085] Induction of pathogenic TH17 cells by inducible salt-sensing kinase SGK1. (2013). https://pubmed.ncbi.nlm.nih.gov/23467085/ DOI: 10.1038/nature11984
Complete structured claim and evidence
Modestly increased NaCl induced SGK1 and promoted IL-23 receptor expression in the tested T-cell program.
Sodium chloride → Mouse IL-23 receptor expression source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/sodium-research/23467085.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "25fdc34faa9d6f0b84dfc9daf98ecc8e09f2486853b9e99bdae552e5ca8c5b2e", "start_char": 0, "end_char": 1656, "text_sha256": "25fdc34faa9d6f0b84dfc9daf98ecc8e09f2486853b9e99bdae552e5ca8c5b2e"}
experimental_model
T-cell transcriptional profiling, kinase loss and experimental autoimmune assays
exposure
NaCl elevation and Sgk1 perturbation
limitations
The SGK1–Foxo1–IL23R pathway is scoped to this immune-cell program, not universal sodium action.
nutrient_topic
Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
organism
Mouse
plain_language
Salt exposure can reinforce responsiveness to an immune signal in this model.
primary_references
[sodium-p23467085] Induction of pathogenic TH17 cells by inducible salt-sensing kinase SGK1. (2013). https://pubmed.ncbi.nlm.nih.gov/23467085/ DOI: 10.1038/nature11984
tissue_or_cell_type
IL-23-responsive TH17 cells
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 577–588
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · T-cell transcriptional profiling, kinase loss and experimental autoimmune assays · source_derived_draft · unverified_draft
### sodium-salt-il23r Modestly increased NaCl induced SGK1 and promoted IL-23 receptor expression in the tested T-cell program. Condition category: normal nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Salt exposure can reinforce responsiveness to an immune signal in this model. organism: Mouse tissue_or_cell_type: IL-23-responsive TH17 cells experimental_model: T-cell transcriptional profiling, kinase loss and experimental autoimmune assays limitations: The SGK1–Foxo1–IL23R pathway is scoped to this immune-cell program, not universal sodium action. exposure: NaCl elevation and Sgk1 perturbation evidence_span: {"source_cache": "artifacts/sodium-research/23467085.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "25fdc34faa9d6f0b84dfc9daf98ecc8e09f2486853b9e99bdae552e5ca8c5b2e", "start_char": 0, "end_char": 1656, "text_sha256": "25fdc34faa9d6f0b84dfc9daf98ecc8e09f2486853b9e99bdae552e5ca8c5b2e"} [sodium-p23467085] Induction of pathogenic TH17 cells by inducible salt-sensing kinase SGK1. (2013). https://pubmed.ncbi.nlm.nih.gov/23467085/ DOI: 10.1038/nature11984
Complete structured claim and evidence
SLC6A19 functioned as a sodium-dependent, chloride-independent neutral amino acid transporter.
Human neutral amino acid transporter B0AT1 / SLC6A19 → Neutral amino acids (assay substrates specified per claim) source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/sodium-research/15286788.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "72277489510231d6da07dacf086404f5f069094a47d7a1a2de9a8392556c3a14", "start_char": 0, "end_char": 1040, "text_sha256": "72277489510231d6da07dacf086404f5f069094a47d7a1a2de9a8392556c3a14"}
experimental_model
Human genetic mapping and heterologous transport-function tests
exposure
Hartnup-associated variants versus normal transporter
limitations
Not every clinical feature of Hartnup disorder was explained; no direct test here of niacin supplementation or sodium shortage.
nutrient_topic
Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
organism
Human SLC6A19
plain_language
Sodium coupling is also used to absorb or recover some amino acids.
primary_references
[sodium-p15286788] Hartnup disorder is caused by mutations in the gene encoding the neutral amino acid transporter SLC6A19. (2004). https://pubmed.ncbi.nlm.nih.gov/15286788/ DOI: 10.1038/ng1406
tissue_or_cell_type
Kidney/intestine transporter; expression assays
transport_effect
raises Sodium-dependent neutral amino acid transport, which is inward.
transport_pool
the expressing cell Sodium-dependent neutral amino acid transport, which is inward.
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 590–601
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human genetic mapping and heterologous transport-function tests · source_derived_draft · unverified_draft
### sodium-b0at1-transport SLC6A19 functioned as a sodium-dependent, chloride-independent neutral amino acid transporter. Condition category: normal nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Sodium coupling is also used to absorb or recover some amino acids. organism: Human SLC6A19 tissue_or_cell_type: Kidney/intestine transporter; expression assays experimental_model: Human genetic mapping and heterologous transport-function tests limitations: Not every clinical feature of Hartnup disorder was explained; no direct test here of niacin supplementation or sodium shortage. exposure: Hartnup-associated variants versus normal transporter evidence_span: {"source_cache": "artifacts/sodium-research/15286788.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "72277489510231d6da07dacf086404f5f069094a47d7a1a2de9a8392556c3a14", "start_char": 0, "end_char": 1040, "text_sha256": "72277489510231d6da07dacf086404f5f069094a47d7a1a2de9a8392556c3a14"} [sodium-p15286788] Hartnup disorder is caused by mutations in the gene encoding the neutral amino acid transporter SLC6A19. (2004). https://pubmed.ncbi.nlm.nih.gov/15286788/ DOI: 10.1038/ng1406
Complete structured claim and evidence
Tested Hartnup-associated SLC6A19 variants reduced neutral amino acid transport in vitro.
Human neutral amino acid transporter B0AT1 / SLC6A19 → Intestinal and renal neutral amino acid transport source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/sodium-research/15286788.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "72277489510231d6da07dacf086404f5f069094a47d7a1a2de9a8392556c3a14", "start_char": 0, "end_char": 1040, "text_sha256": "72277489510231d6da07dacf086404f5f069094a47d7a1a2de9a8392556c3a14"}
experimental_model
Human genetic mapping and heterologous transport-function tests
exposure
Hartnup-associated variants versus normal transporter
limitations
Not every clinical feature of Hartnup disorder was explained; no direct test here of niacin supplementation or sodium shortage.
nutrient_topic
Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
organism
Human SLC6A19
plain_language
Even with sodium and food present, a damaged transporter can limit nutrient transport.
primary_references
[sodium-p15286788] Hartnup disorder is caused by mutations in the gene encoding the neutral amino acid transporter SLC6A19. (2004). https://pubmed.ncbi.nlm.nih.gov/15286788/ DOI: 10.1038/ng1406
tissue_or_cell_type
Kidney/intestine transporter; expression assays
trigger_kind
machinery_impairment Imported condition classification; unverified.
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 603–614
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human genetic mapping and heterologous transport-function tests · source_derived_draft · unverified_draft
### sodium-b0at1-loss Tested Hartnup-associated SLC6A19 variants reduced neutral amino acid transport in vitro. Condition category: machinery_impairment nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Even with sodium and food present, a damaged transporter can limit nutrient transport. organism: Human SLC6A19 tissue_or_cell_type: Kidney/intestine transporter; expression assays experimental_model: Human genetic mapping and heterologous transport-function tests limitations: Not every clinical feature of Hartnup disorder was explained; no direct test here of niacin supplementation or sodium shortage. exposure: Hartnup-associated variants versus normal transporter evidence_span: {"source_cache": "artifacts/sodium-research/15286788.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "72277489510231d6da07dacf086404f5f069094a47d7a1a2de9a8392556c3a14", "start_char": 0, "end_char": 1040, "text_sha256": "72277489510231d6da07dacf086404f5f069094a47d7a1a2de9a8392556c3a14"} [sodium-p15286788] Hartnup disorder is caused by mutations in the gene encoding the neutral amino acid transporter SLC6A19. (2004). https://pubmed.ncbi.nlm.nih.gov/15286788/ DOI: 10.1038/ng1406
Complete structured claim and evidence
Human creatine-transporter expression conferred sodium-dependent creatine uptake with Km 14.9 ± 3.0 micromolar in five experiments.
Human creatine transporter CRT / SLC6A8 → Creatine source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/sodium-research/7945388.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4f936121279583ab698555d2a318900a9dc5a42ecbf294619ee3abcc95c9a2f0", "start_char": 0, "end_char": 910, "text_sha256": "4f936121279583ab698555d2a318900a9dc5a42ecbf294619ee3abcc95c9a2f0"}
experimental_model
Cloning and functional expression
exposure
Radiolabeled creatine uptake
limitations
This primary abstract establishes sodium dependence; no chloride stoichiometry or clinical benefit is inferred.
nutrient_topic
Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
organism
Human SLC6A8 in COS-7 cells
plain_language
Creatine entry has its own sodium-coupled transporter.
primary_references
[sodium-p7945388] The cloning and expression of a human creatine transporter. (1994). https://pubmed.ncbi.nlm.nih.gov/7945388/ DOI: 10.1006/bbrc.1994.2475
tissue_or_cell_type
Cell plasma membrane
transport_effect
raises Expression conferred sodium-dependent creatine uptake.
transport_pool
the expressing cell Expression conferred sodium-dependent creatine uptake.
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 629–640
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cloning and functional expression · source_derived_draft · unverified_draft
### sodium-creatine-transport Human creatine-transporter expression conferred sodium-dependent creatine uptake with Km 14.9 ± 3.0 micromolar in five experiments. Condition category: normal nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Creatine entry has its own sodium-coupled transporter. organism: Human SLC6A8 in COS-7 cells tissue_or_cell_type: Cell plasma membrane experimental_model: Cloning and functional expression limitations: This primary abstract establishes sodium dependence; no chloride stoichiometry or clinical benefit is inferred. exposure: Radiolabeled creatine uptake evidence_span: {"source_cache": "artifacts/sodium-research/7945388.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4f936121279583ab698555d2a318900a9dc5a42ecbf294619ee3abcc95c9a2f0", "start_char": 0, "end_char": 910, "text_sha256": "4f936121279583ab698555d2a318900a9dc5a42ecbf294619ee3abcc95c9a2f0"} [sodium-p7945388] The cloning and expression of a human creatine transporter. (1994). https://pubmed.ncbi.nlm.nih.gov/7945388/ DOI: 10.1006/bbrc.1994.2475
Complete structured claim and evidence
L243P, T262M and the double mutant abolished taurocholate and other bile-acid transport in transfected cells.
Human ileal sodium/bile acid transporter ASBT / SLC10A2 → Ileal epithelial bile acid uptake source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/sodium-research/9109432.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "019508b2d05ec7e21a73ff66bdea9a0b09c6c7e7d8e404de3db49b2a0825ebbe", "start_char": 0, "end_char": 1389, "text_sha256": "019508b2d05ec7e21a73ff66bdea9a0b09c6c7e7d8e404de3db49b2a0825ebbe"}
experimental_model
Human family genetics and transfected COS-cell transport assays
exposure
L243P, T262M and double-mutant constructs
limitations
Family-specific genetic disease; loss of bile-acid transport was tested, whereas individual fat-soluble-vitamin deficiencies were not.
nutrient_topic
Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
organism
Human SLC10A2
plain_language
A sodium-coupled transporter helps recycle bile acids; mutations can break that route.
primary_references
[sodium-p9109432] Primary bile acid malabsorption caused by mutations in the ileal sodium-dependent bile acid transporter gene (SLC10A2). (1997). https://pubmed.ncbi.nlm.nih.gov/9109432/ DOI: 10.1172/jci119355
tissue_or_cell_type
Ileal bile-acid transporter
trigger_kind
machinery_impairment Imported condition classification; unverified.
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 642–653
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human family genetics and transfected COS-cell transport assays · source_derived_draft · unverified_draft
### sodium-asbt-loss L243P, T262M and the double mutant abolished taurocholate and other bile-acid transport in transfected cells. Condition category: machinery_impairment nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A sodium-coupled transporter helps recycle bile acids; mutations can break that route. organism: Human SLC10A2 tissue_or_cell_type: Ileal bile-acid transporter experimental_model: Human family genetics and transfected COS-cell transport assays limitations: Family-specific genetic disease; loss of bile-acid transport was tested, whereas individual fat-soluble-vitamin deficiencies were not. exposure: L243P, T262M and double-mutant constructs evidence_span: {"source_cache": "artifacts/sodium-research/9109432.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "019508b2d05ec7e21a73ff66bdea9a0b09c6c7e7d8e404de3db49b2a0825ebbe", "start_char": 0, "end_char": 1389, "text_sha256": "019508b2d05ec7e21a73ff66bdea9a0b09c6c7e7d8e404de3db49b2a0825ebbe"} [sodium-p9109432] Primary bile acid malabsorption caused by mutations in the ileal sodium-dependent bile acid transporter gene (SLC10A2). (1997). https://pubmed.ncbi.nlm.nih.gov/9109432/ DOI: 10.1172/jci119355
Complete structured claim and evidence
The dysfunctional L243P/T262M constructs retained protein expression and plasma-membrane trafficking.
Human ileal sodium/bile acid transporter ASBT / SLC10A2 → Plasma membrane source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/sodium-research/9109432.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "019508b2d05ec7e21a73ff66bdea9a0b09c6c7e7d8e404de3db49b2a0825ebbe", "start_char": 0, "end_char": 1389, "text_sha256": "019508b2d05ec7e21a73ff66bdea9a0b09c6c7e7d8e404de3db49b2a0825ebbe"}
experimental_model
Human family genetics and transfected COS-cell transport assays
exposure
L243P, T262M and double-mutant constructs
limitations
Family-specific genetic disease; loss of bile-acid transport was tested, whereas individual fat-soluble-vitamin deficiencies were not.
nutrient_topic
Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
organism
Human SLC10A2
plain_language
A transporter can reach the right place but still fail to carry its cargo.
primary_references
[sodium-p9109432] Primary bile acid malabsorption caused by mutations in the ileal sodium-dependent bile acid transporter gene (SLC10A2). (1997). https://pubmed.ncbi.nlm.nih.gov/9109432/ DOI: 10.1172/jci119355
tissue_or_cell_type
Ileal bile-acid transporter
trigger_kind
machinery_impairment Imported condition classification; unverified.
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 655–666
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human family genetics and transfected COS-cell transport assays · source_derived_draft · unverified_draft
### sodium-asbt-trafficking The dysfunctional L243P/T262M constructs retained protein expression and plasma-membrane trafficking. Condition category: machinery_impairment nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A transporter can reach the right place but still fail to carry its cargo. organism: Human SLC10A2 tissue_or_cell_type: Ileal bile-acid transporter experimental_model: Human family genetics and transfected COS-cell transport assays limitations: Family-specific genetic disease; loss of bile-acid transport was tested, whereas individual fat-soluble-vitamin deficiencies were not. exposure: L243P, T262M and double-mutant constructs evidence_span: {"source_cache": "artifacts/sodium-research/9109432.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "019508b2d05ec7e21a73ff66bdea9a0b09c6c7e7d8e404de3db49b2a0825ebbe", "start_char": 0, "end_char": 1389, "text_sha256": "019508b2d05ec7e21a73ff66bdea9a0b09c6c7e7d8e404de3db49b2a0825ebbe"} [sodium-p9109432] Primary bile acid malabsorption caused by mutations in the ileal sodium-dependent bile acid transporter gene (SLC10A2). (1997). https://pubmed.ncbi.nlm.nih.gov/9109432/ DOI: 10.1172/jci119355
Complete structured claim and evidence
The HHRH phenotype included elevated circulating 1,25-dihydroxyvitamin D with normal or low-normal FGF23.
Sodium-phosphate cotransporter NaPi-IIc / SLC34A3 → Circulating calcitriol concentration source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/sodium-research/16358215.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "876374dd0624cf69b89f3f5b17e5be423d7d9a0358f135add88f2493314d2ceb", "start_char": 0, "end_char": 1515, "text_sha256": "876374dd0624cf69b89f3f5b17e5be423d7d9a0358f135add88f2493314d2ceb"}
experimental_model
Mapping and sequencing in families with hereditary hypophosphatemic rickets with hypercalciuria
exposure
SLC34A3 disease-associated mutations in five families
limitations
Genotype–phenotype evidence supports a primary renal defect; downstream calcitriol/calcium pattern is observed, not a dietary sodium intervention.
nutrient_topic
Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
organism
Human
plain_language
A phosphate-handling defect can change the vitamin D environment.
primary_references
[sodium-p16358215] Hereditary hypophosphatemic rickets with hypercalciuria is caused by mutations in the sodium-phosphate cotransporter gene SLC34A3. (2006). https://pubmed.ncbi.nlm.nih.gov/16358215/ DOI: 10.1086/499410
tissue_or_cell_type
Renal proximal tubule and systemic mineral phenotype
trigger_kind
machinery_impairment Imported condition classification; unverified.
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 681–692
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mapping and sequencing in families with hereditary hypophosphatemic rickets with hypercalciuria · source_derived_draft · unverified_draft
### sodium-napi2c-calcitriol The HHRH phenotype included elevated circulating 1,25-dihydroxyvitamin D with normal or low-normal FGF23. Condition category: machinery_impairment nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A phosphate-handling defect can change the vitamin D environment. organism: Human tissue_or_cell_type: Renal proximal tubule and systemic mineral phenotype experimental_model: Mapping and sequencing in families with hereditary hypophosphatemic rickets with hypercalciuria limitations: Genotype–phenotype evidence supports a primary renal defect; downstream calcitriol/calcium pattern is observed, not a dietary sodium intervention. exposure: SLC34A3 disease-associated mutations in five families evidence_span: {"source_cache": "artifacts/sodium-research/16358215.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "876374dd0624cf69b89f3f5b17e5be423d7d9a0358f135add88f2493314d2ceb", "start_char": 0, "end_char": 1515, "text_sha256": "876374dd0624cf69b89f3f5b17e5be423d7d9a0358f135add88f2493314d2ceb"} [sodium-p16358215] Hereditary hypophosphatemic rickets with hypercalciuria is caused by mutations in the sodium-phosphate cotransporter gene SLC34A3. (2006). https://pubmed.ncbi.nlm.nih.gov/16358215/ DOI: 10.1086/499410
Complete structured claim and evidence
The sodium/phosphate-transporter-associated HHRH phenotype included hypercalciuria.
Sodium-phosphate cotransporter NaPi-IIc / SLC34A3 → Urinary calcium excretion source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/sodium-research/16358215.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "876374dd0624cf69b89f3f5b17e5be423d7d9a0358f135add88f2493314d2ceb", "start_char": 0, "end_char": 1515, "text_sha256": "876374dd0624cf69b89f3f5b17e5be423d7d9a0358f135add88f2493314d2ceb"}
experimental_model
Mapping and sequencing in families with hereditary hypophosphatemic rickets with hypercalciuria
exposure
SLC34A3 disease-associated mutations in five families
limitations
Genotype–phenotype evidence supports a primary renal defect; downstream calcitriol/calcium pattern is observed, not a dietary sodium intervention.
nutrient_topic
Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
organism
Human
plain_language
This phosphate disorder can also increase calcium loss into urine.
primary_references
[sodium-p16358215] Hereditary hypophosphatemic rickets with hypercalciuria is caused by mutations in the sodium-phosphate cotransporter gene SLC34A3. (2006). https://pubmed.ncbi.nlm.nih.gov/16358215/ DOI: 10.1086/499410
tissue_or_cell_type
Renal proximal tubule and systemic mineral phenotype
trigger_kind
machinery_impairment Imported condition classification; unverified.
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 694–705
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mapping and sequencing in families with hereditary hypophosphatemic rickets with hypercalciuria · source_derived_draft · unverified_draft
### sodium-napi2c-calcium The sodium/phosphate-transporter-associated HHRH phenotype included hypercalciuria. Condition category: machinery_impairment nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: This phosphate disorder can also increase calcium loss into urine. organism: Human tissue_or_cell_type: Renal proximal tubule and systemic mineral phenotype experimental_model: Mapping and sequencing in families with hereditary hypophosphatemic rickets with hypercalciuria limitations: Genotype–phenotype evidence supports a primary renal defect; downstream calcitriol/calcium pattern is observed, not a dietary sodium intervention. exposure: SLC34A3 disease-associated mutations in five families evidence_span: {"source_cache": "artifacts/sodium-research/16358215.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "876374dd0624cf69b89f3f5b17e5be423d7d9a0358f135add88f2493314d2ceb", "start_char": 0, "end_char": 1515, "text_sha256": "876374dd0624cf69b89f3f5b17e5be423d7d9a0358f135add88f2493314d2ceb"} [sodium-p16358215] Hereditary hypophosphatemic rickets with hypercalciuria is caused by mutations in the sodium-phosphate cotransporter gene SLC34A3. (2006). https://pubmed.ncbi.nlm.nih.gov/16358215/ DOI: 10.1086/499410
Complete structured claim and evidence
Mutagenesis of NBCe1 residues E91 or R298 reduced transport function in the expression assay.
NBCe1-A splice variant → Renal epithelial sodium/bicarbonate transport source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/sodium-research/18441326.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3ca538a7ecb046a47f9246778b3dede99c503a45c6048f75541612c8db37448c", "start_char": 0, "end_char": 1213, "text_sha256": "3ca538a7ecb046a47f9246778b3dede99c503a45c6048f75541612c8db37448c"}
experimental_model
Homology modeling and site-directed mutagenesis with oocyte transport assays
exposure
E91 and R298 mutations and charge-reversal construct
limitations
Structure model plus functional assay; charge rescue does not establish clinical treatment or dietary sodium responsiveness.
nutrient_topic
Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
organism
Human kidney NBCe1 in Xenopus oocytes
plain_language
Acid–base regulation depends on the protein’s structure as well as available sodium.
primary_references
[sodium-p18441326] Entry to "formula tunnel" revealed by SLC4A4 human mutation and structural model. (2008). https://pubmed.ncbi.nlm.nih.gov/18441326/ DOI: 10.1074/jbc.m709819200
tissue_or_cell_type
Sodium/bicarbonate transporter N-terminal domain
trigger_kind
machinery_impairment Imported condition classification; unverified.
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 707–718
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Homology modeling and site-directed mutagenesis with oocyte transport assays · source_derived_draft · unverified_draft
### sodium-nbce1-mutation Mutagenesis of NBCe1 residues E91 or R298 reduced transport function in the expression assay. Condition category: machinery_impairment nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Acid–base regulation depends on the protein’s structure as well as available sodium. organism: Human kidney NBCe1 in Xenopus oocytes tissue_or_cell_type: Sodium/bicarbonate transporter N-terminal domain experimental_model: Homology modeling and site-directed mutagenesis with oocyte transport assays limitations: Structure model plus functional assay; charge rescue does not establish clinical treatment or dietary sodium responsiveness. exposure: E91 and R298 mutations and charge-reversal construct evidence_span: {"source_cache": "artifacts/sodium-research/18441326.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3ca538a7ecb046a47f9246778b3dede99c503a45c6048f75541612c8db37448c", "start_char": 0, "end_char": 1213, "text_sha256": "3ca538a7ecb046a47f9246778b3dede99c503a45c6048f75541612c8db37448c"} [sodium-p18441326] Entry to "formula tunnel" revealed by SLC4A4 human mutation and structural model. (2008). https://pubmed.ncbi.nlm.nih.gov/18441326/ DOI: 10.1074/jbc.m709819200
Complete structured claim and evidence
The E91R/R298E charge-reversal construct restored transport function in the study.
Human kidney NBCe1 E91R/R298E charge-reversal construct → Renal epithelial sodium/bicarbonate transport source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/sodium-research/18441326.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3ca538a7ecb046a47f9246778b3dede99c503a45c6048f75541612c8db37448c", "start_char": 0, "end_char": 1213, "text_sha256": "3ca538a7ecb046a47f9246778b3dede99c503a45c6048f75541612c8db37448c"}
experimental_model
Homology modeling and site-directed mutagenesis with oocyte transport assays
exposure
E91 and R298 mutations and charge-reversal construct
limitations
Structure model plus functional assay; charge rescue does not establish clinical treatment or dietary sodium responsiveness.
nutrient_topic
Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
organism
Human kidney NBCe1 in Xenopus oocytes
plain_language
An engineered protein repair supported a specific interaction between these residues.
primary_references
[sodium-p18441326] Entry to "formula tunnel" revealed by SLC4A4 human mutation and structural model. (2008). https://pubmed.ncbi.nlm.nih.gov/18441326/ DOI: 10.1074/jbc.m709819200
tissue_or_cell_type
Sodium/bicarbonate transporter N-terminal domain
trigger_kind
machinery_impairment Imported condition classification; unverified.
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 720–731
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Homology modeling and site-directed mutagenesis with oocyte transport assays · source_derived_draft · unverified_draft
