Component
Parathyroid hormone secretion
Independent biological entity. Read linked claims for experimental scope and context.
7 recorded relationships. Experimental role, claim status and evidence remain attached to each record.
How nutrients influence it
Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
How nutrients reach it in more than one step
Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.
Tracing routes…
What it does
Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.
What acts on it
In bovine parathyroid slices, extracellular Mg and Ca inhibited PTH release additively, but Mg was less potent on a molar basis.
Experimental context and source evidence
- cross_nutrient
- magnesium -> PTH -> calcium
- experimental_model
- Graded extracellular cations in cultured bovine parathyroid slices
- limitations
- Potency depends on concentrations and preparation; no general human replacement ratio follows.
- nutrient_topic
- Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
- organism
- Bos taurus
- plain_language
- Both ions can signal the gland to release less PTH; calcium and magnesium are not interchangeable inputs.
- primary_references
- [habener-1976-pth-synthesis-secretion] Relative effectiveness of magnesium and calcium on the secretion and biosynthesis of parathyroid hormone in vitro (1976). https://pubmed.ncbi.nlm.nih.gov/1248443/ DOI: 10.1210/endo-98-1-197
- tissue_or_cell_type
- Parathyroid gland
Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 253–263
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Graded extracellular cations in cultured bovine parathyroid slices · source_derived_draft · unverified_draft
### mg-ca-differential-pth-secretory-potency In bovine parathyroid slices, extracellular Mg and Ca inhibited PTH release additively, but Mg was less potent on a molar basis. Condition category: normal nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Both ions can signal the gland to release less PTH; calcium and magnesium are not interchangeable inputs. organism: Bos taurus tissue_or_cell_type: Parathyroid gland experimental_model: Graded extracellular cations in cultured bovine parathyroid slices limitations: Potency depends on concentrations and preparation; no general human replacement ratio follows. cross_nutrient: magnesium -> PTH -> calcium [habener-1976-pth-synthesis-secretion] Relative effectiveness of magnesium and calcium on the secretion and biosynthesis of parathyroid hormone in vitro (1976). https://pubmed.ncbi.nlm.nih.gov/1248443/ DOI: 10.1210/endo-98-1-197
Complete structured claim and evidenceIn intact rat glands, raising Mg from 0.5 to 2 mM suppressed PTH most clearly at moderately low Ca; suppression was small or absent at normal-high Ca and diminished again at very low Ca.
Experimental context and source evidence
- cross_nutrient
- magnesium -> PTH -> calcium
- experimental_model
- Intact rat parathyroid glands in graded Ca/Mg media
- limitations
- An ex-vivo concentration response, not a human threshold; very high 5 mM Mg produced broader suppression.
- nutrient_topic
- Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
- organism
- Rattus norvegicus
- plain_language
- How much extra Mg reduces PTH depends on the calcium signal already reaching the gland.
- primary_references
- [rodriguez-ortiz-2014-pth-context] Magnesium modulates parathyroid hormone secretion and upregulates parathyroid receptor expression at moderately low calcium concentration (2014). https://pubmed.ncbi.nlm.nih.gov/24103811/ DOI: 10.1093/ndt/gft400
- tissue_or_cell_type
- Parathyroid gland
Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 277–287
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Intact rat parathyroid glands in graded Ca/Mg media · source_derived_draft · unverified_draft
### mg-pth-inhibition-depends-on-calcium In intact rat glands, raising Mg from 0.5 to 2 mM suppressed PTH most clearly at moderately low Ca; suppression was small or absent at normal-high Ca and diminished again at very low Ca. Condition category: normal nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: How much extra Mg reduces PTH depends on the calcium signal already reaching the gland. organism: Rattus norvegicus tissue_or_cell_type: Parathyroid gland experimental_model: Intact rat parathyroid glands in graded Ca/Mg media limitations: An ex-vivo concentration response, not a human threshold; very high 5 mM Mg produced broader suppression. cross_nutrient: magnesium -> PTH -> calcium [rodriguez-ortiz-2014-pth-context] Magnesium modulates parathyroid hormone secretion and upregulates parathyroid receptor expression at moderately low calcium concentration (2014). https://pubmed.ncbi.nlm.nih.gov/24103811/ DOI: 10.1093/ndt/gft400
Complete structured claim and evidencePertussis-toxin pretreatment abolished the suppression of PTH release by low Mg in the parathyroid-cell assay.
Experimental context and source evidence
- availability_state
- nutrient_deficiency Imported condition classification; unverified.
- cross_nutrient
- magnesium -> CaSR/PTH -> calcium
- experimental_model
- Dispersed human parathyroid cells from hyperparathyroid tissue
- limitations
- Pharmacologic pathway probe, not evidence for toxin use in patients; no full in-vivo chain tested.
- nutrient_topic
- Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
- organism
- Homo sapiens
- plain_language
- Blocking Gi/o signaling removed the low-Mg secretory brake, placing these signaling proteins in the experimental pathway.
