Component
Urinary cyclic AMP excretion
Measured urinary cAMP output used as a renal response marker after parathyroid extract.
2 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
Parathyroid extract produced only a small urinary cAMP response in the two Mg-deficient patients tested, while glucagon-stimulated plasma cAMP responses were preserved.
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
- Only two challenge studies; urinary cAMP is an organ-response marker, not direct measurement of PTH1R binding or adenylyl-cyclase Mg occupancy.
- nutrient_topic
- Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
- organism
- Homo sapiens
- plain_language
- The kidney responded weakly to the PTH challenge, but another hormone/cAMP response remained functional; Mg deficiency did not disable all signaling equally.
- 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 337–347
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-deficiency-blunts-renal-pth-camp-response Parathyroid extract produced only a small urinary cAMP response in the two Mg-deficient patients tested, while glucagon-stimulated plasma cAMP responses were preserved. Condition category: nutrient_deficiency nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The kidney responded weakly to the PTH challenge, but another hormone/cAMP response remained functional; Mg deficiency did not disable all signaling equally. organism: Homo sapiens tissue_or_cell_type: Blood; parathyroid-kidney axis experimental_model: Human hypomagnesemic hypocalcemia clinical study limitations: Only two challenge studies; urinary cAMP is an organ-response marker, not direct measurement of PTH1R binding or adenylyl-cyclase Mg occupancy. 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 evidence
Where it participates (unsigned role)
A 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.