### sodium-nbce1-rescue The E91R/R298E charge-reversal construct restored transport function in the study. Condition category: machinery_impairment nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: An engineered protein repair supported a specific interaction between these residues. organism: Human kidney NBCe1 in Xenopus oocytes tissue_or_cell_type: Sodium/bicarbonate transporter N-terminal domain experimental_model: Homology modeling and site-directed mutagenesis with oocyte transport assays limitations: Structure model plus functional assay; charge rescue does not establish clinical treatment or dietary sodium responsiveness. exposure: E91 and R298 mutations and charge-reversal construct evidence_span: {"source_cache": "artifacts/sodium-research/18441326.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3ca538a7ecb046a47f9246778b3dede99c503a45c6048f75541612c8db37448c", "start_char": 0, "end_char": 1213, "text_sha256": "3ca538a7ecb046a47f9246778b3dede99c503a45c6048f75541612c8db37448c"} [sodium-p18441326] Entry to "formula tunnel" revealed by SLC4A4 human mutation and structural model. (2008). https://pubmed.ncbi.nlm.nih.gov/18441326/ DOI: 10.1074/jbc.m709819200
Complete structured claim and evidence
A hypoxia-associated conformational change in complex I drove matrix acidification in the proposed and experimentally supported pathway.
Mitochondrial respiratory complex I → Mitochondrial matrix acidification source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/sodium-research/32728214.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2780431aa362c99c816f986e923fd65ed0c0324e8c8674af8ff2a2f9367762c1", "start_char": 0, "end_char": 1533, "text_sha256": "2780431aa362c99c816f986e923fd65ed0c0324e8c8674af8ff2a2f9367762c1"}
experimental_model
Acute-hypoxia cellular and mitochondrial experiments with ion imaging and respiratory/membrane assays
exposure
Acute hypoxia and inhibition of mitochondrial sodium/calcium exchange
limitations
Mechanistic research under hypoxia, including multiple preparations. Do not infer that dietary salt drives this chain, that every tissue responds identically, or that ROS here proves disease.
nutrient_topic
Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
organism
Human and mouse cells; additional rat vascular experiments in the paper
plain_language
Low oxygen can change mitochondrial chemistry before sodium enters.
primary_references
[sodium-p32728214] Na+ controls hypoxic signalling by the mitochondrial respiratory chain. (2020). https://pubmed.ncbi.nlm.nih.gov/32728214/ DOI: 10.1038/s41586-020-2551-y
tissue_or_cell_type
Mitochondrial matrix and inner membrane
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 746–757
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Acute-hypoxia cellular and mitochondrial experiments with ion imaging and respiratory/membrane assays · source_derived_draft · unverified_draft
### sodium-hypoxia-acid A hypoxia-associated conformational change in complex I drove matrix acidification in the proposed and experimentally supported pathway. Condition category: normal nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Low oxygen can change mitochondrial chemistry before sodium enters. organism: Human and mouse cells; additional rat vascular experiments in the paper tissue_or_cell_type: Mitochondrial matrix and inner membrane experimental_model: Acute-hypoxia cellular and mitochondrial experiments with ion imaging and respiratory/membrane assays limitations: Mechanistic research under hypoxia, including multiple preparations. Do not infer that dietary salt drives this chain, that every tissue responds identically, or that ROS here proves disease. exposure: Acute hypoxia and inhibition of mitochondrial sodium/calcium exchange evidence_span: {"source_cache": "artifacts/sodium-research/32728214.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2780431aa362c99c816f986e923fd65ed0c0324e8c8674af8ff2a2f9367762c1", "start_char": 0, "end_char": 1533, "text_sha256": "2780431aa362c99c816f986e923fd65ed0c0324e8c8674af8ff2a2f9367762c1"} [sodium-p32728214] Na+ controls hypoxic signalling by the mitochondrial respiratory chain. (2020). https://pubmed.ncbi.nlm.nih.gov/32728214/ DOI: 10.1038/s41586-020-2551-y
Complete structured claim and evidence
Matrix acidification released free calcium from mitochondrial calcium phosphate deposits.
Mitochondrial matrix acidification → Mitochondrial calcium phosphate deposits source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/sodium-research/32728214.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2780431aa362c99c816f986e923fd65ed0c0324e8c8674af8ff2a2f9367762c1", "start_char": 0, "end_char": 1533, "text_sha256": "2780431aa362c99c816f986e923fd65ed0c0324e8c8674af8ff2a2f9367762c1"}
experimental_model
Acute-hypoxia cellular and mitochondrial experiments with ion imaging and respiratory/membrane assays
exposure
Acute hypoxia and inhibition of mitochondrial sodium/calcium exchange
limitations
Mechanistic research under hypoxia, including multiple preparations. Do not infer that dietary salt drives this chain, that every tissue responds identically, or that ROS here proves disease.
nutrient_topic
Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
organism
Human and mouse cells; additional rat vascular experiments in the paper
plain_language
Calcium stored in deposits became available as free calcium.
primary_references
[sodium-p32728214] Na+ controls hypoxic signalling by the mitochondrial respiratory chain. (2020). https://pubmed.ncbi.nlm.nih.gov/32728214/ DOI: 10.1038/s41586-020-2551-y
tissue_or_cell_type
Mitochondrial matrix and inner membrane
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 759–770
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Acute-hypoxia cellular and mitochondrial experiments with ion imaging and respiratory/membrane assays · source_derived_draft · unverified_draft
### sodium-matrix-calcium Matrix acidification released free calcium from mitochondrial calcium phosphate deposits. Condition category: normal nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Calcium stored in deposits became available as free calcium. organism: Human and mouse cells; additional rat vascular experiments in the paper tissue_or_cell_type: Mitochondrial matrix and inner membrane experimental_model: Acute-hypoxia cellular and mitochondrial experiments with ion imaging and respiratory/membrane assays limitations: Mechanistic research under hypoxia, including multiple preparations. Do not infer that dietary salt drives this chain, that every tissue responds identically, or that ROS here proves disease. exposure: Acute hypoxia and inhibition of mitochondrial sodium/calcium exchange evidence_span: {"source_cache": "artifacts/sodium-research/32728214.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2780431aa362c99c816f986e923fd65ed0c0324e8c8674af8ff2a2f9367762c1", "start_char": 0, "end_char": 1533, "text_sha256": "2780431aa362c99c816f986e923fd65ed0c0324e8c8674af8ff2a2f9367762c1"} [sodium-p32728214] Na+ controls hypoxic signalling by the mitochondrial respiratory chain. (2020). https://pubmed.ncbi.nlm.nih.gov/32728214/ DOI: 10.1038/s41586-020-2551-y
Complete structured claim and evidence
Activation of mitochondrial sodium/calcium exchange promoted sodium import into the matrix during the hypoxic pathway.
Mammalian mitochondrial sodium/calcium exchanger NCLX / SLC8B1 → Sodium import into the mitochondrial matrix source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/sodium-research/32728214.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2780431aa362c99c816f986e923fd65ed0c0324e8c8674af8ff2a2f9367762c1", "start_char": 0, "end_char": 1533, "text_sha256": "2780431aa362c99c816f986e923fd65ed0c0324e8c8674af8ff2a2f9367762c1"}
experimental_model
Acute-hypoxia cellular and mitochondrial experiments with ion imaging and respiratory/membrane assays
exposure
Acute hypoxia and inhibition of mitochondrial sodium/calcium exchange
limitations
Mechanistic research under hypoxia, including multiple preparations. Do not infer that dietary salt drives this chain, that every tissue responds identically, or that ROS here proves disease.
nutrient_topic
Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
organism
Human and mouse cells; additional rat vascular experiments in the paper
plain_language
Calcium handling can bring sodium into the mitochondrion.
primary_references
[sodium-p32728214] Na+ controls hypoxic signalling by the mitochondrial respiratory chain. (2020). https://pubmed.ncbi.nlm.nih.gov/32728214/ DOI: 10.1038/s41586-020-2551-y
tissue_or_cell_type
Mitochondrial matrix and inner membrane
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 772–783
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Acute-hypoxia cellular and mitochondrial experiments with ion imaging and respiratory/membrane assays · source_derived_draft · unverified_draft
### sodium-matrix-sodium Activation of mitochondrial sodium/calcium exchange promoted sodium import into the matrix during the hypoxic pathway. Condition category: normal nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Calcium handling can bring sodium into the mitochondrion. organism: Human and mouse cells; additional rat vascular experiments in the paper tissue_or_cell_type: Mitochondrial matrix and inner membrane experimental_model: Acute-hypoxia cellular and mitochondrial experiments with ion imaging and respiratory/membrane assays limitations: Mechanistic research under hypoxia, including multiple preparations. Do not infer that dietary salt drives this chain, that every tissue responds identically, or that ROS here proves disease. exposure: Acute hypoxia and inhibition of mitochondrial sodium/calcium exchange evidence_span: {"source_cache": "artifacts/sodium-research/32728214.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2780431aa362c99c816f986e923fd65ed0c0324e8c8674af8ff2a2f9367762c1", "start_char": 0, "end_char": 1533, "text_sha256": "2780431aa362c99c816f986e923fd65ed0c0324e8c8674af8ff2a2f9367762c1"} [sodium-p32728214] Na+ controls hypoxic signalling by the mitochondrial respiratory chain. (2020). https://pubmed.ncbi.nlm.nih.gov/32728214/ DOI: 10.1038/s41586-020-2551-y
Complete structured claim and evidence
Matrix sodium interacted with phospholipids and reduced inner-membrane fluidity in the study.
Sodium ion → Inner mitochondrial membrane fluidity source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/sodium-research/32728214.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2780431aa362c99c816f986e923fd65ed0c0324e8c8674af8ff2a2f9367762c1", "start_char": 0, "end_char": 1533, "text_sha256": "2780431aa362c99c816f986e923fd65ed0c0324e8c8674af8ff2a2f9367762c1"}
experimental_model
Acute-hypoxia cellular and mitochondrial experiments with ion imaging and respiratory/membrane assays
exposure
Acute hypoxia and inhibition of mitochondrial sodium/calcium exchange
limitations
Mechanistic research under hypoxia, including multiple preparations. Do not infer that dietary salt drives this chain, that every tissue responds identically, or that ROS here proves disease.
nutrient_topic
Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
organism
Human and mouse cells; additional rat vascular experiments in the paper
plain_language
Sodium changed the physical behavior of a mitochondrial membrane.
primary_references
[sodium-p32728214] Na+ controls hypoxic signalling by the mitochondrial respiratory chain. (2020). https://pubmed.ncbi.nlm.nih.gov/32728214/ DOI: 10.1038/s41586-020-2551-y
tissue_or_cell_type
Mitochondrial matrix and inner membrane
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 785–796
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Acute-hypoxia cellular and mitochondrial experiments with ion imaging and respiratory/membrane assays · source_derived_draft · unverified_draft
### sodium-membrane-fluidity Matrix sodium interacted with phospholipids and reduced inner-membrane fluidity in the study. Condition category: normal nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Sodium changed the physical behavior of a mitochondrial membrane. organism: Human and mouse cells; additional rat vascular experiments in the paper tissue_or_cell_type: Mitochondrial matrix and inner membrane experimental_model: Acute-hypoxia cellular and mitochondrial experiments with ion imaging and respiratory/membrane assays limitations: Mechanistic research under hypoxia, including multiple preparations. Do not infer that dietary salt drives this chain, that every tissue responds identically, or that ROS here proves disease. exposure: Acute hypoxia and inhibition of mitochondrial sodium/calcium exchange evidence_span: {"source_cache": "artifacts/sodium-research/32728214.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2780431aa362c99c816f986e923fd65ed0c0324e8c8674af8ff2a2f9367762c1", "start_char": 0, "end_char": 1533, "text_sha256": "2780431aa362c99c816f986e923fd65ed0c0324e8c8674af8ff2a2f9367762c1"} [sodium-p32728214] Na+ controls hypoxic signalling by the mitochondrial respiratory chain. (2020). https://pubmed.ncbi.nlm.nih.gov/32728214/ DOI: 10.1038/s41586-020-2551-y
Complete structured claim and evidence
The sodium-linked membrane change reduced free ubiquinone mobility between complexes II and III, while transport within supercomplexes was spared.
Sodium ion → Mobility of free ubiquinone between respiratory complexes II and III source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/sodium-research/32728214.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2780431aa362c99c816f986e923fd65ed0c0324e8c8674af8ff2a2f9367762c1", "start_char": 0, "end_char": 1533, "text_sha256": "2780431aa362c99c816f986e923fd65ed0c0324e8c8674af8ff2a2f9367762c1"}
experimental_model
Acute-hypoxia cellular and mitochondrial experiments with ion imaging and respiratory/membrane assays
exposure
Acute hypoxia and inhibition of mitochondrial sodium/calcium exchange
limitations
Mechanistic research under hypoxia, including multiple preparations. Do not infer that dietary salt drives this chain, that every tissue responds identically, or that ROS here proves disease.
nutrient_topic
Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
organism
Human and mouse cells; additional rat vascular experiments in the paper
plain_language
The effect depended on how the respiratory machinery was organized.
primary_references
[sodium-p32728214] Na+ controls hypoxic signalling by the mitochondrial respiratory chain. (2020). https://pubmed.ncbi.nlm.nih.gov/32728214/ DOI: 10.1038/s41586-020-2551-y
tissue_or_cell_type
Mitochondrial matrix and inner membrane
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 798–809
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Acute-hypoxia cellular and mitochondrial experiments with ion imaging and respiratory/membrane assays · source_derived_draft · unverified_draft
### sodium-quinone-mobility The sodium-linked membrane change reduced free ubiquinone mobility between complexes II and III, while transport within supercomplexes was spared. Condition category: normal nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The effect depended on how the respiratory machinery was organized. organism: Human and mouse cells; additional rat vascular experiments in the paper tissue_or_cell_type: Mitochondrial matrix and inner membrane experimental_model: Acute-hypoxia cellular and mitochondrial experiments with ion imaging and respiratory/membrane assays limitations: Mechanistic research under hypoxia, including multiple preparations. Do not infer that dietary salt drives this chain, that every tissue responds identically, or that ROS here proves disease. exposure: Acute hypoxia and inhibition of mitochondrial sodium/calcium exchange evidence_span: {"source_cache": "artifacts/sodium-research/32728214.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2780431aa362c99c816f986e923fd65ed0c0324e8c8674af8ff2a2f9367762c1", "start_char": 0, "end_char": 1533, "text_sha256": "2780431aa362c99c816f986e923fd65ed0c0324e8c8674af8ff2a2f9367762c1"} [sodium-p32728214] Na+ controls hypoxic signalling by the mitochondrial respiratory chain. (2020). https://pubmed.ncbi.nlm.nih.gov/32728214/ DOI: 10.1038/s41586-020-2551-y
Complete structured claim and evidence
The pathway produced complex III superoxide; inhibiting mitochondrial sodium import blocked the response.
Sodium ion → Complex III superoxide production source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/sodium-research/32728214.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2780431aa362c99c816f986e923fd65ed0c0324e8c8674af8ff2a2f9367762c1", "start_char": 0, "end_char": 1533, "text_sha256": "2780431aa362c99c816f986e923fd65ed0c0324e8c8674af8ff2a2f9367762c1"}
experimental_model
Acute-hypoxia cellular and mitochondrial experiments with ion imaging and respiratory/membrane assays
exposure
Acute hypoxia and inhibition of mitochondrial sodium/calcium exchange
limitations
Mechanistic research under hypoxia, including multiple preparations. Do not infer that dietary salt drives this chain, that every tissue responds identically, or that ROS here proves disease.
nutrient_topic
Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
organism
Human and mouse cells; additional rat vascular experiments in the paper
plain_language
A sodium-linked membrane effect contributed to a mitochondrial redox signal.
primary_references
[sodium-p32728214] Na+ controls hypoxic signalling by the mitochondrial respiratory chain. (2020). https://pubmed.ncbi.nlm.nih.gov/32728214/ DOI: 10.1038/s41586-020-2551-y
tissue_or_cell_type
Mitochondrial matrix and inner membrane
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 811–822
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Acute-hypoxia cellular and mitochondrial experiments with ion imaging and respiratory/membrane assays · source_derived_draft · unverified_draft
### sodium-complex3-ros The pathway produced complex III superoxide; inhibiting mitochondrial sodium import blocked the response. Condition category: normal nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A sodium-linked membrane effect contributed to a mitochondrial redox signal. organism: Human and mouse cells; additional rat vascular experiments in the paper tissue_or_cell_type: Mitochondrial matrix and inner membrane experimental_model: Acute-hypoxia cellular and mitochondrial experiments with ion imaging and respiratory/membrane assays limitations: Mechanistic research under hypoxia, including multiple preparations. Do not infer that dietary salt drives this chain, that every tissue responds identically, or that ROS here proves disease. exposure: Acute hypoxia and inhibition of mitochondrial sodium/calcium exchange evidence_span: {"source_cache": "artifacts/sodium-research/32728214.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2780431aa362c99c816f986e923fd65ed0c0324e8c8674af8ff2a2f9367762c1", "start_char": 0, "end_char": 1533, "text_sha256": "2780431aa362c99c816f986e923fd65ed0c0324e8c8674af8ff2a2f9367762c1"} [sodium-p32728214] Na+ controls hypoxic signalling by the mitochondrial respiratory chain. (2020). https://pubmed.ncbi.nlm.nih.gov/32728214/ DOI: 10.1038/s41586-020-2551-y
Complete structured claim and evidence
Intestinal NHE3-null mice developed metabolic acidosis with lower blood bicarbonate.
Mouse sodium/hydrogen exchanger NHE3 / Slc9a3 → Plasma bicarbonate concentration source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/sodium-research/32227118.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0a9c8f006f6b0b8ff35bd7e67c529c9c72e0cf3d3fd29cd46ec8c23942129b39", "start_char": 0, "end_char": 1643, "text_sha256": "0a9c8f006f6b0b8ff35bd7e67c529c9c72e0cf3d3fd29cd46ec8c23942129b39"}
experimental_model
Inducible intestinal epithelial Slc9a3 deletion
exposure
Tamoxifen-induced NHE3 loss
limitations
Genetic machinery failure, not isolated low sodium intake. Gut loss differs from proximal-tubule-specific deletion.
nutrient_topic
Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
organism
Mouse
plain_language
The losses also disturbed acid–base balance.
primary_references
[sodium-p32227118] An inducible intestinal epithelial cell-specific NHE3 knockout mouse model mimicking congenital sodium diarrhea. (2020). https://pubmed.ncbi.nlm.nih.gov/32227118/ DOI: 10.1042/cs20200065
tissue_or_cell_type
Intestine with systemic electrolyte measurements
trigger_kind
machinery_impairment Imported condition classification; unverified.
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 837–848
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Inducible intestinal epithelial Slc9a3 deletion · source_derived_draft · unverified_draft
### sodium-gut-bicarbonate Intestinal NHE3-null mice developed metabolic acidosis with lower blood bicarbonate. Condition category: machinery_impairment nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The losses also disturbed acid–base balance. organism: Mouse tissue_or_cell_type: Intestine with systemic electrolyte measurements experimental_model: Inducible intestinal epithelial Slc9a3 deletion limitations: Genetic machinery failure, not isolated low sodium intake. Gut loss differs from proximal-tubule-specific deletion. exposure: Tamoxifen-induced NHE3 loss evidence_span: {"source_cache": "artifacts/sodium-research/32227118.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0a9c8f006f6b0b8ff35bd7e67c529c9c72e0cf3d3fd29cd46ec8c23942129b39", "start_char": 0, "end_char": 1643, "text_sha256": "0a9c8f006f6b0b8ff35bd7e67c529c9c72e0cf3d3fd29cd46ec8c23942129b39"} [sodium-p32227118] An inducible intestinal epithelial cell-specific NHE3 knockout mouse model mimicking congenital sodium diarrhea. (2020). https://pubmed.ncbi.nlm.nih.gov/32227118/ DOI: 10.1042/cs20200065
Complete structured claim and evidence
Intestinal NHE3-null mice developed hyponatremia.
Mouse sodium/hydrogen exchanger NHE3 / Slc9a3 → Plasma or serum sodium concentration source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/sodium-research/32227118.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0a9c8f006f6b0b8ff35bd7e67c529c9c72e0cf3d3fd29cd46ec8c23942129b39", "start_char": 0, "end_char": 1643, "text_sha256": "0a9c8f006f6b0b8ff35bd7e67c529c9c72e0cf3d3fd29cd46ec8c23942129b39"}
experimental_model
Inducible intestinal epithelial Slc9a3 deletion
exposure
Tamoxifen-induced NHE3 loss
limitations
Genetic machinery failure, not isolated low sodium intake. Gut loss differs from proximal-tubule-specific deletion.
nutrient_topic
Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
organism
Mouse
plain_language
A gut transport defect can affect the measured blood sodium.
primary_references
[sodium-p32227118] An inducible intestinal epithelial cell-specific NHE3 knockout mouse model mimicking congenital sodium diarrhea. (2020). https://pubmed.ncbi.nlm.nih.gov/32227118/ DOI: 10.1042/cs20200065
tissue_or_cell_type
Intestine with systemic electrolyte measurements
trigger_kind
machinery_impairment Imported condition classification; unverified.
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 850–861
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Inducible intestinal epithelial Slc9a3 deletion · source_derived_draft · unverified_draft
### sodium-gut-sodium Intestinal NHE3-null mice developed hyponatremia. Condition category: machinery_impairment nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A gut transport defect can affect the measured blood sodium. organism: Mouse tissue_or_cell_type: Intestine with systemic electrolyte measurements experimental_model: Inducible intestinal epithelial Slc9a3 deletion limitations: Genetic machinery failure, not isolated low sodium intake. Gut loss differs from proximal-tubule-specific deletion. exposure: Tamoxifen-induced NHE3 loss evidence_span: {"source_cache": "artifacts/sodium-research/32227118.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0a9c8f006f6b0b8ff35bd7e67c529c9c72e0cf3d3fd29cd46ec8c23942129b39", "start_char": 0, "end_char": 1643, "text_sha256": "0a9c8f006f6b0b8ff35bd7e67c529c9c72e0cf3d3fd29cd46ec8c23942129b39"} [sodium-p32227118] An inducible intestinal epithelial cell-specific NHE3 knockout mouse model mimicking congenital sodium diarrhea. (2020). https://pubmed.ncbi.nlm.nih.gov/32227118/ DOI: 10.1042/cs20200065
Complete structured claim and evidence
Intestinal NHE3-null mice developed hyperkalemia.
Mouse sodium/hydrogen exchanger NHE3 / Slc9a3 → Plasma potassium concentration source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/sodium-research/32227118.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0a9c8f006f6b0b8ff35bd7e67c529c9c72e0cf3d3fd29cd46ec8c23942129b39", "start_char": 0, "end_char": 1643, "text_sha256": "0a9c8f006f6b0b8ff35bd7e67c529c9c72e0cf3d3fd29cd46ec8c23942129b39"}
experimental_model
Inducible intestinal epithelial Slc9a3 deletion
exposure
Tamoxifen-induced NHE3 loss
limitations
Genetic machinery failure, not isolated low sodium intake. Gut loss differs from proximal-tubule-specific deletion.
nutrient_topic
Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
organism
Mouse
plain_language
Potassium can rise in this model; diarrhea does not impose one universal potassium pattern.
primary_references
[sodium-p32227118] An inducible intestinal epithelial cell-specific NHE3 knockout mouse model mimicking congenital sodium diarrhea. (2020). https://pubmed.ncbi.nlm.nih.gov/32227118/ DOI: 10.1042/cs20200065
tissue_or_cell_type
Intestine with systemic electrolyte measurements
trigger_kind
machinery_impairment Imported condition classification; unverified.
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 863–874
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Inducible intestinal epithelial Slc9a3 deletion · source_derived_draft · unverified_draft
### sodium-gut-potassium Intestinal NHE3-null mice developed hyperkalemia. Condition category: machinery_impairment nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Potassium can rise in this model; diarrhea does not impose one universal potassium pattern. organism: Mouse tissue_or_cell_type: Intestine with systemic electrolyte measurements experimental_model: Inducible intestinal epithelial Slc9a3 deletion limitations: Genetic machinery failure, not isolated low sodium intake. Gut loss differs from proximal-tubule-specific deletion. exposure: Tamoxifen-induced NHE3 loss evidence_span: {"source_cache": "artifacts/sodium-research/32227118.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0a9c8f006f6b0b8ff35bd7e67c529c9c72e0cf3d3fd29cd46ec8c23942129b39", "start_char": 0, "end_char": 1643, "text_sha256": "0a9c8f006f6b0b8ff35bd7e67c529c9c72e0cf3d3fd29cd46ec8c23942129b39"} [sodium-p32227118] An inducible intestinal epithelial cell-specific NHE3 knockout mouse model mimicking congenital sodium diarrhea. (2020). https://pubmed.ncbi.nlm.nih.gov/32227118/ DOI: 10.1042/cs20200065
Complete structured claim and evidence
Intestinal NHE3-null mice had markedly elevated plasma aldosterone.