- primary_references
- [quitterer-2001-magnesium-paradox] Paradoxical block of parathormone secretion is mediated by increased activity of G alpha subunits (2001). https://pubmed.ncbi.nlm.nih.gov/11102444/ DOI: 10.1074/jbc.M007727200
- tissue_or_cell_type
- Parathyroid cells in vitro
- trigger_kind
- nutrient_deficiency Imported condition classification; unverified.
Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 445–455
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Dispersed human parathyroid cells from hyperparathyroid tissue · source_derived_draft · unverified_draft
### pertussis-toxin-removes-low-mg-pth-block Pertussis-toxin pretreatment abolished the suppression of PTH release by low Mg in the parathyroid-cell assay. Condition category: nutrient_deficiency nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Blocking Gi/o signaling removed the low-Mg secretory brake, placing these signaling proteins in the experimental pathway. organism: Homo sapiens tissue_or_cell_type: Parathyroid cells in vitro experimental_model: Dispersed human parathyroid cells from hyperparathyroid tissue limitations: Pharmacologic pathway probe, not evidence for toxin use in patients; no full in-vivo chain tested. cross_nutrient: magnesium -> CaSR/PTH -> calcium [quitterer-2001-magnesium-paradox] Paradoxical block of parathormone secretion is mediated by increased activity of G alpha subunits (2001). https://pubmed.ncbi.nlm.nih.gov/11102444/ DOI: 10.1074/jbc.M007727200
Complete structured claim and evidenceLowering extracellular Mg to 0.1 mM suppressed PTH release from dispersed human parathyroid cells in the tested media.
Experimental context and source evidence
- availability_state
- nutrient_deficiency Imported condition classification; unverified.
- cross_nutrient
- magnesium -> CaSR/PTH -> calcium
- experimental_model
- Dispersed human parathyroid cells from hyperparathyroid tissue
- limitations
- Experiment used hyperparathyroid tissue; culture concentrations are not clinical deficiency cutoffs.
- nutrient_topic
- Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
- organism
- Homo sapiens
- plain_language
- At very low Mg, the gland cells released less PTH even though simple loss of an inhibitory extracellular ion might predict more release.
- primary_references
- [quitterer-2001-magnesium-paradox] Paradoxical block of parathormone secretion is mediated by increased activity of G alpha subunits (2001). https://pubmed.ncbi.nlm.nih.gov/11102444/ DOI: 10.1074/jbc.M007727200
- tissue_or_cell_type
- Parathyroid cells in vitro
- trigger_kind
- nutrient_deficiency Imported condition classification; unverified.
Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 409–419
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Dispersed human parathyroid cells from hyperparathyroid tissue · source_derived_draft · unverified_draft
### very-low-mg-suppresses-pth-in-human-cells Lowering extracellular Mg to 0.1 mM suppressed PTH release from dispersed human parathyroid cells in the tested media. Condition category: nutrient_deficiency nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: At very low Mg, the gland cells released less PTH even though simple loss of an inhibitory extracellular ion might predict more release. organism: Homo sapiens tissue_or_cell_type: Parathyroid cells in vitro experimental_model: Dispersed human parathyroid cells from hyperparathyroid tissue limitations: Experiment used hyperparathyroid tissue; culture concentrations are not clinical deficiency cutoffs. cross_nutrient: magnesium -> CaSR/PTH -> calcium [quitterer-2001-magnesium-paradox] Paradoxical block of parathormone secretion is mediated by increased activity of G alpha subunits (2001). https://pubmed.ncbi.nlm.nih.gov/11102444/ DOI: 10.1074/jbc.M007727200
Complete structured claim and evidenceCaSR potentiation by NPS R-568 strengthens extracellular-calcium-mediated inhibition of PTH secretion in bovine parathyroid cells.
Experimental context and source evidence
- experimental_model
- Bovine parathyroid cells and human CaSR-expressing HEK293 cells
- limitations
- Pharmacological cell experiment; potentiation required extracellular calcium.
- nutrient_topic
- Calcium research collection; topical membership is not evidence of a direct dietary effect. · Calcium
- organism
- Bos taurus
- plain_language
- Greater calcium-sensor activation reduces hormone release.
- primary_references
- [nemeth1998] Calcimimetics with potent and selective activity on the parathyroid calcium receptor (1998). https://pmc.ncbi.nlm.nih.gov/articles/PMC19959/ DOI: 10.1073/pnas.95.7.4040
- tissue_or_cell_type
- Parathyroid cells
Calcium: mechanism-first literature curation (2026-09-17) · lines 25–34
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Bovine parathyroid cells and human CaSR-expressing HEK293 cells · source_derived_draft · unverified_draft
### casr-calcium-pth-suppression CaSR potentiation by NPS R-568 strengthens extracellular-calcium-mediated inhibition of PTH secretion in bovine parathyroid cells. Condition category: normal nutrient_topic: Calcium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Greater calcium-sensor activation reduces hormone release. organism: Bos taurus tissue_or_cell_type: Parathyroid cells experimental_model: Bovine parathyroid cells and human CaSR-expressing HEK293 cells limitations: Pharmacological cell experiment; potentiation required extracellular calcium. [nemeth1998] Calcimimetics with potent and selective activity on the parathyroid calcium receptor (1998). https://pmc.ncbi.nlm.nih.gov/articles/PMC19959/ DOI: 10.1073/pnas.95.7.4040
Complete structured claim and evidence
Where it participates (unsigned role)
Acute Mg administration increased circulating immunoreactive PTH within one minute in the three tested Mg-deficient patients.