Mouse sodium/hydrogen exchanger NHE3 / Slc9a3 → Aldosterone source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/sodium-research/32227118.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0a9c8f006f6b0b8ff35bd7e67c529c9c72e0cf3d3fd29cd46ec8c23942129b39", "start_char": 0, "end_char": 1643, "text_sha256": "0a9c8f006f6b0b8ff35bd7e67c529c9c72e0cf3d3fd29cd46ec8c23942129b39"}
experimental_model
Inducible intestinal epithelial Slc9a3 deletion
exposure
Tamoxifen-induced NHE3 loss
limitations
Genetic machinery failure, not isolated low sodium intake. Gut loss differs from proximal-tubule-specific deletion.
nutrient_topic
Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
organism
Mouse
plain_language
A strong hormonal conservation response did not prevent the phenotype.
primary_references
[sodium-p32227118] An inducible intestinal epithelial cell-specific NHE3 knockout mouse model mimicking congenital sodium diarrhea. (2020). https://pubmed.ncbi.nlm.nih.gov/32227118/ DOI: 10.1042/cs20200065
tissue_or_cell_type
Intestine with systemic electrolyte measurements
trigger_kind
machinery_impairment Imported condition classification; unverified.
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 876–887
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Inducible intestinal epithelial Slc9a3 deletion · source_derived_draft · unverified_draft
### sodium-gut-aldosterone Intestinal NHE3-null mice had markedly elevated plasma aldosterone. Condition category: machinery_impairment nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A strong hormonal conservation response did not prevent the phenotype. organism: Mouse tissue_or_cell_type: Intestine with systemic electrolyte measurements experimental_model: Inducible intestinal epithelial Slc9a3 deletion limitations: Genetic machinery failure, not isolated low sodium intake. Gut loss differs from proximal-tubule-specific deletion. exposure: Tamoxifen-induced NHE3 loss evidence_span: {"source_cache": "artifacts/sodium-research/32227118.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0a9c8f006f6b0b8ff35bd7e67c529c9c72e0cf3d3fd29cd46ec8c23942129b39", "start_char": 0, "end_char": 1643, "text_sha256": "0a9c8f006f6b0b8ff35bd7e67c529c9c72e0cf3d3fd29cd46ec8c23942129b39"} [sodium-p32227118] An inducible intestinal epithelial cell-specific NHE3 knockout mouse model mimicking congenital sodium diarrhea. (2020). https://pubmed.ncbi.nlm.nih.gov/32227118/ DOI: 10.1042/cs20200065
Complete structured claim and evidence
A 30-mmHg perfusion-pressure increase raised sodium excretion fivefold in controls and eightfold in proximal NHE3-null mice.
Mouse sodium/hydrogen exchanger NHE3 / Slc9a3 → Urinary sodium excretion source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/sodium-research/30571224.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "14f3ce82ae25bafc1d5d935be05b3a8d68420b6d8a36fdbbc5d7e89aba77bc33", "start_char": 0, "end_char": 1779, "text_sha256": "14f3ce82ae25bafc1d5d935be05b3a8d68420b6d8a36fdbbc5d7e89aba77bc33"}
experimental_model
Proximal-tubule-specific Slc9a3 knockout and controlled renal perfusion changes
exposure
Genetic deletion; increased perfusion pressure; saline and dietary salt challenges
limitations
Unlike intestinal deletion, the kidney-specific model retained measured baseline plasma sodium, pH and bicarbonate. Tissue context, not a contradiction.
nutrient_topic
Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
organism
Mouse
plain_language
The kidney excreted more sodium in response to pressure when this reabsorption route was missing.
primary_references
[sodium-p30571224] Proximal Tubule-Specific Deletion of the NHE3 (Na+/H+ Exchanger 3) Promotes the Pressure-Natriuresis Response and Lowers Blood Pressure in Mice. (2018). https://pubmed.ncbi.nlm.nih.gov/30571224/ DOI: 10.1161/hypertensionaha.118.10884
tissue_or_cell_type
Kidney proximal tubule
trigger_kind
machinery_impairment Imported condition classification; unverified.
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 889–900
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Proximal-tubule-specific Slc9a3 knockout and controlled renal perfusion changes · source_derived_draft · unverified_draft
### sodium-renal-nhe3-natriuresis A 30-mmHg perfusion-pressure increase raised sodium excretion fivefold in controls and eightfold in proximal NHE3-null mice. Condition category: machinery_impairment nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The kidney excreted more sodium in response to pressure when this reabsorption route was missing. organism: Mouse tissue_or_cell_type: Kidney proximal tubule experimental_model: Proximal-tubule-specific Slc9a3 knockout and controlled renal perfusion changes limitations: Unlike intestinal deletion, the kidney-specific model retained measured baseline plasma sodium, pH and bicarbonate. Tissue context, not a contradiction. exposure: Genetic deletion; increased perfusion pressure; saline and dietary salt challenges evidence_span: {"source_cache": "artifacts/sodium-research/30571224.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "14f3ce82ae25bafc1d5d935be05b3a8d68420b6d8a36fdbbc5d7e89aba77bc33", "start_char": 0, "end_char": 1779, "text_sha256": "14f3ce82ae25bafc1d5d935be05b3a8d68420b6d8a36fdbbc5d7e89aba77bc33"} [sodium-p30571224] Proximal Tubule-Specific Deletion of the NHE3 (Na+/H+ Exchanger 3) Promotes the Pressure-Natriuresis Response and Lowers Blood Pressure in Mice. (2018). https://pubmed.ncbi.nlm.nih.gov/30571224/ DOI: 10.1161/hypertensionaha.118.10884
Complete structured claim and evidence
Proximal-tubule NHE3-null mice had lower basal systolic, diastolic and mean arterial pressure.
Mouse sodium/hydrogen exchanger NHE3 / Slc9a3 → Arterial blood pressure source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/sodium-research/30571224.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "14f3ce82ae25bafc1d5d935be05b3a8d68420b6d8a36fdbbc5d7e89aba77bc33", "start_char": 0, "end_char": 1779, "text_sha256": "14f3ce82ae25bafc1d5d935be05b3a8d68420b6d8a36fdbbc5d7e89aba77bc33"}
experimental_model
Proximal-tubule-specific Slc9a3 knockout and controlled renal perfusion changes
exposure
Genetic deletion; increased perfusion pressure; saline and dietary salt challenges
limitations
Unlike intestinal deletion, the kidney-specific model retained measured baseline plasma sodium, pH and bicarbonate. Tissue context, not a contradiction.
nutrient_topic
Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
organism
Mouse
plain_language
A kidney sodium-transport change can affect blood pressure.
primary_references
[sodium-p30571224] Proximal Tubule-Specific Deletion of the NHE3 (Na+/H+ Exchanger 3) Promotes the Pressure-Natriuresis Response and Lowers Blood Pressure in Mice. (2018). https://pubmed.ncbi.nlm.nih.gov/30571224/ DOI: 10.1161/hypertensionaha.118.10884
tissue_or_cell_type
Kidney proximal tubule
trigger_kind
machinery_impairment Imported condition classification; unverified.
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 902–913
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Proximal-tubule-specific Slc9a3 knockout and controlled renal perfusion changes · source_derived_draft · unverified_draft
### sodium-renal-nhe3-pressure Proximal-tubule NHE3-null mice had lower basal systolic, diastolic and mean arterial pressure. Condition category: machinery_impairment nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A kidney sodium-transport change can affect blood pressure. organism: Mouse tissue_or_cell_type: Kidney proximal tubule experimental_model: Proximal-tubule-specific Slc9a3 knockout and controlled renal perfusion changes limitations: Unlike intestinal deletion, the kidney-specific model retained measured baseline plasma sodium, pH and bicarbonate. Tissue context, not a contradiction. exposure: Genetic deletion; increased perfusion pressure; saline and dietary salt challenges evidence_span: {"source_cache": "artifacts/sodium-research/30571224.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "14f3ce82ae25bafc1d5d935be05b3a8d68420b6d8a36fdbbc5d7e89aba77bc33", "start_char": 0, "end_char": 1779, "text_sha256": "14f3ce82ae25bafc1d5d935be05b3a8d68420b6d8a36fdbbc5d7e89aba77bc33"} [sodium-p30571224] Proximal Tubule-Specific Deletion of the NHE3 (Na+/H+ Exchanger 3) Promotes the Pressure-Natriuresis Response and Lowers Blood Pressure in Mice. (2018). https://pubmed.ncbi.nlm.nih.gov/30571224/ DOI: 10.1161/hypertensionaha.118.10884
Complete structured claim and evidence
Kidney-specific NHE3 deletion did not change the measured baseline plasma sodium, pH or bicarbonate.
Mouse sodium/hydrogen exchanger NHE3 / Slc9a3 → Plasma or serum sodium concentration source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/sodium-research/30571224.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "14f3ce82ae25bafc1d5d935be05b3a8d68420b6d8a36fdbbc5d7e89aba77bc33", "start_char": 0, "end_char": 1779, "text_sha256": "14f3ce82ae25bafc1d5d935be05b3a8d68420b6d8a36fdbbc5d7e89aba77bc33"}
experimental_model
Proximal-tubule-specific Slc9a3 knockout and controlled renal perfusion changes
exposure
Genetic deletion; increased perfusion pressure; saline and dietary salt challenges
limitations
Unlike intestinal deletion, the kidney-specific model retained measured baseline plasma sodium, pH and bicarbonate. Tissue context, not a contradiction.
nutrient_topic
Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
organism
Mouse
plain_language
Changed sodium handling need not produce a changed blood sodium value.
primary_references
[sodium-p30571224] Proximal Tubule-Specific Deletion of the NHE3 (Na+/H+ Exchanger 3) Promotes the Pressure-Natriuresis Response and Lowers Blood Pressure in Mice. (2018). https://pubmed.ncbi.nlm.nih.gov/30571224/ DOI: 10.1161/hypertensionaha.118.10884
tissue_or_cell_type
Kidney proximal tubule
trigger_kind
machinery_impairment Imported condition classification; unverified.
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 915–926
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Proximal-tubule-specific Slc9a3 knockout and controlled renal perfusion changes · source_derived_draft · unverified_draft
### sodium-renal-nhe3-marker Kidney-specific NHE3 deletion did not change the measured baseline plasma sodium, pH or bicarbonate. Condition category: machinery_impairment nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Changed sodium handling need not produce a changed blood sodium value. organism: Mouse tissue_or_cell_type: Kidney proximal tubule experimental_model: Proximal-tubule-specific Slc9a3 knockout and controlled renal perfusion changes limitations: Unlike intestinal deletion, the kidney-specific model retained measured baseline plasma sodium, pH and bicarbonate. Tissue context, not a contradiction. exposure: Genetic deletion; increased perfusion pressure; saline and dietary salt challenges evidence_span: {"source_cache": "artifacts/sodium-research/30571224.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "14f3ce82ae25bafc1d5d935be05b3a8d68420b6d8a36fdbbc5d7e89aba77bc33", "start_char": 0, "end_char": 1779, "text_sha256": "14f3ce82ae25bafc1d5d935be05b3a8d68420b6d8a36fdbbc5d7e89aba77bc33"} [sodium-p30571224] Proximal Tubule-Specific Deletion of the NHE3 (Na+/H+ Exchanger 3) Promotes the Pressure-Natriuresis Response and Lowers Blood Pressure in Mice. (2018). https://pubmed.ncbi.nlm.nih.gov/30571224/ DOI: 10.1161/hypertensionaha.118.10884
Complete structured claim and evidence
Affected individuals had salt wasting with hyperkalemia and acidosis despite mineralocorticoid unresponsiveness.
Epithelial sodium channel → Plasma potassium concentration source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/sodium-research/8589714.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c85f54f2086e1dc34cabaa8e4521a157bfeb5512b7882ca214ddfa2597b9bc4e", "start_char": 0, "end_char": 696, "text_sha256": "c85f54f2086e1dc34cabaa8e4521a157bfeb5512b7882ca214ddfa2597b9bc4e"}
experimental_model
Human family genetics and sodium-channel functional testing
exposure
Loss-of-function alpha- or beta-subunit variants in five kindreds
limitations
Autosomal recessive pseudohypoaldosteronism; not ordinary dietary sodium deficiency and not proof that additional aldosterone can repair the channel.
nutrient_topic
Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
organism
Human
plain_language
Sodium-channel failure can impair the normal balance of potassium and acid as well as sodium.
primary_references
[sodium-p8589714] Mutations in subunits of the epithelial sodium channel cause salt wasting with hyperkalaemic acidosis, pseudohypoaldosteronism type 1. (1996). https://pubmed.ncbi.nlm.nih.gov/8589714/ DOI: 10.1038/ng0396-248
tissue_or_cell_type
ENaC-dependent epithelia and systemic electrolyte phenotype
trigger_kind
machinery_impairment Imported condition classification; unverified.
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 941–952
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human family genetics and sodium-channel functional testing · source_derived_draft · unverified_draft
### sodium-enac-loss-potassium Affected individuals had salt wasting with hyperkalemia and acidosis despite mineralocorticoid unresponsiveness. Condition category: machinery_impairment nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Sodium-channel failure can impair the normal balance of potassium and acid as well as sodium. organism: Human tissue_or_cell_type: ENaC-dependent epithelia and systemic electrolyte phenotype experimental_model: Human family genetics and sodium-channel functional testing limitations: Autosomal recessive pseudohypoaldosteronism; not ordinary dietary sodium deficiency and not proof that additional aldosterone can repair the channel. exposure: Loss-of-function alpha- or beta-subunit variants in five kindreds evidence_span: {"source_cache": "artifacts/sodium-research/8589714.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c85f54f2086e1dc34cabaa8e4521a157bfeb5512b7882ca214ddfa2597b9bc4e", "start_char": 0, "end_char": 696, "text_sha256": "c85f54f2086e1dc34cabaa8e4521a157bfeb5512b7882ca214ddfa2597b9bc4e"} [sodium-p8589714] Mutations in subunits of the epithelial sodium channel cause salt wasting with hyperkalaemic acidosis, pseudohypoaldosteronism type 1. (1996). https://pubmed.ncbi.nlm.nih.gov/8589714/ DOI: 10.1038/ng0396-248
Complete structured claim and evidence
The beta-subunit P616L mutant increased amiloride-sensitive sodium current 8.8-fold versus normal subunits in oocytes.
Human ENaC beta-subunit P616L variant as numbered in the 1995 study → ENaC-mediated sodium current source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/sodium-research/8524790.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "31f8bb4c6f32108b9d6042db6ec60ed8c77b21af322621a2cb0fd9c2aa7236a1", "start_char": 0, "end_char": 1598, "text_sha256": "31f8bb4c6f32108b9d6042db6ec60ed8c77b21af322621a2cb0fd9c2aa7236a1"}
experimental_model
Human kindred analysis and oocyte channel-expression comparison
exposure
P616L as numbered in the paper
limitations
Gain-of-function genetic disease; no implication that this mutation is caused by salt intake.
nutrient_topic
Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
organism
Human variant in Xenopus oocytes
plain_language
A mutation can make sodium entry excessive even without a defective sodium supply.
primary_references
[sodium-p8524790] A de novo missense mutation of the beta subunit of the epithelial sodium channel causes hypertension and Liddle syndrome, identifying a proline-rich segment critical for regulation of channel activity. (1995). https://pubmed.ncbi.nlm.nih.gov/8524790/ DOI: 10.1073/pnas.92.25.11495
tissue_or_cell_type
ENaC beta-subunit regulatory tail
trigger_kind
machinery_impairment Imported condition classification; unverified.
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 954–965
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human kindred analysis and oocyte channel-expression comparison · source_derived_draft · unverified_draft
### sodium-liddle-current The beta-subunit P616L mutant increased amiloride-sensitive sodium current 8.8-fold versus normal subunits in oocytes. Condition category: machinery_impairment nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A mutation can make sodium entry excessive even without a defective sodium supply. organism: Human variant in Xenopus oocytes tissue_or_cell_type: ENaC beta-subunit regulatory tail experimental_model: Human kindred analysis and oocyte channel-expression comparison limitations: Gain-of-function genetic disease; no implication that this mutation is caused by salt intake. exposure: P616L as numbered in the paper evidence_span: {"source_cache": "artifacts/sodium-research/8524790.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "31f8bb4c6f32108b9d6042db6ec60ed8c77b21af322621a2cb0fd9c2aa7236a1", "start_char": 0, "end_char": 1598, "text_sha256": "31f8bb4c6f32108b9d6042db6ec60ed8c77b21af322621a2cb0fd9c2aa7236a1"} [sodium-p8524790] A de novo missense mutation of the beta subunit of the epithelial sodium channel causes hypertension and Liddle syndrome, identifying a proline-rich segment critical for regulation of channel activity. (1995). https://pubmed.ncbi.nlm.nih.gov/8524790/ DOI: 10.1073/pnas.92.25.11495
Complete structured claim and evidence
Supplemented preterm infants had fewer recorded serum sodium values below 135 mmol/L.
Sodium → Plasma or serum sodium concentration source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/sodium-research/25406227.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a3c6cd28e4896dc8cdaeaacb7d524c55098b87dd5bf9d028ce49ba544832e339", "start_char": 0, "end_char": 1645, "text_sha256": "a3c6cd28e4896dc8cdaeaacb7d524c55098b87dd5bf9d028ce49ba544832e339"}
experimental_model
Randomized masked trial in 53 infants born before 32 weeks
exposure
4 mEq/kg/day supplemental sodium versus placebo, days 7–35
limitations
Study regimen, not a dosing recommendation. Small neonatal trial; improved weight gain is not proof that every blood sodium measurement diagnoses total-body depletion.
nutrient_topic
Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
organism
Human preterm infants
plain_language
Very premature infants can need a different sodium provision than older children or adults.
primary_references
[sodium-p25406227] Impact of Early Sodium Supplementation on Hyponatremia and Growth in Premature Infants: A Randomized Controlled Trial. (2016). https://pubmed.ncbi.nlm.nih.gov/25406227/ DOI: 10.1177/0148607114558303
tissue_or_cell_type
Whole-body growth and serum sodium
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 967–978
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized masked trial in 53 infants born before 32 weeks · source_derived_draft · unverified_draft
### sodium-preterm-sodium Supplemented preterm infants had fewer recorded serum sodium values below 135 mmol/L. Condition category: nutrient_deficiency nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Very premature infants can need a different sodium provision than older children or adults. organism: Human preterm infants tissue_or_cell_type: Whole-body growth and serum sodium experimental_model: Randomized masked trial in 53 infants born before 32 weeks limitations: Study regimen, not a dosing recommendation. Small neonatal trial; improved weight gain is not proof that every blood sodium measurement diagnoses total-body depletion. exposure: 4 mEq/kg/day supplemental sodium versus placebo, days 7–35 evidence_span: {"source_cache": "artifacts/sodium-research/25406227.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a3c6cd28e4896dc8cdaeaacb7d524c55098b87dd5bf9d028ce49ba544832e339", "start_char": 0, "end_char": 1645, "text_sha256": "a3c6cd28e4896dc8cdaeaacb7d524c55098b87dd5bf9d028ce49ba544832e339"} [sodium-p25406227] Impact of Early Sodium Supplementation on Hyponatremia and Growth in Premature Infants: A Randomized Controlled Trial. (2016). https://pubmed.ncbi.nlm.nih.gov/25406227/ DOI: 10.1177/0148607114558303
Complete structured claim and evidence
Length and head-circumference growth did not differ significantly between treatment groups.
Sodium → Preterm infant length and head-circumference growth source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/sodium-research/25406227.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a3c6cd28e4896dc8cdaeaacb7d524c55098b87dd5bf9d028ce49ba544832e339", "start_char": 0, "end_char": 1645, "text_sha256": "a3c6cd28e4896dc8cdaeaacb7d524c55098b87dd5bf9d028ce49ba544832e339"}
experimental_model
Randomized masked trial in 53 infants born before 32 weeks
exposure
4 mEq/kg/day supplemental sodium versus placebo, days 7–35
limitations
Study regimen, not a dosing recommendation. Small neonatal trial; improved weight gain is not proof that every blood sodium measurement diagnoses total-body depletion.
nutrient_topic
Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
organism
Human preterm infants
plain_language
The observed growth benefit was not uniform across every growth measurement.
primary_references
[sodium-p25406227] Impact of Early Sodium Supplementation on Hyponatremia and Growth in Premature Infants: A Randomized Controlled Trial. (2016). https://pubmed.ncbi.nlm.nih.gov/25406227/ DOI: 10.1177/0148607114558303
tissue_or_cell_type
Whole-body growth and serum sodium
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 993–1004
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized masked trial in 53 infants born before 32 weeks · source_derived_draft · unverified_draft
### sodium-preterm-limits Length and head-circumference growth did not differ significantly between treatment groups. Condition category: nutrient_deficiency nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The observed growth benefit was not uniform across every growth measurement. organism: Human preterm infants tissue_or_cell_type: Whole-body growth and serum sodium experimental_model: Randomized masked trial in 53 infants born before 32 weeks limitations: Study regimen, not a dosing recommendation. Small neonatal trial; improved weight gain is not proof that every blood sodium measurement diagnoses total-body depletion. exposure: 4 mEq/kg/day supplemental sodium versus placebo, days 7–35 evidence_span: {"source_cache": "artifacts/sodium-research/25406227.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a3c6cd28e4896dc8cdaeaacb7d524c55098b87dd5bf9d028ce49ba544832e339", "start_char": 0, "end_char": 1645, "text_sha256": "a3c6cd28e4896dc8cdaeaacb7d524c55098b87dd5bf9d028ce49ba544832e339"} [sodium-p25406227] Impact of Early Sodium Supplementation on Hyponatremia and Growth in Premature Infants: A Randomized Controlled Trial. (2016). https://pubmed.ncbi.nlm.nih.gov/25406227/ DOI: 10.1177/0148607114558303
Complete structured claim and evidence
Brain sodium and chloride overshot normal control contents by 24 hours after rapid correction.
Desmopressin / dDAVP → Brain sodium and chloride content source_derived_draftungraded
Experimental context and source evidence
availability_state
biomarker_context Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/sodium-research/8096428.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7f7a7712c9e952343e279ae89e0d1051857c4188820819def597a430fdaf9e4c", "start_char": 0, "end_char": 1587, "text_sha256": "7f7a7712c9e952343e279ae89e0d1051857c4188820819def597a430fdaf9e4c"}
experimental_model
Sustained dDAVP-induced hyponatremia followed by withdrawal and tissue measurements
exposure
14 days hyponatremia; sodium rose from 104 to 139 mmol/L over 24 hours after withdrawal
limitations
Extreme experimental correction; records tissue reaccumulation, not a safe human correction rate or direct proof of myelin injury in this study.
nutrient_topic
Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
organism
Rat
plain_language
The brain’s electrolyte content changed quickly after blood sodium rose.
primary_references
[sodium-p8096428] Rapid correction of hyponatremia produces differential effects on brain osmolyte and electrolyte reaccumulation in rats. (1993). https://pubmed.ncbi.nlm.nih.gov/8096428/ DOI: 10.1016/0006-8993(93)91564-9
tissue_or_cell_type
Brain water, electrolytes and organic osmolytes
trigger_kind
biomarker_context Imported condition classification; unverified.
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 1019–1030
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Sustained dDAVP-induced hyponatremia followed by withdrawal and tissue measurements · source_derived_draft · unverified_draft
### sodium-brain-electrolytes Brain sodium and chloride overshot normal control contents by 24 hours after rapid correction. Condition category: biomarker_context nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The brain’s electrolyte content changed quickly after blood sodium rose. organism: Rat tissue_or_cell_type: Brain water, electrolytes and organic osmolytes experimental_model: Sustained dDAVP-induced hyponatremia followed by withdrawal and tissue measurements limitations: Extreme experimental correction; records tissue reaccumulation, not a safe human correction rate or direct proof of myelin injury in this study. exposure: 14 days hyponatremia; sodium rose from 104 to 139 mmol/L over 24 hours after withdrawal evidence_span: {"source_cache": "artifacts/sodium-research/8096428.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7f7a7712c9e952343e279ae89e0d1051857c4188820819def597a430fdaf9e4c", "start_char": 0, "end_char": 1587, "text_sha256": "7f7a7712c9e952343e279ae89e0d1051857c4188820819def597a430fdaf9e4c"} [sodium-p8096428] Rapid correction of hyponatremia produces differential effects on brain osmolyte and electrolyte reaccumulation in rats. (1993). https://pubmed.ncbi.nlm.nih.gov/8096428/ DOI: 10.1016/0006-8993(93)91564-9
Complete structured claim and evidence
Most organic osmolytes required five or more days to recover; glutamate was an exception that recovered within 24 hours.
Desmopressin / dDAVP → Brain organic osmolyte content source_derived_draftungraded
Experimental context and source evidence
availability_state
biomarker_context Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/sodium-research/8096428.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7f7a7712c9e952343e279ae89e0d1051857c4188820819def597a430fdaf9e4c", "start_char": 0, "end_char": 1587, "text_sha256": "7f7a7712c9e952343e279ae89e0d1051857c4188820819def597a430fdaf9e4c"}
experimental_model
Sustained dDAVP-induced hyponatremia followed by withdrawal and tissue measurements
exposure
14 days hyponatremia; sodium rose from 104 to 139 mmol/L over 24 hours after withdrawal
limitations
Extreme experimental correction; records tissue reaccumulation, not a safe human correction rate or direct proof of myelin injury in this study.
nutrient_topic
Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
organism
Rat
plain_language
Different brain solutes adapt on different timelines.
primary_references
[sodium-p8096428] Rapid correction of hyponatremia produces differential effects on brain osmolyte and electrolyte reaccumulation in rats. (1993). https://pubmed.ncbi.nlm.nih.gov/8096428/ DOI: 10.1016/0006-8993(93)91564-9
tissue_or_cell_type
Brain water, electrolytes and organic osmolytes
trigger_kind
biomarker_context Imported condition classification; unverified.
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 1032–1043
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Sustained dDAVP-induced hyponatremia followed by withdrawal and tissue measurements · source_derived_draft · unverified_draft
### sodium-brain-osmolytes Most organic osmolytes required five or more days to recover; glutamate was an exception that recovered within 24 hours. Condition category: biomarker_context nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Different brain solutes adapt on different timelines. organism: Rat tissue_or_cell_type: Brain water, electrolytes and organic osmolytes experimental_model: Sustained dDAVP-induced hyponatremia followed by withdrawal and tissue measurements limitations: Extreme experimental correction; records tissue reaccumulation, not a safe human correction rate or direct proof of myelin injury in this study. exposure: 14 days hyponatremia; sodium rose from 104 to 139 mmol/L over 24 hours after withdrawal evidence_span: {"source_cache": "artifacts/sodium-research/8096428.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7f7a7712c9e952343e279ae89e0d1051857c4188820819def597a430fdaf9e4c", "start_char": 0, "end_char": 1587, "text_sha256": "7f7a7712c9e952343e279ae89e0d1051857c4188820819def597a430fdaf9e4c"} [sodium-p8096428] Rapid correction of hyponatremia produces differential effects on brain osmolyte and electrolyte reaccumulation in rats. (1993). https://pubmed.ncbi.nlm.nih.gov/8096428/ DOI: 10.1016/0006-8993(93)91564-9
Complete structured claim and evidence
Hyponatremia below 130 mmol/L occurred in 29/142 versus 16/150 participants receiving reduced-osmolarity versus standard ORS; affected participants were symptom-free.
Oral rehydration solutions (formulation specified per study) → Plasma or serum sodium concentration source_derived_draftungraded
Experimental context and source evidence
availability_state
biomarker_context Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/sodium-research/10440307.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "cd7239d3f0a151f53930364ba35b974cd938a67bc4282e4b67a02e24f68e9969", "start_char": 0, "end_char": 2141, "text_sha256": "cd7239d3f0a151f53930364ba35b974cd938a67bc4282e4b67a02e24f68e9969"}
experimental_model
Randomized double-blind comparison in 300 adults with severe cholera
exposure
Reduced-osmolarity versus then-standard WHO oral rehydration solution
limitations
Historical formulation comparison; not a current formulation recommendation. Both sodium and other solution properties changed; no isolated sodium effect.
nutrient_topic
Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
organism
Human
plain_language
Replacing fluid is not just replacing water: solution composition affected blood sodium.
primary_references
[sodium-p10440307] Efficacy and safety of oral rehydration solution with reduced osmolarity in adults with cholera: a randomised double-blind clinical trial. CHOICE study group. (1999). https://pubmed.ncbi.nlm.nih.gov/10440307/ DOI: 10.1016/s0140-6736(98)09332-5
tissue_or_cell_type
Intestinal fluid loss and serum sodium
trigger_kind
biomarker_context Imported condition classification; unverified.
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 1045–1056
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized double-blind comparison in 300 adults with severe cholera · source_derived_draft · unverified_draft
### sodium-ors-sodium Hyponatremia below 130 mmol/L occurred in 29/142 versus 16/150 participants receiving reduced-osmolarity versus standard ORS; affected participants were symptom-free. Condition category: biomarker_context nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Replacing fluid is not just replacing water: solution composition affected blood sodium. organism: Human tissue_or_cell_type: Intestinal fluid loss and serum sodium experimental_model: Randomized double-blind comparison in 300 adults with severe cholera limitations: Historical formulation comparison; not a current formulation recommendation. Both sodium and other solution properties changed; no isolated sodium effect. exposure: Reduced-osmolarity versus then-standard WHO oral rehydration solution evidence_span: {"source_cache": "artifacts/sodium-research/10440307.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "cd7239d3f0a151f53930364ba35b974cd938a67bc4282e4b67a02e24f68e9969", "start_char": 0, "end_char": 2141, "text_sha256": "cd7239d3f0a151f53930364ba35b974cd938a67bc4282e4b67a02e24f68e9969"} [sodium-p10440307] Efficacy and safety of oral rehydration solution with reduced osmolarity in adults with cholera: a randomised double-blind clinical trial. CHOICE study group. (1999). https://pubmed.ncbi.nlm.nih.gov/10440307/ DOI: 10.1016/s0140-6736(98)09332-5
Complete structured claim and evidence
The ORS groups did not differ significantly in initial 24-hour stool output, total stool output or diarrhea duration.
Oral rehydration solutions (formulation specified per study) → Stool output in adult cholera source_derived_draftungraded
Experimental context and source evidence
availability_state
biomarker_context Imported condition classification; unverified.
evidence_span
{"source_cache": "artifacts/sodium-research/10440307.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "cd7239d3f0a151f53930364ba35b974cd938a67bc4282e4b67a02e24f68e9969", "start_char": 0, "end_char": 2141, "text_sha256": "cd7239d3f0a151f53930364ba35b974cd938a67bc4282e4b67a02e24f68e9969"}
experimental_model
Randomized double-blind comparison in 300 adults with severe cholera
exposure
Reduced-osmolarity versus then-standard WHO oral rehydration solution
limitations
Historical formulation comparison; not a current formulation recommendation. Both sodium and other solution properties changed; no isolated sodium effect.
nutrient_topic
Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
organism
Human
plain_language
A lower-osmolarity formulation did not improve those clinical endpoints in this adult cholera trial.
primary_references
[sodium-p10440307] Efficacy and safety of oral rehydration solution with reduced osmolarity in adults with cholera: a randomised double-blind clinical trial. CHOICE study group. (1999). https://pubmed.ncbi.nlm.nih.gov/10440307/ DOI: 10.1016/s0140-6736(98)09332-5
tissue_or_cell_type
Intestinal fluid loss and serum sodium
trigger_kind
biomarker_context Imported condition classification; unverified.
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 1058–1069
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized double-blind comparison in 300 adults with severe cholera · source_derived_draft · unverified_draft
### sodium-ors-stool The ORS groups did not differ significantly in initial 24-hour stool output, total stool output or diarrhea duration. Condition category: biomarker_context nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A lower-osmolarity formulation did not improve those clinical endpoints in this adult cholera trial. organism: Human tissue_or_cell_type: Intestinal fluid loss and serum sodium experimental_model: Randomized double-blind comparison in 300 adults with severe cholera limitations: Historical formulation comparison; not a current formulation recommendation. Both sodium and other solution properties changed; no isolated sodium effect. exposure: Reduced-osmolarity versus then-standard WHO oral rehydration solution evidence_span: {"source_cache": "artifacts/sodium-research/10440307.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "cd7239d3f0a151f53930364ba35b974cd938a67bc4282e4b67a02e24f68e9969", "start_char": 0, "end_char": 2141, "text_sha256": "cd7239d3f0a151f53930364ba35b974cd938a67bc4282e4b67a02e24f68e9969"} [sodium-p10440307] Efficacy and safety of oral rehydration solution with reduced osmolarity in adults with cholera: a randomised double-blind clinical trial. CHOICE study group. (1999). https://pubmed.ncbi.nlm.nih.gov/10440307/ DOI: 10.1016/s0140-6736(98)09332-5
Complete structured claim and evidence
Low-sodium DASH versus high-sodium control produced mean systolic differences of 7.1 mmHg without hypertension and 11.5 mmHg with hypertension.
Sodium → Arterial blood pressure source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/sodium-research/11136953.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7664fc223f123220dd64755a1e9bc4ee3e9942e09b5de444bd789f210f449133", "start_char": 0, "end_char": 1987, "text_sha256": "7664fc223f123220dd64755a1e9bc4ee3e9942e09b5de444bd789f210f449133"}
experimental_model
Randomized controlled feeding trial in 412 participants
exposure
Three sodium levels for 30 days each within assigned DASH or control diet
limitations
Blood-pressure trial, not a hard-outcome trial; DASH changes multiple nutrients and foods. Its combined effect cannot be assigned to one mineral.
nutrient_topic
Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
organism
Human adults with and without hypertension
plain_language
Diet composition and sodium reduction had a combined effect.
primary_references
[sodium-p11136953] Effects on blood pressure of reduced dietary sodium and the Dietary Approaches to Stop Hypertension (DASH) diet. DASH-Sodium Collaborative Research Group. (2001). https://pubmed.ncbi.nlm.nih.gov/11136953/ DOI: 10.1056/nejm200101043440101
tissue_or_cell_type
Systemic blood pressure
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 1084–1095
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized controlled feeding trial in 412 participants · source_derived_draft · unverified_draft
### sodium-dash-combination Low-sodium DASH versus high-sodium control produced mean systolic differences of 7.1 mmHg without hypertension and 11.5 mmHg with hypertension. Condition category: normal nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Diet composition and sodium reduction had a combined effect. organism: Human adults with and without hypertension tissue_or_cell_type: Systemic blood pressure experimental_model: Randomized controlled feeding trial in 412 participants limitations: Blood-pressure trial, not a hard-outcome trial; DASH changes multiple nutrients and foods. Its combined effect cannot be assigned to one mineral. exposure: Three sodium levels for 30 days each within assigned DASH or control diet evidence_span: {"source_cache": "artifacts/sodium-research/11136953.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7664fc223f123220dd64755a1e9bc4ee3e9942e09b5de444bd789f210f449133", "start_char": 0, "end_char": 1987, "text_sha256": "7664fc223f123220dd64755a1e9bc4ee3e9942e09b5de444bd789f210f449133"} [sodium-p11136953] Effects on blood pressure of reduced dietary sodium and the Dietary Approaches to Stop Hypertension (DASH) diet. DASH-Sodium Collaborative Research Group. (2001). https://pubmed.ncbi.nlm.nih.gov/11136953/ DOI: 10.1056/nejm200101043440101
Complete structured claim and evidence
Fractional calcium absorption adapted to calcium intake but was not significantly altered by salt intake.
Sodium chloride → Fractional intestinal calcium absorption source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/sodium-research/18410231.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f831f038a6c4249510bbeeae68778a216f1c36aa440e33816072959d1a07fefa", "start_char": 0, "end_char": 1558, "text_sha256": "f831f038a6c4249510bbeeae68778a216f1c36aa440e33816072959d1a07fefa"}
experimental_model
Randomized crossover with stable-isotope calcium measures and compartmental modeling in 11 completers
exposure
Four five-week calcium/salt diet combinations: 518 or 1284 mg calcium; 3.9 or 11.2 g salt daily
limitations
Small study; bone balance was modeled, fractures were not measured. Salt means sodium chloride, not elemental sodium.
nutrient_topic
Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
organism
Human postmenopausal women
plain_language
The kidney calcium loss was not matched by a measured salt-driven increase in absorption.
primary_references
[sodium-p18410231] Sodium and bone health: impact of moderately high and low salt intakes on calcium metabolism in postmenopausal women. (2008). https://pubmed.ncbi.nlm.nih.gov/18410231/ DOI: 10.1359/jbmr.080408
tissue_or_cell_type
Intestinal, renal and modeled skeletal calcium balance
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 1110–1121
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized crossover with stable-isotope calcium measures and compartmental modeling in 11 completers · source_derived_draft · unverified_draft
### sodium-salt-calcium-absorption Fractional calcium absorption adapted to calcium intake but was not significantly altered by salt intake. Condition category: normal nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The kidney calcium loss was not matched by a measured salt-driven increase in absorption. organism: Human postmenopausal women tissue_or_cell_type: Intestinal, renal and modeled skeletal calcium balance experimental_model: Randomized crossover with stable-isotope calcium measures and compartmental modeling in 11 completers limitations: Small study; bone balance was modeled, fractures were not measured. Salt means sodium chloride, not elemental sodium. exposure: Four five-week calcium/salt diet combinations: 518 or 1284 mg calcium; 3.9 or 11.2 g salt daily evidence_span: {"source_cache": "artifacts/sodium-research/18410231.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f831f038a6c4249510bbeeae68778a216f1c36aa440e33816072959d1a07fefa", "start_char": 0, "end_char": 1558, "text_sha256": "f831f038a6c4249510bbeeae68778a216f1c36aa440e33816072959d1a07fefa"} [sodium-p18410231] Sodium and bone health: impact of moderately high and low salt intakes on calcium metabolism in postmenopausal women. (2008). https://pubmed.ncbi.nlm.nih.gov/18410231/ DOI: 10.1359/jbmr.080408
Complete structured claim and evidence
Higher salt shifted modeled bone calcium balance from positive to negative on the higher-calcium diet; balance was negative at both salt levels on the lower-calcium diet.
Sodium chloride → Modeled bone calcium balance source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/sodium-research/18410231.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f831f038a6c4249510bbeeae68778a216f1c36aa440e33816072959d1a07fefa", "start_char": 0, "end_char": 1558, "text_sha256": "f831f038a6c4249510bbeeae68778a216f1c36aa440e33816072959d1a07fefa"}
experimental_model
Randomized crossover with stable-isotope calcium measures and compartmental modeling in 11 completers
exposure
Four five-week calcium/salt diet combinations: 518 or 1284 mg calcium; 3.9 or 11.2 g salt daily
limitations
Small study; bone balance was modeled, fractures were not measured. Salt means sodium chloride, not elemental sodium.
nutrient_topic
Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
organism
Human postmenopausal women
plain_language
Calcium intake changed the context of the modeled salt effect; this was not a fracture trial.
primary_references
[sodium-p18410231] Sodium and bone health: impact of moderately high and low salt intakes on calcium metabolism in postmenopausal women. (2008). https://pubmed.ncbi.nlm.nih.gov/18410231/ DOI: 10.1359/jbmr.080408
tissue_or_cell_type
Intestinal, renal and modeled skeletal calcium balance
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 1123–1134
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized crossover with stable-isotope calcium measures and compartmental modeling in 11 completers · source_derived_draft · unverified_draft
### sodium-salt-bone-model Higher salt shifted modeled bone calcium balance from positive to negative on the higher-calcium diet; balance was negative at both salt levels on the lower-calcium diet. Condition category: normal nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Calcium intake changed the context of the modeled salt effect; this was not a fracture trial. organism: Human postmenopausal women tissue_or_cell_type: Intestinal, renal and modeled skeletal calcium balance experimental_model: Randomized crossover with stable-isotope calcium measures and compartmental modeling in 11 completers limitations: Small study; bone balance was modeled, fractures were not measured. Salt means sodium chloride, not elemental sodium. exposure: Four five-week calcium/salt diet combinations: 518 or 1284 mg calcium; 3.9 or 11.2 g salt daily evidence_span: {"source_cache": "artifacts/sodium-research/18410231.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f831f038a6c4249510bbeeae68778a216f1c36aa440e33816072959d1a07fefa", "start_char": 0, "end_char": 1558, "text_sha256": "f831f038a6c4249510bbeeae68778a216f1c36aa440e33816072959d1a07fefa"} [sodium-p18410231] Sodium and bone health: impact of moderately high and low salt intakes on calcium metabolism in postmenopausal women. (2008). https://pubmed.ncbi.nlm.nih.gov/18410231/ DOI: 10.1359/jbmr.080408
Complete structured claim and evidence
The 6-g/day salt increase reduced free-water clearance while increasing urine osmolyte excretion.
Sodium chloride → Renal free-water clearance source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/sodium-research/28414302.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "099d2bd468b387701a756371dde0732e2eba2b5d15d02948a99fc96c3df3046d", "start_char": 0, "end_char": 2118, "text_sha256": "099d2bd468b387701a756371dde0732e2eba2b5d15d02948a99fc96c3df3046d"}
experimental_model
Two controlled confinement studies lasting 105 and 205 days, totaling 10 men
exposure
6, 9 and 12 g/day salt; other nutrients held constant
limitations
Small all-male long-duration study; reduced free-water clearance is not creation of water. Do not extrapolate to acute salt ingestion, all populations or immune effects.
nutrient_topic
Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
organism
Human healthy men
plain_language
The kidneys adjusted water conservation during sustained salt exposure.
primary_references
[sodium-p28414302] Increased salt consumption induces body water conservation and decreases fluid intake. (2017). https://pubmed.ncbi.nlm.nih.gov/28414302/ DOI: 10.1172/jci88530
tissue_or_cell_type
Whole-body water and osmolyte balance
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 1136–1147
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Two controlled confinement studies lasting 105 and 205 days, totaling 10 men · source_derived_draft · unverified_draft
### sodium-salt-water-clearance The 6-g/day salt increase reduced free-water clearance while increasing urine osmolyte excretion. Condition category: normal nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The kidneys adjusted water conservation during sustained salt exposure. organism: Human healthy men tissue_or_cell_type: Whole-body water and osmolyte balance experimental_model: Two controlled confinement studies lasting 105 and 205 days, totaling 10 men limitations: Small all-male long-duration study; reduced free-water clearance is not creation of water. Do not extrapolate to acute salt ingestion, all populations or immune effects. exposure: 6, 9 and 12 g/day salt; other nutrients held constant evidence_span: {"source_cache": "artifacts/sodium-research/28414302.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "099d2bd468b387701a756371dde0732e2eba2b5d15d02948a99fc96c3df3046d", "start_char": 0, "end_char": 2118, "text_sha256": "099d2bd468b387701a756371dde0732e2eba2b5d15d02948a99fc96c3df3046d"} [sodium-p28414302] Increased salt consumption induces body water conservation and decreases fluid intake. (2017). https://pubmed.ncbi.nlm.nih.gov/28414302/ DOI: 10.1172/jci88530
Complete structured claim and evidence
Fluid intake was lower at 12 g/day salt in these long-duration controlled studies.
Sodium chloride → Fluid intake source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/sodium-research/28414302.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "099d2bd468b387701a756371dde0732e2eba2b5d15d02948a99fc96c3df3046d", "start_char": 0, "end_char": 2118, "text_sha256": "099d2bd468b387701a756371dde0732e2eba2b5d15d02948a99fc96c3df3046d"}
experimental_model
Two controlled confinement studies lasting 105 and 205 days, totaling 10 men
exposure
6, 9 and 12 g/day salt; other nutrients held constant
limitations
Small all-male long-duration study; reduced free-water clearance is not creation of water. Do not extrapolate to acute salt ingestion, all populations or immune effects.
nutrient_topic
Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
organism
Human healthy men
plain_language
Long-term fluid behavior in this setting did not follow a simple more-salt–more-drinking rule.
primary_references
[sodium-p28414302] Increased salt consumption induces body water conservation and decreases fluid intake. (2017). https://pubmed.ncbi.nlm.nih.gov/28414302/ DOI: 10.1172/jci88530
tissue_or_cell_type
Whole-body water and osmolyte balance
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 1149–1160
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Two controlled confinement studies lasting 105 and 205 days, totaling 10 men · source_derived_draft · unverified_draft
### sodium-salt-drinking Fluid intake was lower at 12 g/day salt in these long-duration controlled studies. Condition category: normal nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Long-term fluid behavior in this setting did not follow a simple more-salt–more-drinking rule. organism: Human healthy men tissue_or_cell_type: Whole-body water and osmolyte balance experimental_model: Two controlled confinement studies lasting 105 and 205 days, totaling 10 men limitations: Small all-male long-duration study; reduced free-water clearance is not creation of water. Do not extrapolate to acute salt ingestion, all populations or immune effects. exposure: 6, 9 and 12 g/day salt; other nutrients held constant evidence_span: {"source_cache": "artifacts/sodium-research/28414302.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "099d2bd468b387701a756371dde0732e2eba2b5d15d02948a99fc96c3df3046d", "start_char": 0, "end_char": 2118, "text_sha256": "099d2bd468b387701a756371dde0732e2eba2b5d15d02948a99fc96c3df3046d"} [sodium-p28414302] Increased salt consumption induces body water conservation and decreases fluid intake. (2017). https://pubmed.ncbi.nlm.nih.gov/28414302/ DOI: 10.1172/jci88530
Complete structured claim and evidence
Ouabain-sensitive extrusion was approximately three sodium ions per ATP hydrolyzed in resealed erythrocyte ghosts.
Sodium-potassium ATPase complexes → Sodium-pump-mediated sodium efflux source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
Sodium export couples to potassium-supported pump cycling and magnesium-dependent energy use.
experimental_model
Radiotracer sodium and ATP-hydrolysis assay.
limitations
This measurement does not itself establish an exact two-potassium ratio.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Human
plain_language
ATP consumption pays for sodium extrusion while potassium is available externally.
primary_references
[garrahan-1967-pump] The stoicheiometry of the sodium pump (1967). https://pmc.ncbi.nlm.nih.gov/articles/PMC1365482/ DOI: 10.1113/jphysiol.1967.sp008297
tissue_or_cell_type
Erythrocyte membrane
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 587–597
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Radiotracer sodium and ATP-hydrolysis assay. · source_derived_draft · unverified_draft
### k-pump-sodium-atp-coupling Ouabain-sensitive extrusion was approximately three sodium ions per ATP hydrolyzed in resealed erythrocyte ghosts. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: ATP consumption pays for sodium extrusion while potassium is available externally. organism: Human tissue_or_cell_type: Erythrocyte membrane experimental_model: Radiotracer sodium and ATP-hydrolysis assay. limitations: This measurement does not itself establish an exact two-potassium ratio. cross_nutrient: Sodium export couples to potassium-supported pump cycling and magnesium-dependent energy use. [garrahan-1967-pump] The stoicheiometry of the sodium pump (1967). https://pmc.ncbi.nlm.nih.gov/articles/PMC1365482/ DOI: 10.1113/jphysiol.1967.sp008297
Complete structured claim and evidence
Sodium-24 and potassium-42 experiments demonstrated ouabain-sensitive sodium efflux and potassium influx in human red cells.
Sodium-potassium ATPase complexes → Sodium-pump-mediated potassium influx source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
Magnesium-dependent ATP chemistry is coupled to sodium and potassium handling by the pump; serum magnesium is not the enzyme-site concentration.
experimental_model
Human red cells and resealed ghosts; ATP/Mg loading, ouabain, sodium-24, potassium-42 and gamma-phosphorus-32 ATP.
limitations
This experiment found unequal fluxes but did not itself measure an exact 3:2 ratio.
nutrient_topic
Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
organism
Homo sapiens
plain_language
The pump moves the two nutrient ions in opposite directions.
primary_references
[garrahan-1967-nka] The stoicheiometry of the sodium pump (1967). https://doi.org/10.1113/jphysiol.1967.sp008297 DOI: 10.1113/jphysiol.1967.sp008297
tissue_or_cell_type
Erythrocytes
transport_direction
Sodium outward; potassium inward.
Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 832–843
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human red cells and resealed ghosts; ATP/Mg loading, ouabain, sodium-24, potassium-42 and gamma-phosphorus-32 ATP. · source_derived_draft · unverified_draft
### mg-nka-isotope-opposed-flux Sodium-24 and potassium-42 experiments demonstrated ouabain-sensitive sodium efflux and potassium influx in human red cells. Condition category: normal nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The pump moves the two nutrient ions in opposite directions. organism: Homo sapiens tissue_or_cell_type: Erythrocytes experimental_model: Human red cells and resealed ghosts; ATP/Mg loading, ouabain, sodium-24, potassium-42 and gamma-phosphorus-32 ATP. limitations: This experiment found unequal fluxes but did not itself measure an exact 3:2 ratio. cross_nutrient: Magnesium-dependent ATP chemistry is coupled to sodium and potassium handling by the pump; serum magnesium is not the enzyme-site concentration. transport_direction: Sodium outward; potassium inward. [garrahan-1967-nka] The stoicheiometry of the sodium pump (1967). https://doi.org/10.1113/jphysiol.1967.sp008297 DOI: 10.1113/jphysiol.1967.sp008297
Complete structured claim and evidence
Pre-steady-state pig-kidney pump experiments identified Mg as an essential activator of ATP-dependent phosphorylation.