Experimental context and source evidence
- availability_state
- nutrient_deficiency Imported condition classification; unverified.
- cross_nutrient
- magnesium -> PTH -> calcium
- experimental_model
- Human hypomagnesemic hypocalcemia clinical study
- limitations
- Three infusion experiments; timing supports but does not directly visualize secretory machinery.
- nutrient_topic
- Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
- organism
- Homo sapiens
- plain_language
- The fast hormone rise supports release of stored PTH after Mg restoration, rather than requiring new hormone synthesis first.
- primary_references
- [rude-1976-human-pth-resistance] Functional hypoparathyroidism and parathyroid hormone end-organ resistance in human magnesium deficiency (1976). https://pubmed.ncbi.nlm.nih.gov/182417/ DOI: 10.1111/j.1365-2265.1976.tb01947.x
- tissue_or_cell_type
- Blood; parathyroid-kidney axis
- trigger_kind
- nutrient_deficiency Imported condition classification; unverified.
Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 313–323
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human hypomagnesemic hypocalcemia clinical study · source_derived_draft · unverified_draft
### mg-repletion-rapidly-releases-pth Acute Mg administration increased circulating immunoreactive PTH within one minute in the three tested Mg-deficient patients. Condition category: nutrient_deficiency nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The fast hormone rise supports release of stored PTH after Mg restoration, rather than requiring new hormone synthesis first. organism: Homo sapiens tissue_or_cell_type: Blood; parathyroid-kidney axis experimental_model: Human hypomagnesemic hypocalcemia clinical study limitations: Three infusion experiments; timing supports but does not directly visualize secretory machinery. cross_nutrient: magnesium -> PTH -> calcium [rude-1976-human-pth-resistance] Functional hypoparathyroidism and parathyroid hormone end-organ resistance in human magnesium deficiency (1976). https://pubmed.ncbi.nlm.nih.gov/182417/ DOI: 10.1111/j.1365-2265.1976.tb01947.x
Complete structured claim and evidenceA child with primary hypomagnesemia retained calcemic and renal phosphate/cAMP responses to parathyroid extract during Mg depletion despite impaired endogenous PTH secretion.
Experimental context and source evidence
- availability_state
- nutrient_deficiency Imported condition classification; unverified.
- cross_nutrient
- magnesium -> PTH -> calcium/phosphate
- experimental_model
- Single-child Mg withdrawal/repletion with hormone challenge
- limitations
- Single case; shows PTH resistance is not obligatory. Primary hypomagnesemia was not genetically assigned in this study.
- nutrient_topic
- Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
- organism
- Homo sapiens
- plain_language
- In this child the main failure was releasing the hormone; tissues could still respond when hormone was provided.
- primary_references
- [suh-1973-preserved-pth-response] Pathogenesis of Hypocalcemia in Primary Hypomagnesemia: Normal End-Organ Responsiveness to Parathyroid Hormone, Impaired Parathyroid Gland Function (1973). https://www.jci.org/articles/view/107159 DOI: 10.1172/JCI107159
- tissue_or_cell_type
- Blood and kidney
- trigger_kind
- nutrient_deficiency Imported condition classification; unverified.
Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 397–407
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Single-child Mg withdrawal/repletion with hormone challenge · source_derived_draft · unverified_draft
### primary-hypomagnesemia-can-preserve-pth-response A child with primary hypomagnesemia retained calcemic and renal phosphate/cAMP responses to parathyroid extract during Mg depletion despite impaired endogenous PTH secretion. Condition category: nutrient_deficiency nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: In this child the main failure was releasing the hormone; tissues could still respond when hormone was provided. organism: Homo sapiens tissue_or_cell_type: Blood and kidney experimental_model: Single-child Mg withdrawal/repletion with hormone challenge limitations: Single case; shows PTH resistance is not obligatory. Primary hypomagnesemia was not genetically assigned in this study. cross_nutrient: magnesium -> PTH -> calcium/phosphate [suh-1973-preserved-pth-response] Pathogenesis of Hypocalcemia in Primary Hypomagnesemia: Normal End-Organ Responsiveness to Parathyroid Hormone, Impaired Parathyroid Gland Function (1973). https://www.jci.org/articles/view/107159 DOI: 10.1172/JCI107159
Complete structured claim and evidence
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.