Mg2+ → Sodium-potassium ATPase phosphorylation source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
Magnesium-dependent ATP chemistry is coupled to sodium and potassium handling by the pump; serum magnesium is not the enzyme-site concentration.
experimental_model
Pig-kidney Na/K-ATPase rapid-mixing phosphorylation; Na-containing, K-free medium; varied ATP and MgCl2.
limitations
Na-containing, K-free assay; not the full physiological transport cycle.
nutrient_topic
Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
organism
Sus scrofa
plain_language
Magnesium enables the ATP-driven phosphate-transfer step of the sodium pump.
primary_references
[campos-1992-nka] Effects of magnesium and ATP on pre-steady-state phosphorylation kinetics of the Na+,K(+)-ATPase (1992). https://pubmed.ncbi.nlm.nih.gov/1314673/ DOI: 10.1016/0005-2736(92)90161-e
tissue_or_cell_type
Kidney enzyme
Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 771–781
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Pig-kidney Na/K-ATPase rapid-mixing phosphorylation; Na-containing, K-free medium; varied ATP and MgCl2. · source_derived_draft · unverified_draft
### mg-nka-phosphorylation-requirement Pre-steady-state pig-kidney pump experiments identified Mg as an essential activator of ATP-dependent phosphorylation. Condition category: normal nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Magnesium enables the ATP-driven phosphate-transfer step of the sodium pump. organism: Sus scrofa tissue_or_cell_type: Kidney enzyme experimental_model: Pig-kidney Na/K-ATPase rapid-mixing phosphorylation; Na-containing, K-free medium; varied ATP and MgCl2. limitations: Na-containing, K-free assay; not the full physiological transport cycle. cross_nutrient: Magnesium-dependent ATP chemistry is coupled to sodium and potassium handling by the pump; serum magnesium is not the enzyme-site concentration. [campos-1992-nka] Effects of magnesium and ATP on pre-steady-state phosphorylation kinetics of the Na+,K(+)-ATPase (1992). https://pubmed.ncbi.nlm.nih.gov/1314673/ DOI: 10.1016/0005-2736(92)90161-e
Complete structured claim and evidence
Adding KCl after ATP phosphorylation accelerated dephosphorylation of pig-kidney Na/K-ATPase.
Potassium ion → Sodium-potassium ATPase dephosphorylation source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
Magnesium-dependent ATP chemistry is coupled to sodium and potassium handling by the pump; serum magnesium is not the enzyme-site concentration.
experimental_model
Pig-kidney enzyme stopped-flow RH421 fluorescence; sequential ATP then KCl mixing.
limitations
Stopped-flow assay; no dietary or magnesium-depletion intervention.
nutrient_topic
Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
organism
Sus scrofa
plain_language
Potassium promotes the phosphate-removal part of the pump cycle.
primary_references
[kane-1998-nka] Dephosphorylation kinetics of pig kidney Na+,K+-ATPase (1998). https://pubmed.ncbi.nlm.nih.gov/9521778/ DOI: 10.1021/bi972813e
tissue_or_cell_type
Kidney enzyme
Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 807–817
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Pig-kidney enzyme stopped-flow RH421 fluorescence; sequential ATP then KCl mixing. · source_derived_draft · unverified_draft
### mg-nka-potassium-dephosphorylation Adding KCl after ATP phosphorylation accelerated dephosphorylation of pig-kidney Na/K-ATPase. Condition category: normal nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Potassium promotes the phosphate-removal part of the pump cycle. organism: Sus scrofa tissue_or_cell_type: Kidney enzyme experimental_model: Pig-kidney enzyme stopped-flow RH421 fluorescence; sequential ATP then KCl mixing. limitations: Stopped-flow assay; no dietary or magnesium-depletion intervention. cross_nutrient: Magnesium-dependent ATP chemistry is coupled to sodium and potassium handling by the pump; serum magnesium is not the enzyme-site concentration. [kane-1998-nka] Dephosphorylation kinetics of pig kidney Na+,K+-ATPase (1998). https://pubmed.ncbi.nlm.nih.gov/9521778/ DOI: 10.1021/bi972813e
Complete structured claim and evidence
Lowering bath K from 5.0 to 2.7 mM reduced ventricular pump current and increased intracellular sodium.
Extracellular potassium concentration → Sodium-potassium ATPase complexes source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
cross_nutrient
Low extracellular potassium compromises sodium extrusion.
experimental_model
Rat ventricular patch clamp/Na fluorescence.
limitations
Acute bath manipulation; not dietary depletion.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Rat
plain_language
With less extracellular potassium, sodium extrusion slowed.
primary_references
[aronsen-2015-cardiac] Hypokalaemia induces Ca2+ overload and Ca2+ waves in ventricular myocytes by reducing Na+,K+-ATPase alpha2 activity (2015). https://pmc.ncbi.nlm.nih.gov/articles/PMC4376427/ DOI: 10.1113/jphysiol.2014.279893
tissue_or_cell_type
Ventricular myocytes
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 610–620
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rat ventricular patch clamp/Na fluorescence. · source_derived_draft · unverified_draft
### k-low-cardiac-pump-current Lowering bath K from 5.0 to 2.7 mM reduced ventricular pump current and increased intracellular sodium. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: With less extracellular potassium, sodium extrusion slowed. organism: Rat tissue_or_cell_type: Ventricular myocytes experimental_model: Rat ventricular patch clamp/Na fluorescence. limitations: Acute bath manipulation; not dietary depletion. cross_nutrient: Low extracellular potassium compromises sodium extrusion. [aronsen-2015-cardiac] Hypokalaemia induces Ca2+ overload and Ca2+ waves in ventricular myocytes by reducing Na+,K+-ATPase alpha2 activity (2015). https://pmc.ncbi.nlm.nih.gov/articles/PMC4376427/ DOI: 10.1113/jphysiol.2014.279893
Complete structured claim and evidence
Pump inhibition during low-K exposure increased sodium sensed by NCX and favored cellular calcium loading.
Sodium-potassium ATPase complexes → Na+/Ca2+ exchanger 1 / SLC8A1 source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
cross_nutrient
Potassium-to-sodium-to-calcium coupling is experimentally supported; dietary effect magnitude is untested.
experimental_model
Rat ventricular ion assays plus modeling.
limitations
NCX microdomain interpretation; source ouabain units differ between methods and figure legends.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Rat
plain_language
Potassium-dependent sodium pumping helps the exchanger remove calcium.
primary_references
[aronsen-2015-cardiac] Hypokalaemia induces Ca2+ overload and Ca2+ waves in ventricular myocytes by reducing Na+,K+-ATPase alpha2 activity (2015). https://pmc.ncbi.nlm.nih.gov/articles/PMC4376427/ DOI: 10.1113/jphysiol.2014.279893
tissue_or_cell_type
Ventricular myocytes
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 622–632
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rat ventricular ion assays plus modeling. · source_derived_draft · unverified_draft
### k-low-cardiac-ncx-calcium Pump inhibition during low-K exposure increased sodium sensed by NCX and favored cellular calcium loading. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Potassium-dependent sodium pumping helps the exchanger remove calcium. organism: Rat tissue_or_cell_type: Ventricular myocytes experimental_model: Rat ventricular ion assays plus modeling. limitations: NCX microdomain interpretation; source ouabain units differ between methods and figure legends. cross_nutrient: Potassium-to-sodium-to-calcium coupling is experimentally supported; dietary effect magnitude is untested. [aronsen-2015-cardiac] Hypokalaemia induces Ca2+ overload and Ca2+ waves in ventricular myocytes by reducing Na+,K+-ATPase alpha2 activity (2015). https://pmc.ncbi.nlm.nih.gov/articles/PMC4376427/ DOI: 10.1113/jphysiol.2014.279893
Complete structured claim and evidence
Human cardiac NCX1 exchanges calcium and sodium in opposing directions across the membrane.
Na+/Ca2+ exchanger 1 / SLC8A1 → Calcium ion source_derived_draftungraded
Experimental context and source evidence
compartment_description
Plasma membrane
experimental_model
Human cardiac NCX1; cryo-EM and functional exchange assays
limitations
Net direction depends on electrochemical gradients and voltage; NCX1 is not an ATP-hydrolyzing pump.
nutrient_topic
Calcium research collection; topical membership is not evidence of a direct dietary effect. · Calcium
organism
Homo sapiens
plain_language
NCX1 couples calcium movement to sodium moving the other way.
primary_references
[ca-xue2023] Structural mechanisms of the human cardiac sodium-calcium exchanger NCX1 (2023). https://pubmed.ncbi.nlm.nih.gov/37794011/ DOI: 10.1038/s41467-023-41885-4
research_relationship_category
transport
tissue_or_cell_type
Cardiac NCX1 expression system
transport_effect
depends Reversible exchange: forward mode extrudes calcium and reverse mode admits it, which the record states.
transport_or_reaction_direction
Reversible Na+/Ca2+ exchange; forward calcium extrusion or reverse calcium entry
transport_pool
cytosolic calcium Reversible exchange: forward mode extrudes calcium and reverse mode admits it, which the record states.
Calcium: mechanism-first literature curation (2026-09-17) · lines 625–637
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human cardiac NCX1; cryo-EM and functional exchange assays · source_derived_draft · unverified_draft
### ca-ncx1-calcium-sodium-exchange Human cardiac NCX1 exchanges calcium and sodium in opposing directions across the membrane. Condition category: normal nutrient_topic: Calcium research collection; topical membership is not evidence of a direct dietary effect. plain_language: NCX1 couples calcium movement to sodium moving the other way. organism: Homo sapiens tissue_or_cell_type: Cardiac NCX1 expression system experimental_model: Human cardiac NCX1; cryo-EM and functional exchange assays limitations: Net direction depends on electrochemical gradients and voltage; NCX1 is not an ATP-hydrolyzing pump. research_relationship_category: transport transport_or_reaction_direction: Reversible Na+/Ca2+ exchange; forward calcium extrusion or reverse calcium entry compartment_description: Plasma membrane [ca-xue2023] Structural mechanisms of the human cardiac sodium-calcium exchanger NCX1 (2023). https://pubmed.ncbi.nlm.nih.gov/37794011/ DOI: 10.1038/s41467-023-41885-4
Complete structured claim and evidence
Sgk1 phosphorylated Nedd4-2 at Ser444 and less strongly Ser338 in Xenopus constructs.
Serum and glucocorticoid-regulated kinase 1 → NEDD4-like E3 ubiquitin protein ligase source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
This biochemical sodium-channel pathway contributes to the machinery for K handling.
evidence_location
Figure 2.
experimental_model
Expression, kinase-dead and site-mutant experiments
limitations
Residue numbers are construct/species-specific; nutritional K sensing was not tested.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Xenopus laevis
plain_language
SGK1 modifies the protein that normally restrains sodium channels.
primary_references
[debonneville-2001-sgk-nedd4] Phosphorylation of Nedd4-2 by Sgk1 regulates epithelial Na(+) channel cell surface expression (2001). https://pubmed.ncbi.nlm.nih.gov/11742982/ DOI: 10.1093/emboj/20.24.7052
tissue_or_cell_type
Oocytes
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 408–419
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Expression, kinase-dead and site-mutant experiments · source_derived_draft · unverified_draft
### renal-sgk1-phosphorylates-nedd4l Sgk1 phosphorylated Nedd4-2 at Ser444 and less strongly Ser338 in Xenopus constructs. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: SGK1 modifies the protein that normally restrains sodium channels. organism: Xenopus laevis tissue_or_cell_type: Oocytes experimental_model: Expression, kinase-dead and site-mutant experiments limitations: Residue numbers are construct/species-specific; nutritional K sensing was not tested. cross_nutrient: This biochemical sodium-channel pathway contributes to the machinery for K handling. evidence_location: Figure 2. [debonneville-2001-sgk-nedd4] Phosphorylation of Nedd4-2 by Sgk1 regulates epithelial Na(+) channel cell surface expression (2001). https://pubmed.ncbi.nlm.nih.gov/11742982/ DOI: 10.1093/emboj/20.24.7052
Complete structured claim and evidence
SGK-dependent Nedd4-2 phosphorylation reduced its ENaC interaction and increased ENaC surface expression in oocytes.
SGK-phosphorylated NEDD4L → ENaC surface abundance source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
Higher sodium-channel availability can support the secretory machinery used for K balance.
evidence_location
Figures 3-5; interaction and anti-FLAG surface-labeling experiments.
experimental_model
Oocyte binding, current and surface-labeling assays
limitations
Molecular sufficiency does not establish exclusive control in intact kidneys.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Xenopus laevis
plain_language
Phosphorylation weakens the sodium-channel removal signal, leaving more channels at the surface.
primary_references
[debonneville-2001-sgk-nedd4] Phosphorylation of Nedd4-2 by Sgk1 regulates epithelial Na(+) channel cell surface expression (2001). https://pubmed.ncbi.nlm.nih.gov/11742982/ DOI: 10.1093/emboj/20.24.7052
tissue_or_cell_type
Oocytes
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 421–432
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Oocyte binding, current and surface-labeling assays · source_derived_draft · unverified_draft
### renal-phospho-nedd4l-releases-enac SGK-dependent Nedd4-2 phosphorylation reduced its ENaC interaction and increased ENaC surface expression in oocytes. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Phosphorylation weakens the sodium-channel removal signal, leaving more channels at the surface. organism: Xenopus laevis tissue_or_cell_type: Oocytes experimental_model: Oocyte binding, current and surface-labeling assays limitations: Molecular sufficiency does not establish exclusive control in intact kidneys. cross_nutrient: Higher sodium-channel availability can support the secretory machinery used for K balance. evidence_location: Figures 3-5; interaction and anti-FLAG surface-labeling experiments. [debonneville-2001-sgk-nedd4] Phosphorylation of Nedd4-2 by Sgk1 regulates epithelial Na(+) channel cell surface expression (2001). https://pubmed.ncbi.nlm.nih.gov/11742982/ DOI: 10.1093/emboj/20.24.7052
Complete structured claim and evidence
Benzamil inhibition of sodium absorption abolished the flow-stimulated increase in K secretion in rabbit CCDs.
Epithelial sodium channel → Distal renal potassium secretion source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
Sodium transport through ENaC supports potassium secretion.
evidence_location
Figure 7 and associated Results.
experimental_model
Benzamil pretreatment and flow increase
limitations
Other species/segments can show ENaC-independent components; no universal requirement claimed.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Oryctolagus cuniculus
plain_language
Sodium entry through ENaC supports potassium secretion in this perfused segment.
primary_references
[liu-2007-calcium-flow] Ca2+ dependence of flow-stimulated K secretion in the mammalian cortical collecting duct (2007). https://journals.physiology.org/doi/10.1152/ajprenal.00057.2007 DOI: 10.1152/ajprenal.00057.2007
tissue_or_cell_type
Cortical collecting duct
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 382–393
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Benzamil pretreatment and flow increase · source_derived_draft · unverified_draft
### renal-enac-supports-rabbit-flow-k-secretion Benzamil inhibition of sodium absorption abolished the flow-stimulated increase in K secretion in rabbit CCDs. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Sodium entry through ENaC supports potassium secretion in this perfused segment. organism: Oryctolagus cuniculus tissue_or_cell_type: Cortical collecting duct experimental_model: Benzamil pretreatment and flow increase limitations: Other species/segments can show ENaC-independent components; no universal requirement claimed. cross_nutrient: Sodium transport through ENaC supports potassium secretion. evidence_location: Figure 7 and associated Results. [liu-2007-calcium-flow] Ca2+ dependence of flow-stimulated K secretion in the mammalian cortical collecting duct (2007). https://journals.physiology.org/doi/10.1152/ajprenal.00057.2007 DOI: 10.1152/ajprenal.00057.2007
Complete structured claim and evidence
Cloned renal NKCC2 supported bumetanide-sensitive sodium-potassium-chloride cotransport in oocytes, distinct from NCC potassium-independent NaCl transport.
Sodium-potassium-chloride cotransporter 2 → NKCC2-mediated ion influx source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
Potassium is a transported participant in this sodium/chloride entry mechanism.
evidence_location
Primary abstract; functional oocyte characterization.
experimental_model
Cloned renal cotransporter expression
limitations
Transport identity, not a dietary deficiency threshold; individual splice variants are not generalized.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Mammalian proteins in Xenopus laevis oocytes
plain_language
NKCC2 moves potassium together with sodium and chloride; the related NCC transporter does not require potassium as cargo.
primary_references
[gamba-1994-nkcc2] Molecular cloning, primary structure, and characterization of two members of the mammalian electroneutral sodium-(potassium)-chloride cotransporter family expressed in kidney (1994). https://www.sciencedirect.com/science/article/pii/S0021925817324997 DOI: 10.1016/S0021-9258(17)32499-7
tissue_or_cell_type
Heterologous cell membrane
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 548–559
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cloned renal cotransporter expression · source_derived_draft · unverified_draft
### renal-nkcc2-couples-potassium-to-salt-influx Cloned renal NKCC2 supported bumetanide-sensitive sodium-potassium-chloride cotransport in oocytes, distinct from NCC potassium-independent NaCl transport. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: NKCC2 moves potassium together with sodium and chloride; the related NCC transporter does not require potassium as cargo. organism: Mammalian proteins in Xenopus laevis oocytes tissue_or_cell_type: Heterologous cell membrane experimental_model: Cloned renal cotransporter expression limitations: Transport identity, not a dietary deficiency threshold; individual splice variants are not generalized. cross_nutrient: Potassium is a transported participant in this sodium/chloride entry mechanism. evidence_location: Primary abstract; functional oocyte characterization. [gamba-1994-nkcc2] Molecular cloning, primary structure, and characterization of two members of the mammalian electroneutral sodium-(potassium)-chloride cotransporter family expressed in kidney (1994). https://www.sciencedirect.com/science/article/pii/S0021925817324997 DOI: 10.1016/S0021-9258(17)32499-7
Complete structured claim and evidence
Low-potassium feeding on high salt reduced sodium excretion; NCC deletion blunted the blood-pressure response.
Thiazide-sensitive sodium-chloride cotransporter → Renal sodium reabsorption source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
cross_nutrient
Potassium restriction changes sodium handling through NCC.
evidence_location
Figure 2A-C.
experimental_model
Wild-type versus Slc12a3-null dietary study
limitations
Knockout tests pathway contribution, not exclusive control of pressure.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Mus musculus
plain_language
Potassium scarcity can make sodium retention easier through NCC.
primary_references
[terker-2015-k-voltage-chloride] Potassium Modulates Electrolyte Balance and Blood Pressure through Effects on Distal Cell Voltage and Chloride (2015). https://pmc.ncbi.nlm.nih.gov/articles/PMC4332769/ DOI: 10.1016/j.cmet.2014.12.006
tissue_or_cell_type
Kidney
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 112–123
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Wild-type versus Slc12a3-null dietary study · source_derived_draft · unverified_draft
### renal-low-k-ncc-salt-retention Low-potassium feeding on high salt reduced sodium excretion; NCC deletion blunted the blood-pressure response. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Potassium scarcity can make sodium retention easier through NCC. organism: Mus musculus tissue_or_cell_type: Kidney experimental_model: Wild-type versus Slc12a3-null dietary study limitations: Knockout tests pathway contribution, not exclusive control of pressure. cross_nutrient: Potassium restriction changes sodium handling through NCC. evidence_location: Figure 2A-C. [terker-2015-k-voltage-chloride] Potassium Modulates Electrolyte Balance and Blood Pressure through Effects on Distal Cell Voltage and Chloride (2015). https://pmc.ncbi.nlm.nih.gov/articles/PMC4332769/ DOI: 10.1016/j.cmet.2014.12.006
Complete structured claim and evidence
OSR1 phosphorylated human NCC at Thr46, Thr55 and Thr60; Thr60 mutation impaired chloride-depletion-induced NCC activation.
Oxidative stress responsive kinase 1 → Thiazide-sensitive sodium-chloride cotransporter source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
Defines the sodium/chloride transporter step of the potassium switch.
evidence_location
Primary abstract; phosphosite mapping, docking and Thr60Ala assays.
experimental_model
Recombinant phosphosite mapping and cell mutants
limitations
The dietary K response was not tested in this experiment.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Human protein; HEK293/mpkDCT cells
plain_language
A kinase modifies the sodium-chloride transporter at regulatory sites.
primary_references
[richardson-2008-spak-osr1-ncc] Activation of the thiazide-sensitive Na+-Cl- cotransporter by the WNK-regulated kinases SPAK and OSR1 (2008). https://pubmed.ncbi.nlm.nih.gov/18270262/ DOI: 10.1242/jcs.025312
tissue_or_cell_type
Biochemical assay and cultured kidney-derived cells
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 177–188
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant phosphosite mapping and cell mutants · source_derived_draft · unverified_draft
### renal-oxsr1-phosphorylates-ncc OSR1 phosphorylated human NCC at Thr46, Thr55 and Thr60; Thr60 mutation impaired chloride-depletion-induced NCC activation. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A kinase modifies the sodium-chloride transporter at regulatory sites. organism: Human protein; HEK293/mpkDCT cells tissue_or_cell_type: Biochemical assay and cultured kidney-derived cells experimental_model: Recombinant phosphosite mapping and cell mutants limitations: The dietary K response was not tested in this experiment. cross_nutrient: Defines the sodium/chloride transporter step of the potassium switch. evidence_location: Primary abstract; phosphosite mapping, docking and Thr60Ala assays. [richardson-2008-spak-osr1-ncc] Activation of the thiazide-sensitive Na+-Cl- cotransporter by the WNK-regulated kinases SPAK and OSR1 (2008). https://pubmed.ncbi.nlm.nih.gov/18270262/ DOI: 10.1242/jcs.025312
Complete structured claim and evidence
SPAK phosphorylated human NCC at Thr46, Thr55 and Thr60; Thr60 mutation impaired chloride-depletion-induced NCC activation.
STE20/SPS1-related proline/alanine-rich kinase → Thiazide-sensitive sodium-chloride cotransporter source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
Defines the sodium/chloride transporter step of the potassium switch.
evidence_location
Primary abstract; phosphosite mapping, docking and Thr60Ala assays.
experimental_model
Recombinant phosphosite mapping and cell mutants
limitations
The dietary K response was not tested in this experiment.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Human protein; HEK293/mpkDCT cells
plain_language
A kinase modifies the sodium-chloride transporter at regulatory sites.
primary_references
[richardson-2008-spak-osr1-ncc] Activation of the thiazide-sensitive Na+-Cl- cotransporter by the WNK-regulated kinases SPAK and OSR1 (2008). https://pubmed.ncbi.nlm.nih.gov/18270262/ DOI: 10.1242/jcs.025312
tissue_or_cell_type
Biochemical assay and cultured kidney-derived cells
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 164–175
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant phosphosite mapping and cell mutants · source_derived_draft · unverified_draft
### renal-stk39-phosphorylates-ncc SPAK phosphorylated human NCC at Thr46, Thr55 and Thr60; Thr60 mutation impaired chloride-depletion-induced NCC activation. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A kinase modifies the sodium-chloride transporter at regulatory sites. organism: Human protein; HEK293/mpkDCT cells tissue_or_cell_type: Biochemical assay and cultured kidney-derived cells experimental_model: Recombinant phosphosite mapping and cell mutants limitations: The dietary K response was not tested in this experiment. cross_nutrient: Defines the sodium/chloride transporter step of the potassium switch. evidence_location: Primary abstract; phosphosite mapping, docking and Thr60Ala assays. [richardson-2008-spak-osr1-ncc] Activation of the thiazide-sensitive Na+-Cl- cotransporter by the WNK-regulated kinases SPAK and OSR1 (2008). https://pubmed.ncbi.nlm.nih.gov/18270262/ DOI: 10.1242/jcs.025312
Complete structured claim and evidence
Adding luminal choline chloride or RbCl reduced renin release, whereas the tested sodium salts without chloride did not.
Chloride ion → Juxtaglomerular renin secretion source_derived_draftungraded
Experimental context and source evidence
evidence_span
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experimental_model
Perfused isolated juxtaglomerular apparatus
exposure
Luminal ion substitutions and 1 µM bumetanide
limitations
Tubular luminal signal; plasma chloride alone does not reproduce it.
nutrient_topic
Chloride research collection; topical membership is not evidence of a direct dietary effect. · Chloride
organism
Rabbit
plain_language
The kidney’s salt sensor responded specifically to chloride delivery in this experiment.
primary_references
[chloride-p2012204] Renin release from isolated juxtaglomerular apparatus depends on macula densa chloride transport. (1991). https://pubmed.ncbi.nlm.nih.gov/2012204/ DOI: 10.1152/ajprenal.1991.260.4.f486
tissue_or_cell_type
Macula densa and renin-secreting apparatus
Chloride: transport, acid-base balance, nutrient interactions and loss states (2026-09-17) · lines 562–573
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Perfused isolated juxtaglomerular apparatus · source_derived_draft · unverified_draft
### chloride-macula-chloride-renin Adding luminal choline chloride or RbCl reduced renin release, whereas the tested sodium salts without chloride did not. Condition category: normal nutrient_topic: Chloride research collection; topical membership is not evidence of a direct dietary effect. plain_language: The kidney’s salt sensor responded specifically to chloride delivery in this experiment. organism: Rabbit tissue_or_cell_type: Macula densa and renin-secreting apparatus experimental_model: Perfused isolated juxtaglomerular apparatus limitations: Tubular luminal signal; plasma chloride alone does not reproduce it. exposure: Luminal ion substitutions and 1 µM bumetanide evidence_span: {"source_cache": "artifacts/chloride-research/2012204.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8ce0dd9b0315d2f3148f4edcc7d2e511984122ac2d50fa813a03e9b473b73dac", "start_char": 0, "end_char": 1695, "text_sha256": "8ce0dd9b0315d2f3148f4edcc7d2e511984122ac2d50fa813a03e9b473b73dac"} [chloride-p2012204] Renin release from isolated juxtaglomerular apparatus depends on macula densa chloride transport. (1991). https://pubmed.ncbi.nlm.nih.gov/2012204/ DOI: 10.1152/ajprenal.1991.260.4.f486
Complete structured claim and evidence
Luminal bumetanide increased renin release during high-NaCl perfusion, supporting cotransporter-dependent sensing.
Sodium-potassium-chloride cotransporter 2 → Juxtaglomerular renin secretion source_derived_draftungraded
Experimental context and source evidence
evidence_span
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experimental_model
Perfused isolated juxtaglomerular apparatus
exposure
Luminal ion substitutions and 1 µM bumetanide
limitations
Pharmacological evidence for macula-densa Na-K-2Cl transport; molecular NKCC2 was not genetically tested in this experiment.
nutrient_topic
Chloride research collection; topical membership is not evidence of a direct dietary effect. · Chloride
organism
Rabbit
plain_language
The chloride must engage the transport system to produce the usual signal.
primary_references
[chloride-p2012204] Renin release from isolated juxtaglomerular apparatus depends on macula densa chloride transport. (1991). https://pubmed.ncbi.nlm.nih.gov/2012204/ DOI: 10.1152/ajprenal.1991.260.4.f486
tissue_or_cell_type
Macula densa and renin-secreting apparatus
Chloride: transport, acid-base balance, nutrient interactions and loss states (2026-09-17) · lines 575–586
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Perfused isolated juxtaglomerular apparatus · source_derived_draft · unverified_draft
### chloride-macula-transport-renin Luminal bumetanide increased renin release during high-NaCl perfusion, supporting cotransporter-dependent sensing. Condition category: normal nutrient_topic: Chloride research collection; topical membership is not evidence of a direct dietary effect. plain_language: The chloride must engage the transport system to produce the usual signal. organism: Rabbit tissue_or_cell_type: Macula densa and renin-secreting apparatus experimental_model: Perfused isolated juxtaglomerular apparatus limitations: Pharmacological evidence for macula-densa Na-K-2Cl transport; molecular NKCC2 was not genetically tested in this experiment. exposure: Luminal ion substitutions and 1 µM bumetanide evidence_span: {"source_cache": "artifacts/chloride-research/2012204.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8ce0dd9b0315d2f3148f4edcc7d2e511984122ac2d50fa813a03e9b473b73dac", "start_char": 0, "end_char": 1695, "text_sha256": "8ce0dd9b0315d2f3148f4edcc7d2e511984122ac2d50fa813a03e9b473b73dac"} [chloride-p2012204] Renin release from isolated juxtaglomerular apparatus depends on macula densa chloride transport. (1991). https://pubmed.ncbi.nlm.nih.gov/2012204/ DOI: 10.1152/ajprenal.1991.260.4.f486
Complete structured claim and evidence
Slc4a8 deletion abolished the thiazide-sensitive NaCl absorption measured in cortical collecting ducts.
Mouse sodium-driven chloride/bicarbonate exchanger / Slc4a8 → Renal sodium reabsorption source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/chloride-research/20389022.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e38f38d6be0ba6db309bcc35de163f9dd6db62963c41864ca0b7fe6c24a31ddb", "start_char": 0, "end_char": 1550, "text_sha256": "e38f38d6be0ba6db309bcc35de163f9dd6db62963c41864ca0b7fe6c24a31ddb"}
experimental_model
Gene deletion and perfused collecting ducts
exposure
Slc4a8, NCC and ENaC perturbations
limitations
Mouse electroneutral transport; thiazide sensitivity alone does not identify NCC.
nutrient_topic
Chloride research collection; topical membership is not evidence of a direct dietary effect. · Chloride
organism
Mouse
plain_language
Sodium and chloride can be reabsorbed through a coupled exchanger system beyond NCC.
primary_references
[chloride-p20389022] The Na+-dependent chloride-bicarbonate exchanger SLC4A8 mediates an electroneutral Na+ reabsorption process in the renal cortical collecting ducts of mice. (2010). https://pubmed.ncbi.nlm.nih.gov/20389022/ DOI: 10.1172/jci40145
tissue_or_cell_type
Cortical collecting duct
Chloride: transport, acid-base balance, nutrient interactions and loss states (2026-09-17) · lines 536–547
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Gene deletion and perfused collecting ducts · source_derived_draft · unverified_draft
### chloride-ndcbe-sodium Slc4a8 deletion abolished the thiazide-sensitive NaCl absorption measured in cortical collecting ducts. Condition category: normal nutrient_topic: Chloride research collection; topical membership is not evidence of a direct dietary effect. plain_language: Sodium and chloride can be reabsorbed through a coupled exchanger system beyond NCC. organism: Mouse tissue_or_cell_type: Cortical collecting duct experimental_model: Gene deletion and perfused collecting ducts limitations: Mouse electroneutral transport; thiazide sensitivity alone does not identify NCC. exposure: Slc4a8, NCC and ENaC perturbations evidence_span: {"source_cache": "artifacts/chloride-research/20389022.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e38f38d6be0ba6db309bcc35de163f9dd6db62963c41864ca0b7fe6c24a31ddb", "start_char": 0, "end_char": 1550, "text_sha256": "e38f38d6be0ba6db309bcc35de163f9dd6db62963c41864ca0b7fe6c24a31ddb"} [chloride-p20389022] The Na+-dependent chloride-bicarbonate exchanger SLC4A8 mediates an electroneutral Na+ reabsorption process in the renal cortical collecting ducts of mice. (2010). https://pubmed.ncbi.nlm.nih.gov/20389022/ DOI: 10.1172/jci40145
Complete structured claim and evidence
Rat SVCT1 expressed in Xenopus oocytes mediated stereospecific, concentrative uptake of reduced L-ascorbate driven by the sodium electrochemical gradient.
Rat sodium-dependent vitamin C transporter 1 / Slc23a1 → L-Ascorbate source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
true
experimental_model
Rat cDNA transporters expressed in Xenopus oocytes; mammalian tissue distribution
exposure
Heterologous cDNA expression and uptake assays
limitations
Primary abstract only; no inferred human kinetic constants.
nutrient_topic
Vitamin C research collection; topical membership is not evidence of a direct dietary effect. · Vitamin C
organism
Rattus norvegicus protein in Xenopus laevis
plain_language
SVCT1 uses a sodium gradient to bring reduced vitamin C into cells.
primary_references
[tsukaguchi1999] A family of mammalian Na+-dependent L-ascorbic acid transporters. (1999). https://pubmed.ncbi.nlm.nih.gov/10331392/ DOI: 10.1038/19986
tissue_or_cell_type
Oocyte plasma membrane
transport_effect
raises Stereospecific concentrative uptake driven by the sodium electrochemical gradient.
transport_pool
the expressing cell Stereospecific concentrative uptake driven by the sodium electrochemical gradient.
Vitamin C: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 104–115
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rat cDNA transporters expressed in Xenopus oocytes; mammalian tissue distribution · source_derived_draft · unverified_draft
### vc-transport-svct1-uptake Rat SVCT1 expressed in Xenopus oocytes mediated stereospecific, concentrative uptake of reduced L-ascorbate driven by the sodium electrochemical gradient. Condition category: normal nutrient_topic: Vitamin C research collection; topical membership is not evidence of a direct dietary effect. plain_language: SVCT1 uses a sodium gradient to bring reduced vitamin C into cells. organism: Rattus norvegicus protein in Xenopus laevis tissue_or_cell_type: Oocyte plasma membrane experimental_model: Rat cDNA transporters expressed in Xenopus oocytes; mammalian tissue distribution limitations: Primary abstract only; no inferred human kinetic constants. exposure: Heterologous cDNA expression and uptake assays cross_nutrient: true [tsukaguchi1999] A family of mammalian Na+-dependent L-ascorbic acid transporters. (1999). https://pubmed.ncbi.nlm.nih.gov/10331392/ DOI: 10.1038/19986
Complete structured claim and evidence
Rat SVCT2 expressed in Xenopus oocytes mediated stereospecific, concentrative uptake of reduced L-ascorbate driven by the sodium electrochemical gradient.
Rat sodium-dependent vitamin C transporter 2 / Slc23a2 → L-Ascorbate source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
true
experimental_model
Rat cDNA transporters expressed in Xenopus oocytes; mammalian tissue distribution
exposure
Heterologous cDNA expression and uptake assays
limitations
Primary abstract only; no inferred human kinetic constants.
nutrient_topic
Vitamin C research collection; topical membership is not evidence of a direct dietary effect. · Vitamin C
organism
Rattus norvegicus protein in Xenopus laevis
plain_language
SVCT2 uses a sodium gradient to bring reduced vitamin C into cells.
primary_references
[tsukaguchi1999] A family of mammalian Na+-dependent L-ascorbic acid transporters. (1999). https://pubmed.ncbi.nlm.nih.gov/10331392/ DOI: 10.1038/19986
tissue_or_cell_type
Oocyte plasma membrane
transport_effect
raises Stereospecific concentrative uptake driven by the sodium electrochemical gradient.
transport_pool
the expressing cell Stereospecific concentrative uptake driven by the sodium electrochemical gradient.
Vitamin C: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 117–128
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rat cDNA transporters expressed in Xenopus oocytes; mammalian tissue distribution · source_derived_draft · unverified_draft
### vc-transport-svct2-uptake Rat SVCT2 expressed in Xenopus oocytes mediated stereospecific, concentrative uptake of reduced L-ascorbate driven by the sodium electrochemical gradient. Condition category: normal nutrient_topic: Vitamin C research collection; topical membership is not evidence of a direct dietary effect. plain_language: SVCT2 uses a sodium gradient to bring reduced vitamin C into cells. organism: Rattus norvegicus protein in Xenopus laevis tissue_or_cell_type: Oocyte plasma membrane experimental_model: Rat cDNA transporters expressed in Xenopus oocytes; mammalian tissue distribution limitations: Primary abstract only; no inferred human kinetic constants. exposure: Heterologous cDNA expression and uptake assays cross_nutrient: true [tsukaguchi1999] A family of mammalian Na+-dependent L-ascorbic acid transporters. (1999). https://pubmed.ncbi.nlm.nih.gov/10331392/ DOI: 10.1038/19986
Complete structured claim and evidence
Slc23a1 deletion raised renal ascorbate fractional excretion about 16–18-fold in female mice and 6–7-fold in males; female reabsorption was essentially abolished.
Mouse Slc23a1 gene → Renal ascorbate fractional excretion source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
cross_nutrient
false
experimental_model
Slc23a1 knockout mice and wild-type controls
exposure
Slc23a1 knockout versus wild type
limitations
Sex-specific renal clearances; inulin clearance was unchanged. This is transporter loss, not low intake.
nutrient_topic
Vitamin C research collection; topical membership is not evidence of a direct dietary effect. · Vitamin C
organism
Mus musculus
plain_language
Removing SVCT1 made mice lose more filtered vitamin C in urine.
primary_references
[corpe2010] Vitamin C transporter Slc23a1 links renal reabsorption, vitamin C tissue accumulation, and perinatal survival in mice. (2010). https://pubmed.ncbi.nlm.nih.gov/20200446/ DOI: 10.1172/jci39191
tissue_or_cell_type
Kidney
trigger_kind
machinery_impairment Imported condition classification; unverified.
Vitamin C: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 143–154
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Slc23a1 knockout mice and wild-type controls · source_derived_draft · unverified_draft
### vc-transport-svct1-renal-loss Slc23a1 deletion raised renal ascorbate fractional excretion about 16–18-fold in female mice and 6–7-fold in males; female reabsorption was essentially abolished. Condition category: machinery_impairment nutrient_topic: Vitamin C research collection; topical membership is not evidence of a direct dietary effect. plain_language: Removing SVCT1 made mice lose more filtered vitamin C in urine. organism: Mus musculus tissue_or_cell_type: Kidney experimental_model: Slc23a1 knockout mice and wild-type controls limitations: Sex-specific renal clearances; inulin clearance was unchanged. This is transporter loss, not low intake. exposure: Slc23a1 knockout versus wild type cross_nutrient: false [corpe2010] Vitamin C transporter Slc23a1 links renal reabsorption, vitamin C tissue accumulation, and perinatal survival in mice. (2010). https://pubmed.ncbi.nlm.nih.gov/20200446/ DOI: 10.1172/jci39191
Complete structured claim and evidence
Rat NIS expressed in Xenopus oocytes transported iodide with two sodium ions per anion and generated inward electrogenic transport.
Rat sodium/iodide symporter / Slc5a5 → NIS sodium-iodide cotransport source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
true
experimental_model
Rat NIS expressed in Xenopus laevis oocytes; electrophysiology and tracer uptake
exposure
Tracer uptake and electrophysiology; apparent sodium affinity 28 ± 3 mM and iodide affinity 33 ± 9 micromolar.
limitations
Rat-protein assay parameters are not dietary sodium requirements or human iodide thresholds.
nutrient_topic
Iodine research collection; topical membership is not evidence of a direct dietary effect. · Iodine
organism
Rat protein in Xenopus laevis oocytes
plain_language
NIS uses sodium movement to carry iodide into cells.
primary_references
[iodine-trans-stoichiometry1997] Thyroid Na+/I- symporter. Mechanism, stoichiometry, and specificity. (1997). https://pubmed.ncbi.nlm.nih.gov/9341168/ DOI: 10.1074/jbc.272.43.27230
tissue_or_cell_type
Oocyte plasma membrane
Iodine: thyroid hormone production, deficiency, excess and nutrient interactions (2026-09-17) · lines 167–178
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rat NIS expressed in Xenopus laevis oocytes; electrophysiology and tracer uptake · source_derived_draft · unverified_draft
### iodine-trans-sodium-coupling Rat NIS expressed in Xenopus oocytes transported iodide with two sodium ions per anion and generated inward electrogenic transport. Condition category: normal nutrient_topic: Iodine research collection; topical membership is not evidence of a direct dietary effect. plain_language: NIS uses sodium movement to carry iodide into cells. organism: Rat protein in Xenopus laevis oocytes tissue_or_cell_type: Oocyte plasma membrane experimental_model: Rat NIS expressed in Xenopus laevis oocytes; electrophysiology and tracer uptake limitations: Rat-protein assay parameters are not dietary sodium requirements or human iodide thresholds. exposure: Tracer uptake and electrophysiology; apparent sodium affinity 28 ± 3 mM and iodide affinity 33 ± 9 micromolar. cross_nutrient: true [iodine-trans-stoichiometry1997] Thyroid Na+/I- symporter. Mechanism, stoichiometry, and specificity. (1997). https://pubmed.ncbi.nlm.nih.gov/9341168/ DOI: 10.1074/jbc.272.43.27230
Complete structured claim and evidence
Thermodynamic fits to rat IEC-6 NIS transport data estimated an iodide Kd of 224 micromolar without sodium binding and 22.4 micromolar in the sodium-bound state.
Sodium ion → NIS affinity for iodide source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
true
experimental_model
Endogenous rat NIS in IEC-6 intestinal epithelial cells; initial-rate transport and statistical thermodynamic fitting
exposure
Initial-rate iodide uptake at 5, 10, 20 or 60 micromolar iodide with 0–260 mM sodium; two-minute incubations; constant osmolarity.
limitations
Kd values depend on the authors’ transport model; the finding does not show that eating extra salt improves iodine status.
nutrient_topic
Iodine research collection; topical membership is not evidence of a direct dietary effect. · Iodine
organism
Rattus norvegicus
plain_language
Sodium binding makes NIS bind iodide more readily.
primary_references
[iodine-trans-sodium-affinity2014] Physiological sodium concentrations enhance the iodide affinity of the Na+/I- symporter. (2014). https://pubmed.ncbi.nlm.nih.gov/24888603/ DOI: 10.1038/ncomms4948
tissue_or_cell_type
IEC-6 intestinal epithelial cells
Iodine: thyroid hormone production, deficiency, excess and nutrient interactions (2026-09-17) · lines 180–191
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Endogenous rat NIS in IEC-6 intestinal epithelial cells; initial-rate transport and statistical thermodynamic fitting · source_derived_draft · unverified_draft
### iodine-trans-sodium-affinity Thermodynamic fits to rat IEC-6 NIS transport data estimated an iodide Kd of 224 micromolar without sodium binding and 22.4 micromolar in the sodium-bound state. Condition category: normal nutrient_topic: Iodine research collection; topical membership is not evidence of a direct dietary effect. plain_language: Sodium binding makes NIS bind iodide more readily. organism: Rattus norvegicus tissue_or_cell_type: IEC-6 intestinal epithelial cells experimental_model: Endogenous rat NIS in IEC-6 intestinal epithelial cells; initial-rate transport and statistical thermodynamic fitting limitations: Kd values depend on the authors’ transport model; the finding does not show that eating extra salt improves iodine status. exposure: Initial-rate iodide uptake at 5, 10, 20 or 60 micromolar iodide with 0–260 mM sodium; two-minute incubations; constant osmolarity. cross_nutrient: true [iodine-trans-sodium-affinity2014] Physiological sodium concentrations enhance the iodide affinity of the Na+/I- symporter. (2014). https://pubmed.ncbi.nlm.nih.gov/24888603/ DOI: 10.1038/ncomms4948
Complete structured claim and evidence
Expression of cloned human SLC5A6 in HRPE cells conferred sodium-dependent uptake of biotin.
Human sodium-dependent multivitamin transporter / SLC5A6 → Cellular biotin uptake source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
true
experimental_model
Human SMVT cloned from JAR cells, expressed in human retinal pigment epithelial cells and Xenopus laevis oocytes
exposure
Human SMVT cDNA expression; substrate concentrations not specified in the abstract.
limitations
Heterologous human-protein experiments establish transport properties; they do not quantify whole-body absorption or nutrient deficiency from supplement competition.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens (protein and HRPE expression cells)
plain_language
SMVT carries biotin into cells using sodium-dependent transport.
primary_references
[b5-trans-wang1999] Human placental Na+-dependent multivitamin transporter. Cloning, functional expression, gene structure, and chromosomal localization. (1999). https://pubmed.ncbi.nlm.nih.gov/10329687/ DOI: 10.1074/jbc.274.21.14875
tissue_or_cell_type
HRPE cell plasma membrane
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 171–182
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human SMVT cloned from JAR cells, expressed in human retinal pigment epithelial cells and Xenopus laevis oocytes · source_derived_draft · unverified_draft
### b5-trans-smvt-biotin Expression of cloned human SLC5A6 in HRPE cells conferred sodium-dependent uptake of biotin. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: SMVT carries biotin into cells using sodium-dependent transport. organism: Homo sapiens (protein and HRPE expression cells) tissue_or_cell_type: HRPE cell plasma membrane experimental_model: Human SMVT cloned from JAR cells, expressed in human retinal pigment epithelial cells and Xenopus laevis oocytes limitations: Heterologous human-protein experiments establish transport properties; they do not quantify whole-body absorption or nutrient deficiency from supplement competition. exposure: Human SMVT cDNA expression; substrate concentrations not specified in the abstract. cross_nutrient: true [b5-trans-wang1999] Human placental Na+-dependent multivitamin transporter. Cloning, functional expression, gene structure, and chromosomal localization. (1999). https://pubmed.ncbi.nlm.nih.gov/10329687/ DOI: 10.1074/jbc.274.21.14875
Complete structured claim and evidence
Expression of cloned human SLC5A6 in HRPE cells conferred sodium-dependent uptake of lipoate.
Human sodium-dependent multivitamin transporter / SLC5A6 → Cellular free lipoate uptake source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
true
experimental_model
Human SMVT cloned from JAR cells, expressed in human retinal pigment epithelial cells and Xenopus laevis oocytes
exposure
Human SMVT cDNA expression; substrate concentrations not specified in the abstract.
limitations
Heterologous human-protein experiments establish transport properties; they do not quantify whole-body absorption or nutrient deficiency from supplement competition.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens (protein and HRPE expression cells)
plain_language
SMVT carries lipoate into cells using sodium-dependent transport.
primary_references
[b5-trans-wang1999] Human placental Na+-dependent multivitamin transporter. Cloning, functional expression, gene structure, and chromosomal localization. (1999). https://pubmed.ncbi.nlm.nih.gov/10329687/ DOI: 10.1074/jbc.274.21.14875
tissue_or_cell_type
HRPE cell plasma membrane
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 184–195
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human SMVT cloned from JAR cells, expressed in human retinal pigment epithelial cells and Xenopus laevis oocytes · source_derived_draft · unverified_draft
### b5-trans-smvt-lipoate Expression of cloned human SLC5A6 in HRPE cells conferred sodium-dependent uptake of lipoate. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: SMVT carries lipoate into cells using sodium-dependent transport. organism: Homo sapiens (protein and HRPE expression cells) tissue_or_cell_type: HRPE cell plasma membrane experimental_model: Human SMVT cloned from JAR cells, expressed in human retinal pigment epithelial cells and Xenopus laevis oocytes limitations: Heterologous human-protein experiments establish transport properties; they do not quantify whole-body absorption or nutrient deficiency from supplement competition. exposure: Human SMVT cDNA expression; substrate concentrations not specified in the abstract. cross_nutrient: true [b5-trans-wang1999] Human placental Na+-dependent multivitamin transporter. Cloning, functional expression, gene structure, and chromosomal localization. (1999). https://pubmed.ncbi.nlm.nih.gov/10329687/ DOI: 10.1074/jbc.274.21.14875
Complete structured claim and evidence
Expression of cloned human SLC5A6 in HRPE cells conferred sodium-dependent uptake of pantothenate.
Human sodium-dependent multivitamin transporter / SLC5A6 → Cellular pantothenate uptake source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
true
experimental_model
Human SMVT cloned from JAR cells, expressed in human retinal pigment epithelial cells and Xenopus laevis oocytes
exposure
Human SMVT cDNA expression; substrate concentrations not specified in the abstract.
limitations
Heterologous human-protein experiments establish transport properties; they do not quantify whole-body absorption or nutrient deficiency from supplement competition.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens (protein and HRPE expression cells)
plain_language
SMVT carries pantothenate into cells using sodium-dependent transport.
primary_references
[b5-trans-wang1999] Human placental Na+-dependent multivitamin transporter. Cloning, functional expression, gene structure, and chromosomal localization. (1999). https://pubmed.ncbi.nlm.nih.gov/10329687/ DOI: 10.1074/jbc.274.21.14875
tissue_or_cell_type
HRPE cell plasma membrane
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 158–169
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human SMVT cloned from JAR cells, expressed in human retinal pigment epithelial cells and Xenopus laevis oocytes · source_derived_draft · unverified_draft
### b5-trans-smvt-pantothenate Expression of cloned human SLC5A6 in HRPE cells conferred sodium-dependent uptake of pantothenate. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: SMVT carries pantothenate into cells using sodium-dependent transport. organism: Homo sapiens (protein and HRPE expression cells) tissue_or_cell_type: HRPE cell plasma membrane experimental_model: Human SMVT cloned from JAR cells, expressed in human retinal pigment epithelial cells and Xenopus laevis oocytes limitations: Heterologous human-protein experiments establish transport properties; they do not quantify whole-body absorption or nutrient deficiency from supplement competition. exposure: Human SMVT cDNA expression; substrate concentrations not specified in the abstract. cross_nutrient: true [b5-trans-wang1999] Human placental Na+-dependent multivitamin transporter. Cloning, functional expression, gene structure, and chromosomal localization. (1999). https://pubmed.ncbi.nlm.nih.gov/10329687/ DOI: 10.1074/jbc.274.21.14875
Complete structured claim and evidence
Sodium-dependence kinetics of human SLC5A6-mediated pantothenate uptake supported a 2:1 sodium:pantothenate coupling ratio.
Sodium ion → Pantothenate (vitamin B5) source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
true
experimental_model
Human SMVT cloned from JAR cells, expressed in human retinal pigment epithelial cells and Xenopus laevis oocytes
exposure
Sodium concentration-response of cloned human SMVT-mediated vitamin uptake.
limitations
Heterologous human-protein experiments establish transport properties; they do not quantify whole-body absorption or nutrient deficiency from supplement competition. The ratio is inferred from transport kinetics, rather than direct counting of individual cotransport events.
nutrient_topic
Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
organism
Homo sapiens
plain_language
Two sodium ions accompany each pantothenate molecule in the reported SMVT transport model.
primary_references
[b5-trans-wang1999] Human placental Na+-dependent multivitamin transporter. Cloning, functional expression, gene structure, and chromosomal localization. (1999). https://pubmed.ncbi.nlm.nih.gov/10329687/ DOI: 10.1074/jbc.274.21.14875
tissue_or_cell_type
HRPE cell plasma membrane
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 197–208
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human SMVT cloned from JAR cells, expressed in human retinal pigment epithelial cells and Xenopus laevis oocytes · source_derived_draft · unverified_draft
### b5-trans-two-sodium-pantothenate Sodium-dependence kinetics of human SLC5A6-mediated pantothenate uptake supported a 2:1 sodium:pantothenate coupling ratio. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Two sodium ions accompany each pantothenate molecule in the reported SMVT transport model. organism: Homo sapiens tissue_or_cell_type: HRPE cell plasma membrane experimental_model: Human SMVT cloned from JAR cells, expressed in human retinal pigment epithelial cells and Xenopus laevis oocytes limitations: Heterologous human-protein experiments establish transport properties; they do not quantify whole-body absorption or nutrient deficiency from supplement competition. The ratio is inferred from transport kinetics, rather than direct counting of individual cotransport events. exposure: Sodium concentration-response of cloned human SMVT-mediated vitamin uptake. cross_nutrient: true [b5-trans-wang1999] Human placental Na+-dependent multivitamin transporter. Cloning, functional expression, gene structure, and chromosomal localization. (1999). https://pubmed.ncbi.nlm.nih.gov/10329687/ DOI: 10.1074/jbc.274.21.14875
Complete structured claim and evidence
A fitted five-state model of human SMIT2 currents included cooperative Na+ binding and a likely rate-limiting return of empty transporter.
Sodium ion → SLC5A11 (human SMIT2) source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/inositol-research/24944204.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "12216ce12672706d91e22c9fbc1ebc5dbe77444e9869048f8a0d456f621cb41e", "start_char": 0, "end_char": 1647, "text_sha256": "12216ce12672706d91e22c9fbc1ebc5dbe77444e9869048f8a0d456f621cb41e"}
experimental_model
Voltage clamp and kinetic model fitting
exposure
Sodium and voltage manipulations
limitations
Cooperative sodium binding and turnover were model-derived; this is not a clinical sodium recommendation.
nutrient_topic
Inositol research collection; topical membership is not evidence of a direct dietary effect. · Inositol (stereoisomer family)
organism
Human SMIT2 in Xenopus oocytes
plain_language
The sodium gradient is part of the transport machinery, rather than inositol moving independently of ions.
primary_references
[ino-p24944204] The transport mechanism of the human sodium/myo-inositol transporter 2 (SMIT2/SGLT6), a member of the LeuT structural family. (2014). https://pubmed.ncbi.nlm.nih.gov/24944204/ DOI: 10.1152/ajpcell.00054.2014
tissue_or_cell_type
Heterologous membrane transport
Inositol: synthesis, signaling, mineral interactions and conditional deficiency (2026-09-17) · lines 340–351
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Voltage clamp and kinetic model fitting · source_derived_draft · unverified_draft
### ino-smit2-sodium A fitted five-state model of human SMIT2 currents included cooperative Na+ binding and a likely rate-limiting return of empty transporter. Condition category: normal nutrient_topic: Inositol research collection; topical membership is not evidence of a direct dietary effect. plain_language: The sodium gradient is part of the transport machinery, rather than inositol moving independently of ions. organism: Human SMIT2 in Xenopus oocytes tissue_or_cell_type: Heterologous membrane transport experimental_model: Voltage clamp and kinetic model fitting limitations: Cooperative sodium binding and turnover were model-derived; this is not a clinical sodium recommendation. exposure: Sodium and voltage manipulations evidence_span: {"source_cache": "artifacts/inositol-research/24944204.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "12216ce12672706d91e22c9fbc1ebc5dbe77444e9869048f8a0d456f621cb41e", "start_char": 0, "end_char": 1647, "text_sha256": "12216ce12672706d91e22c9fbc1ebc5dbe77444e9869048f8a0d456f621cb41e"} [ino-p24944204] The transport mechanism of the human sodium/myo-inositol transporter 2 (SMIT2/SGLT6), a member of the LeuT structural family. (2014). https://pubmed.ncbi.nlm.nih.gov/24944204/ DOI: 10.1152/ajpcell.00054.2014
Complete structured claim and evidence
Human SMIT2 expression increased D-chiro-inositol uptake 159-fold in rat L6 cells.
SLC5A11 (human SMIT2) → D-chiro-inositol source_derived_draftungraded
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
The transporter can carry a second inositol stereoisomer.
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 D-chiro-inositol uptake 159-fold.
transport_pool
the expressing cell Expression increased D-chiro-inositol uptake 159-fold.
Inositol: synthesis, signaling, mineral interactions and conditional deficiency (2026-09-17) · lines 301–312
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-dci Human SMIT2 expression increased D-chiro-inositol uptake 159-fold in rat L6 cells. Condition category: normal nutrient_topic: Inositol research collection; topical membership is not evidence of a direct dietary effect. plain_language: The transporter can carry a second inositol stereoisomer. 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
Human SMIT2 expression increased myo-inositol uptake 37-fold relative to vector control in rat L6 cells.
SLC5A11 (human SMIT2) → Myo-inositol source_derived_draftungraded
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
Human SLC41A1-associated Mg efflux in HEK293 cells fell sharply when extracellular sodium was replaced in the Kolisek assay.
SLC41A1 → Cellular magnesium efflux source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
Sodium availability affected measured magnesium export in this assay; coupling is contested.
evidence-system
Human construct overexpression; mag-fura-2; extracellular Na replacement
experimental_model
Human construct overexpression; mag-fura-2; extracellular Na replacement
limitations
Indirect free-ion assay and overexpression; conflicts with sodium-independent isotope flux in a different construct/protocol.
nutrient_topic
Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
organism
Human protein and human-derived cells
plain_language
This experiment supported sodium-coupled export of magnesium.
primary_references
[kolisek-2012-slc41a1] Human gene SLC41A1 encodes for the Na+/Mg2+ exchanger (2012). https://pubmed.ncbi.nlm.nih.gov/22031603/ DOI: 10.1152/ajpcell.00289.2011
tissue
HEK293 cells
tissue_or_cell_type
HEK293 cells
transport_direction
Mg2+ from cytosol toward extracellular solution.
Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1165–1178
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human construct overexpression; mag-fura-2; extracellular Na replacement · source_derived_draft · unverified_draft
### slc41a1-sodium-dependent-efflux Human SLC41A1-associated Mg efflux in HEK293 cells fell sharply when extracellular sodium was replaced in the Kolisek assay. Condition category: normal nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: This experiment supported sodium-coupled export of magnesium. organism: Human protein and human-derived cells tissue_or_cell_type: HEK293 cells experimental_model: Human construct overexpression; mag-fura-2; extracellular Na replacement limitations: Indirect free-ion assay and overexpression; conflicts with sodium-independent isotope flux in a different construct/protocol. cross_nutrient: Sodium availability affected measured magnesium export in this assay; coupling is contested. transport_direction: Mg2+ from cytosol toward extracellular solution. evidence-system: Human construct overexpression; mag-fura-2; extracellular Na replacement tissue: HEK293 cells [kolisek-2012-slc41a1] Human gene SLC41A1 encodes for the Na+/Mg2+ exchanger (2012). https://pubmed.ncbi.nlm.nih.gov/22031603/ DOI: 10.1152/ajpcell.00289.2011
Complete structured claim and evidence
Mouse SLC41A1 expressed in HEK293 cells supported Mg extrusion without extracellular sodium in the Arjona isotope assay.
SLC41A1 → Cellular magnesium efflux source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
This assay challenges obligatory sodium dependence of SLC41A1-associated magnesium extrusion.
evidence-system
Mouse SLC41A1 construct; stable-isotope 25Mg measurements
experimental_model
Mouse SLC41A1 construct; stable-isotope 25Mg measurements
limitations
Different ortholog, loading and readout from the sodium-dependent report; physiological coupling remains unresolved.
nutrient_topic
Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
organism
Mouse protein; human-derived cells
plain_language
A different experiment found magnesium export that did not require sodium.
primary_references
[arjona-2019-slc41a1] SLC41A1 is essential for magnesium homeostasis in vivo (2019). https://pubmed.ncbi.nlm.nih.gov/30417250/ DOI: 10.1007/s00424-018-2234-9
tissue
HEK293 cells
tissue_or_cell_type
HEK293 cells
transport_direction
Mg2+ from cytosol toward extracellular solution.
Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1180–1193
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mouse SLC41A1 construct; stable-isotope 25Mg measurements · source_derived_draft · unverified_draft
### slc41a1-sodium-independent-efflux Mouse SLC41A1 expressed in HEK293 cells supported Mg extrusion without extracellular sodium in the Arjona isotope assay. Condition category: normal nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A different experiment found magnesium export that did not require sodium. organism: Mouse protein; human-derived cells tissue_or_cell_type: HEK293 cells experimental_model: Mouse SLC41A1 construct; stable-isotope 25Mg measurements limitations: Different ortholog, loading and readout from the sodium-dependent report; physiological coupling remains unresolved. cross_nutrient: This assay challenges obligatory sodium dependence of SLC41A1-associated magnesium extrusion. transport_direction: Mg2+ from cytosol toward extracellular solution. evidence-system: Mouse SLC41A1 construct; stable-isotope 25Mg measurements tissue: HEK293 cells [arjona-2019-slc41a1] SLC41A1 is essential for magnesium homeostasis in vivo (2019). https://pubmed.ncbi.nlm.nih.gov/30417250/ DOI: 10.1007/s00424-018-2234-9
Complete structured claim and evidence
Human PDXK showed lower substrate Km with potassium than sodium, whereas sodium supported over twice the maximal activity.
Potassium ion → Pyridoxal kinase / PDXK source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
Potassium/sodium-B6 enzyme kinetics.
evidence_location
Full text: Metal binding and enzyme activity; Figure 1
experimental_model
Purified recombinant human PDXK kinetics and crystallography.
exposure
Kinetic assays at pH 7.3.
limitations
Lower Km is not a direct binding constant; results do not define dietary sodium/potassium effects.
nutrient_topic
Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B6
organism
Homo sapiens
plain_language
Potassium and sodium affect different kinetic properties.
primary_references
[safo2007] Crystal Structure of human pyridoxal kinase: structural basis of M(+) and M(2+) activation. (2007). https://pubmed.ncbi.nlm.nih.gov/17766369/ DOI: 10.1110/ps.073022107
tissue_or_cell_type
Purified human enzyme
Vitamin B6: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 203–215
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Purified recombinant human PDXK kinetics and crystallography. · source_derived_draft · unverified_draft
### b6-transport-pdxk-k-na Human PDXK showed lower substrate Km with potassium than sodium, whereas sodium supported over twice the maximal activity. Condition category: normal nutrient_topic: Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Potassium and sodium affect different kinetic properties. organism: Homo sapiens tissue_or_cell_type: Purified human enzyme experimental_model: Purified recombinant human PDXK kinetics and crystallography. limitations: Lower Km is not a direct binding constant; results do not define dietary sodium/potassium effects. exposure: Kinetic assays at pH 7.3. evidence_location: Full text: Metal binding and enzyme activity; Figure 1 cross_nutrient: Potassium/sodium-B6 enzyme kinetics. [safo2007] Crystal Structure of human pyridoxal kinase: structural basis of M(+) and M(2+) activation. (2007). https://pubmed.ncbi.nlm.nih.gov/17766369/ DOI: 10.1110/ps.073022107
Complete structured claim and evidence
SLC19A2-mediated uptake did not require extracellular sodium and increased with an outward proton gradient.
Human thiamine transporter 1 / SLC19A2 → Cellular free-thiamine uptake source_derived_draftungraded
Experimental context and source evidence
evidence-scope
HeLa cells
evidence_locator
Abstract
evidence_spans
[{"source_document": "artifacts/thiamine_transport_sources/dutta-1999-slc19a2-source-record.json", "source_field": "resultList.result[0].abstractText", "start_char": 0, "end_char": 1275}]
experimental_model
Human placental cDNA expressed in HeLa cells; radiotracer uptake.
limitations
Does not establish an exact proton stoichiometry.
nutrient_topic
Thiamine research collection; topical membership is not evidence of a direct dietary effect. · Thiamine (vitamin B1)
organism
Homo sapiens
plain_language
B1 entry in this assay depended on proton conditions without sodium cotransport.
primary_references
[dutta-1999-slc19a2] Cloning of the human thiamine transporter, a member of the folate transporter family (1999). https://pubmed.ncbi.nlm.nih.gov/10542220/ DOI: 10.1074/jbc.274.45.31925
tissue_or_cell_type
HeLa cells
Thiamine: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 135–147
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human placental cDNA expressed in HeLa cells; radiotracer uptake. · source_derived_draft · unverified_draft
### b1-slc19a2-sodium-independence SLC19A2-mediated uptake did not require extracellular sodium and increased with an outward proton gradient. Condition category: normal nutrient_topic: Thiamine research collection; topical membership is not evidence of a direct dietary effect. plain_language: B1 entry in this assay depended on proton conditions without sodium cotransport. organism: Homo sapiens tissue_or_cell_type: HeLa cells experimental_model: Human placental cDNA expressed in HeLa cells; radiotracer uptake. limitations: Does not establish an exact proton stoichiometry. evidence_spans: [{"source_document": "artifacts/thiamine_transport_sources/dutta-1999-slc19a2-source-record.json", "source_field": "resultList.result[0].abstractText", "start_char": 0, "end_char": 1275}] evidence_locator: Abstract evidence-scope: HeLa cells [dutta-1999-slc19a2] Cloning of the human thiamine transporter, a member of the folate transporter family (1999). https://pubmed.ncbi.nlm.nih.gov/10542220/ DOI: 10.1074/jbc.274.45.31925
Complete structured claim and evidence
Human RFVT2 expression increased riboflavin uptake in HEK293 cells; uptake did not require extracellular sodium or chloride.
Riboflavin transporter 2 / SLC52A2 → Riboflavin (vitamin B2) source_derived_draftungraded
Experimental context and source evidence
evidence_location
Abstract; comparative HEK293 transport assays
experimental_model
Human RFVT2 expression and radiotracer uptake
exposure
Transient expression; extracellular-ion substitution.
limitations
Older name hRFT3 maps to SLC52A2, not SLC52A3; tissue mRNA enrichment is not transport flux.
nutrient_topic
Riboflavin research collection; topical membership is not evidence of a direct dietary effect. · Riboflavin (vitamin B2)
organism
Homo sapiens
plain_language
RFVT2 provides a route for riboflavin entry into cells.
primary_references
[transport-rfvt2-2010] Identification and comparative functional characterization of a new human riboflavin transporter hRFT3 expressed in the brain. (2010). https://doi.org/10.3945/jn.110.122911 DOI: 10.3945/jn.110.122911
tissue_or_cell_type
HEK293 cells
transport_effect
raises Expression increased riboflavin uptake in HEK293 cells.
transport_pool
the expressing cell Expression increased riboflavin uptake in HEK293 cells.
Riboflavin: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 150–161
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human RFVT2 expression and radiotracer uptake · source_derived_draft · unverified_draft
### transport-rfvt2-influx Human RFVT2 expression increased riboflavin uptake in HEK293 cells; uptake did not require extracellular sodium or chloride. Condition category: normal nutrient_topic: Riboflavin research collection; topical membership is not evidence of a direct dietary effect. plain_language: RFVT2 provides a route for riboflavin entry into cells. organism: Homo sapiens tissue_or_cell_type: HEK293 cells experimental_model: Human RFVT2 expression and radiotracer uptake limitations: Older name hRFT3 maps to SLC52A2, not SLC52A3; tissue mRNA enrichment is not transport flux. exposure: Transient expression; extracellular-ion substitution. evidence_location: Abstract; comparative HEK293 transport assays [transport-rfvt2-2010] Identification and comparative functional characterization of a new human riboflavin transporter hRFT3 expressed in the brain. (2010). https://doi.org/10.3945/jn.110.122911 DOI: 10.3945/jn.110.122911
Complete structured claim and evidence
At fixed sodium intake, potassium depletion reduced urinary sodium from 110 to 83 mmol/day in this crossover.
Potassium → Urinary sodium excretion source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
cross_nutrient
Potassium -> sodium balance.
experimental_model
12 hypertensive adults; ten-day periods.
exposure
16 versus 96 mmol/day K; sodium 120 mmol/day.
limitations
Supports retention physiology; the human study did not measure the Kir4.1-WNK-NCC chain.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Homo sapiens
plain_language
A potassium shortage changed how the kidney handled sodium.
primary_references
[k-krishna1991] Potassium depletion exacerbates essential hypertension (1991). https://pubmed.ncbi.nlm.nih.gov/2058867/ DOI: 10.7326/0003-4819-115-2-77
tissue_or_cell_type
Kidney and urine
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1509–1520
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · 12 hypertensive adults; ten-day periods. · source_derived_draft · unverified_draft
### k-depletion-human-sodium-retention At fixed sodium intake, potassium depletion reduced urinary sodium from 110 to 83 mmol/day in this crossover. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A potassium shortage changed how the kidney handled sodium. organism: Homo sapiens tissue_or_cell_type: Kidney and urine experimental_model: 12 hypertensive adults; ten-day periods. limitations: Supports retention physiology; the human study did not measure the Kir4.1-WNK-NCC chain. cross_nutrient: Potassium -> sodium balance. exposure: 16 versus 96 mmol/day K; sodium 120 mmol/day. [k-krishna1991] Potassium depletion exacerbates essential hypertension (1991). https://pubmed.ncbi.nlm.nih.gov/2058867/ DOI: 10.7326/0003-4819-115-2-77
Complete structured claim and evidence
Mg restriction reduced cleaved alpha/gamma ENaC abundance and blunted amiloride-induced sodium excretion in mice.
Magnesium → Epithelial sodium channel source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
cross_nutrient
magnesium -> sodium -> potassium
experimental_model
Dietary restriction in C57BL/6J mice with renal transport assays
limitations
Cleaved subunits and amiloride response support ENaC inhibition; the molecular cause was unresolved.
nutrient_topic
Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
organism
Mus musculus
plain_language
With less dietary Mg, these kidneys reduced the sodium entry pathway that normally helps drive potassium secretion.
primary_references
[maeoka-2025-enac-romk] Hypomagnesaemia-associated hypokalaemia requires activation of both ENaC and ROMK (2025). https://pubmed.ncbi.nlm.nih.gov/41137719/ DOI: 10.1113/JP287704
tissue_or_cell_type
Kidney distal nephron
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 154–164
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Dietary restriction in C57BL/6J mice with renal transport assays · source_derived_draft · unverified_draft
### mg-restriction-reduces-enac-activity Mg restriction reduced cleaved alpha/gamma ENaC abundance and blunted amiloride-induced sodium excretion in mice. Condition category: nutrient_deficiency nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: With less dietary Mg, these kidneys reduced the sodium entry pathway that normally helps drive potassium secretion. organism: Mus musculus tissue_or_cell_type: Kidney distal nephron experimental_model: Dietary restriction in C57BL/6J mice with renal transport assays limitations: Cleaved subunits and amiloride response support ENaC inhibition; the molecular cause was unresolved. cross_nutrient: magnesium -> sodium -> potassium [maeoka-2025-enac-romk] Hypomagnesaemia-associated hypokalaemia requires activation of both ENaC and ROMK (2025). https://pubmed.ncbi.nlm.nih.gov/41137719/ DOI: 10.1113/JP287704
Complete structured claim and evidence
Combined Na/Mg restriction increased native ROMK activity in DCT2/CNT and lowered plasma K, while ENaC cleavage markers were preserved relative to normal diet.
Magnesium → Renal outer medullary potassium channel / KCNJ1 source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
cross_nutrient
magnesium -> sodium -> potassium
duration
Seven days
experimental_contrast
{"combination": "joint", "comparator": "Normal diet", "conditions": [{"entity_slug": "sodium", "state": "Restricted"}, {"entity_slug": "magnesium", "state": "Restricted"}], "effect_direction": "increase", "endpoint": "Native ROMK activity in DCT2/CNT", "intervention": "Combined dietary sodium and magnesium restriction"} Primary abstract PMID 41137719 / DOI 10.1113/JP287704 rechecked 2026-09-20. This comparison must not be separated into two single-deficiency effects.
experimental_model
Dietary restriction in C57BL/6J mice with renal transport assays
limitations
Co-occurrence supports the proposed mechanism; intracellular Mg and distal Na delivery were not directly measured.
nutrient_topic
Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
organism
Mus musculus
plain_language
In this combined shortage, the Mg-sensitive potassium pathway was more active while the sodium pathway that supports potassium exit remained available.
primary_references
[maeoka-2025-enac-romk] Hypomagnesaemia-associated hypokalaemia requires activation of both ENaC and ROMK (2025). https://pubmed.ncbi.nlm.nih.gov/41137719/ DOI: 10.1113/JP287704
tissue_or_cell_type
Kidney distal nephron
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 178–189
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Dietary restriction in C57BL/6J mice with renal transport assays · source_derived_draft · unverified_draft
### combined-na-mg-restriction-romk-hypokalemia Combined Na/Mg restriction increased native ROMK activity in DCT2/CNT and lowered plasma K, while ENaC cleavage markers were preserved relative to normal diet. Condition category: nutrient_deficiency nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: In this combined shortage, the Mg-sensitive potassium pathway was more active while the sodium pathway that supports potassium exit remained available. organism: Mus musculus tissue_or_cell_type: Kidney distal nephron experimental_model: Dietary restriction in C57BL/6J mice with renal transport assays limitations: Co-occurrence supports the proposed mechanism; intracellular Mg and distal Na delivery were not directly measured. cross_nutrient: magnesium -> sodium -> potassium duration: Seven days [maeoka-2025-enac-romk] Hypomagnesaemia-associated hypokalaemia requires activation of both ENaC and ROMK (2025). https://pubmed.ncbi.nlm.nih.gov/41137719/ DOI: 10.1113/JP287704
Complete structured claim and evidence
The mouse findings support a model in which sustained ENaC sodium entry and higher ROMK conductance jointly favor potassium secretion during combined Na/Mg restriction.
Epithelial sodium channel → Distal renal potassium secretion source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
cross_nutrient
magnesium -> sodium -> potassium
experimental_model
Dietary restriction in C57BL/6J mice with renal transport assays
limitations
Integrated mechanism supported across experiments; enhanced distal Na delivery was not demonstrated and is not required by these data.
nutrient_topic
Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
organism
Mus musculus
plain_language
Sodium entry changes the electrical conditions for potassium exit; lifting the Mg brake on ROMK matters when that driving force is available.
primary_references
[maeoka-2025-enac-romk] Hypomagnesaemia-associated hypokalaemia requires activation of both ENaC and ROMK (2025). https://pubmed.ncbi.nlm.nih.gov/41137719/ DOI: 10.1113/JP287704 [yang-2010-romk-magnesium] Magnesium modulates ROMK channel-mediated potassium secretion (2010). https://pubmed.ncbi.nlm.nih.gov/21030597/ DOI: 10.1681/ASN.2010060617
spatial_transport_direction
Na+: tubular lumen to cell via ENaC; K+: cell to lumen via ROMK.
tissue_or_cell_type
Kidney distal nephron
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 203–215
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Dietary restriction in C57BL/6J mice with renal transport assays · source_derived_draft · unverified_draft
### mg-romk-enac-conditional-k-secretory-chain The mouse findings support a model in which sustained ENaC sodium entry and higher ROMK conductance jointly favor potassium secretion during combined Na/Mg restriction. Condition category: nutrient_deficiency nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Sodium entry changes the electrical conditions for potassium exit; lifting the Mg brake on ROMK matters when that driving force is available. organism: Mus musculus tissue_or_cell_type: Kidney distal nephron experimental_model: Dietary restriction in C57BL/6J mice with renal transport assays limitations: Integrated mechanism supported across experiments; enhanced distal Na delivery was not demonstrated and is not required by these data. cross_nutrient: magnesium -> sodium -> potassium spatial_transport_direction: Na+: tubular lumen to cell via ENaC; K+: cell to lumen via ROMK. [maeoka-2025-enac-romk] Hypomagnesaemia-associated hypokalaemia requires activation of both ENaC and ROMK (2025). https://pubmed.ncbi.nlm.nih.gov/41137719/ DOI: 10.1113/JP287704 [yang-2010-romk-magnesium] Magnesium modulates ROMK channel-mediated potassium secretion (2010). https://pubmed.ncbi.nlm.nih.gov/21030597/ DOI: 10.1681/ASN.2010060617
Complete structured claim and evidence

Availability and dependencies

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

The glucose transporter fails despite available nutrients

Condition: machinery_impairment · A disease-associated SGLT1 mutation.

Normal role: SGLT1 couples intestinal sodium and sugar uptake.

Recorded consequence: Loss of sodium-dependent glucose transport and glucose/galactose malabsorption.

Scope: Human family and expressed transporter; inherited machinery impairment.

Renal glucose recovery is lost

Condition: machinery_impairment · Slc5a2 deletion.

Normal role: SGLT2 recovers filtered glucose in the early proximal tubule.

Recorded consequence: Glucosuria and polyuria with residual later glucose reabsorption.

Scope: Mouse genetic model; no measured volume depletion.

An amino acid transporter loses function

Condition: machinery_impairment · Disease-associated SLC6A19 variants.

Normal role: B0AT1 transports neutral amino acids.

Recorded consequence: Reduced neutral amino acid transport.

Scope: Human Hartnup genetics and in-vitro testing; not a dietary sodium deficiency.

Bile acid recycling fails

Condition: machinery_impairment · Dysfunctional SLC10A2 mutations.

Normal role: ASBT reclaims bile acids at the ileum.

Recorded consequence: Loss of bile-acid uptake despite protein reaching the membrane.

Scope: Human family with primary bile acid malabsorption; cell assays.

A sodium/phosphate transporter defect links phosphate, vitamin D and calcium

Condition: machinery_impairment · Disease-associated SLC34A3 variants.

Normal role: NaPi-IIc supports renal phosphate conservation.

Recorded consequence: Renal phosphate wasting with high calcitriol and hypercalciuria.

Scope: Human hereditary hypophosphatemic rickets with hypercalciuria.

Sodium/bicarbonate transport is impaired by protein changes

Condition: machinery_impairment · Mutations at E91 or R298.

Normal role: Kidney NBCe1 contributes to bicarbonate transport.

Recorded consequence: Reduced transport, with functional rescue in an engineered charge-reversal construct.

Scope: Human transporter expressed in oocytes.

Intestinal sodium conservation fails

Condition: machinery_impairment · Intestinal epithelial Slc9a3 deletion.

Normal role: NHE3 contributes to intestinal sodium and fluid absorption.

Recorded consequence: Alkaline diarrhea, low blood sodium/bicarbonate and high potassium/aldosterone.

Scope: Inducible mouse intestinal knockout.

Renal sodium reabsorption is reduced

Condition: machinery_impairment · Kidney proximal-tubule-specific deletion.

Normal role: Proximal-tubule NHE3 contributes to sodium recovery.

Recorded consequence: Greater natriuresis and lower blood pressure.

Scope: Mouse kidney-specific knockout; baseline blood sodium and bicarbonate unchanged.

ENaC fails despite mineralocorticoid signaling

Condition: machinery_impairment · Loss-of-function ENaC alpha or beta variants.

Normal role: ENaC supports epithelial sodium entry.

Recorded consequence: Severe neonatal salt wasting, hyperkalemia and metabolic acidosis.

Scope: Human inherited pseudohypoaldosteronism type 1.

A sodium channel is overactive

Condition: machinery_impairment · De novo beta-subunit P616L mutation.

Normal role: ENaC activity is normally regulated.

Recorded consequence: Increased sodium current and inherited hypertension.

Scope: Liddle syndrome family and functional oocyte assay.

Sodium provision can limit growth in very premature infants

Condition: nutrient_deficiency · Risk of late hyponatremia during early preterm feeding.

Normal role: Adequate sodium provision supports growth in this population.

Recorded consequence: Supplementation reduced low-sodium reports and increased weight-gain velocity.

Scope: Randomized neonatal trial; not a general adult supplementation claim.

Low blood sodium accompanies exercise-associated weight gain

Condition: biomarker_context · Endurance exercise with varying fluid intake and weight change.

Normal role: Blood sodium must be interpreted with water balance.

Recorded consequence: Weight gain was associated with hyponatremia.

Scope: Human runner cohort; biomarker interpretation, not established total-body sodium deficiency.

Brain solutes recover at different speeds

Condition: biomarker_context · Rapid reversal of sustained experimental hyponatremia.

Normal role: Brain cells regulate water with electrolytes and organic osmolytes.

Recorded consequence: Electrolytes recovered faster than most organic osmolytes.

Scope: Rat dDAVP model; concentration adaptation, not dietary salt deficiency.

Replacement-fluid composition matters during major intestinal losses

Condition: biomarker_context · Severe adult cholera treated with two historical ORS formulations.

Normal role: Glucose/electrolyte solutions are used in oral rehydration.

Recorded consequence: Reduced-osmolarity ORS caused more symptom-free biochemical hyponatremia without significant stool-output benefit.

Scope: Adult cholera trial; do not generalize to all diarrhea or current treatment choices.

The sources

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

Calcium: mechanism-first literature curation (2026-09-17)AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · unverified_draftRead preserved source
Chloride: transport, acid-base balance, nutrient interactions and loss states (2026-09-17)AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · unverified_draftRead preserved source
Inositol: synthesis, signaling, mineral interactions and conditional deficiency (2026-09-17)AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · unverified_draftRead preserved source
Iodine: thyroid hormone production, deficiency, excess and nutrient interactions (2026-09-17)AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · unverified_draftRead preserved source
Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17)AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · unverified_draftRead preserved source
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17)AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · unverified_draftRead preserved source
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17)AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · unverified_draftRead preserved source
Riboflavin: mechanisms, deficiency and nutrient interactions (2026-09-17)AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · unverified_draftRead preserved source
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17)AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · unverified_draftRead preserved source
Thiamine: mechanisms, deficiency and nutrient interactions (2026-09-17)AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · unverified_draftRead preserved source
Vitamin B6: mechanisms, deficiency and nutrient interactions (2026-09-17)AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · unverified_draftRead preserved source
Vitamin C: mechanisms, deficiency and nutrient interactions (2026-09-17)AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · unverified_draftRead preserved source

Recorded disagreements

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

Is SLC41A1-associated magnesium efflux obligatorily sodium dependent?Human-SLC41A1 fluorescence experiments found strong Na dependence; mouse-SLC41A1 isotope experiments found efflux without Na.Read the recorded disagreement

Open questions in this collection

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

Can a blood sodium value predict a tissue-specific sodium transport rate?The whole-body ratio and local electrochemical gradients are distinct; these studies do not establish a universal conversion.
Which findings diagnose sodium depletion independently of hyponatremia in a particular person?Intake, losses, body-water status, kidney function and hormones must be considered; these studies do not validate one universal blood cutoff for depletion.
Does the observed salt-related calcium loss produce a predictable long-term fracture risk?The selected crossover measured calcium handling and modeled balance, not incident fractures or decades of uncompensated loss.
Does improving sodium intake improve vitamin or other nutrient uptake in people whose sodium balance is already adequate?Sodium-dependent transport in vesicles, oocytes or cultured cells is not a clinical supplementation result.
Does impaired bile-acid recycling cause a specific fat-soluble vitamin deficit in every SLC10A2 disorder?The selected primary transport study did not quantify each vitamin; that downstream chain needs its own patient evidence.
How general is the hypoxic NCLX–membrane–ubiquinone mechanism across tissues and chronic disease?The recorded chain retains its acute experimental setting; dietary and clinical extrapolations are untested here.
How strongly do these experimental salt-sensitive immune pathways contribute to human disease at usual intakes?Cell-culture and mouse disease models establish mechanisms within their settings, not population-specific human causation or treatment effects.

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

Evidence, AI assistance and curation standards

Sodium

The mechanisms

Serum-water sodium correlated strongly with (exchangeable sodium + exchangeable potassium)/total body water in the studied patients.

Normal intestinal SGLT1 couples glucose entry to the inward sodium electrochemical gradient.

Human OCTN2 expression increased sodium-dependent carnitine uptake with an apparent Km of 4.34 micromolar.

SLC34A3 mutations segregated with renal phosphate wasting and hypophosphatemic rickets in the studied families.

NCLX overexpression increased sodium-dependent mitochondrial calcium efflux; silencing reduced it and heterologous rescue restored it.

Aldosterone increased collecting-duct sgk mRNA within 30 minutes through mineralocorticoid receptors without requiring new protein synthesis.

Intestinal NHE3 deletion produced persistent watery, alkaline diarrhea.

The alpha- or beta-subunit variants identified in affected families caused loss of channel activity.

Weight gain during the marathon was independently associated with hyponatremia, odds ratio 4.2 (95% CI 2.2–8.2).

Mean weight-gain velocity was 26.9 versus 22.9 g/kg/day with supplementation versus placebo.

The higher-salt diet increased urinary calcium excretion in the crossover trial (P=0.0008).

High-to-intermediate sodium reduction lowered systolic pressure by 2.1 mmHg on the control diet and 1.3 mmHg on DASH; intermediate-to-low reduction lowered it by another 4.6 and 1.7 mmHg respectively.

Serum sodium correlated only partly or poorly with the isolated body-composition ratios, including exchangeable sodium/body weight.

The familial SGLT1 missense variant abolished sodium-dependent glucose transport in injected oocytes.

Early proximal glucose reabsorption was 78 ± 6% in wild-type mice and absent in Sglt2-null mice.

Sglt2-null mice had glucosuria and polyuria without differences in plasma glucose or GFR versus controls.

The human Nav1.4–beta1 structure resolved its pore and voltage-sensing domains, supporting a molecular account of sodium permeation.

Analysis of the Nav1.4 structure and previously characterized residues supported an allosteric blocking mechanism of fast inactivation.

Current reversal measurements supported uptake of one glutamate anion with three sodium ions and one proton, coupled to outward movement of one potassium ion.

Increasing extracellular potassium around cells loaded with sodium and glutamate evoked an outward, blocker-sensitive reversed transport current.

Coexpression of mouse sgk with the three ENaC subunits increased sodium current in Xenopus oocytes.

Vasopressin increased apical AQP2 labeling and shifted AQP2 from intracellular vesicles toward the apical membrane.

Water permeability rose during vasopressin exposure and fell after withdrawal in parallel with AQP2 redistribution.

Nax directly interacted with sodium/potassium-pump alpha subunits in the study.

The sodium-associated increase in SFO lactate production occurred in wild-type but not Nax-knockout mice.

Lactate stimulated the activity of SFO GABAergic neurons.

Increased NaCl enhanced cytokine-induced TH17 differentiation in human and mouse T-cell cultures.

Silencing or chemical inhibition of p38/MAPK blocked the high-salt enhancement of TH17 differentiation in the study.

Silencing or chemical inhibition of NFAT5 blocked the high-salt enhancement of TH17 differentiation in the study.

Silencing or chemical inhibition of SGK1 blocked the high-salt enhancement of TH17 differentiation in the study.

Mice fed a high-salt diet developed more severe experimental autoimmune encephalomyelitis.

The study identified SGK1-dependent deactivation of Foxo1 in the TH17 program.

Foxo1 acted as a direct repressor of IL-23 receptor expression in the study.

Modestly increased NaCl induced SGK1 and promoted IL-23 receptor expression in the tested T-cell program.

SLC6A19 functioned as a sodium-dependent, chloride-independent neutral amino acid transporter.

Tested Hartnup-associated SLC6A19 variants reduced neutral amino acid transport in vitro.

Human creatine-transporter expression conferred sodium-dependent creatine uptake with Km 14.9 ± 3.0 micromolar in five experiments.

L243P, T262M and the double mutant abolished taurocholate and other bile-acid transport in transfected cells.

The dysfunctional L243P/T262M constructs retained protein expression and plasma-membrane trafficking.

The HHRH phenotype included elevated circulating 1,25-dihydroxyvitamin D with normal or low-normal FGF23.

The sodium/phosphate-transporter-associated HHRH phenotype included hypercalciuria.

Mutagenesis of NBCe1 residues E91 or R298 reduced transport function in the expression assay.

The E91R/R298E charge-reversal construct restored transport function in the study.

A hypoxia-associated conformational change in complex I drove matrix acidification in the proposed and experimentally supported pathway.

Matrix acidification released free calcium from mitochondrial calcium phosphate deposits.

Activation of mitochondrial sodium/calcium exchange promoted sodium import into the matrix during the hypoxic pathway.

Matrix sodium interacted with phospholipids and reduced inner-membrane fluidity in the study.

The sodium-linked membrane change reduced free ubiquinone mobility between complexes II and III, while transport within supercomplexes was spared.

The pathway produced complex III superoxide; inhibiting mitochondrial sodium import blocked the response.

Intestinal NHE3-null mice developed metabolic acidosis with lower blood bicarbonate.

Intestinal NHE3-null mice developed hyponatremia.

Intestinal NHE3-null mice developed hyperkalemia.

Intestinal NHE3-null mice had markedly elevated plasma aldosterone.

A 30-mmHg perfusion-pressure increase raised sodium excretion fivefold in controls and eightfold in proximal NHE3-null mice.

Proximal-tubule NHE3-null mice had lower basal systolic, diastolic and mean arterial pressure.

Kidney-specific NHE3 deletion did not change the measured baseline plasma sodium, pH or bicarbonate.

Affected individuals had salt wasting with hyperkalemia and acidosis despite mineralocorticoid unresponsiveness.

The beta-subunit P616L mutant increased amiloride-sensitive sodium current 8.8-fold versus normal subunits in oocytes.

Supplemented preterm infants had fewer recorded serum sodium values below 135 mmol/L.

Length and head-circumference growth did not differ significantly between treatment groups.

Brain sodium and chloride overshot normal control contents by 24 hours after rapid correction.

Most organic osmolytes required five or more days to recover; glutamate was an exception that recovered within 24 hours.

Hyponatremia below 130 mmol/L occurred in 29/142 versus 16/150 participants receiving reduced-osmolarity versus standard ORS; affected participants were symptom-free.

The ORS groups did not differ significantly in initial 24-hour stool output, total stool output or diarrhea duration.

Low-sodium DASH versus high-sodium control produced mean systolic differences of 7.1 mmHg without hypertension and 11.5 mmHg with hypertension.

Fractional calcium absorption adapted to calcium intake but was not significantly altered by salt intake.

Higher salt shifted modeled bone calcium balance from positive to negative on the higher-calcium diet; balance was negative at both salt levels on the lower-calcium diet.

The 6-g/day salt increase reduced free-water clearance while increasing urine osmolyte excretion.

Fluid intake was lower at 12 g/day salt in these long-duration controlled studies.

Ouabain-sensitive extrusion was approximately three sodium ions per ATP hydrolyzed in resealed erythrocyte ghosts.

Sodium-24 and potassium-42 experiments demonstrated ouabain-sensitive sodium efflux and potassium influx in human red cells.

Pre-steady-state pig-kidney pump experiments identified Mg as an essential activator of ATP-dependent phosphorylation.

Adding KCl after ATP phosphorylation accelerated dephosphorylation of pig-kidney Na/K-ATPase.

Lowering bath K from 5.0 to 2.7 mM reduced ventricular pump current and increased intracellular sodium.

Pump inhibition during low-K exposure increased sodium sensed by NCX and favored cellular calcium loading.

Human cardiac NCX1 exchanges calcium and sodium in opposing directions across the membrane.

Sgk1 phosphorylated Nedd4-2 at Ser444 and less strongly Ser338 in Xenopus constructs.

SGK-dependent Nedd4-2 phosphorylation reduced its ENaC interaction and increased ENaC surface expression in oocytes.