6533b7d4fe1ef96bd126326b
RESEARCH PRODUCT
Increased Gastrin and Calcitonin Secretion after Oral Calcium or Peptones Administration in Patients with Hypercalciuria: A Clue to an Alteration in Calcium-Sensing Receptor Activity
Valeria ValdesOrnella SangalettiGabriele Bianchi-porroMassimo BarrellaTarcisio VagoMaurizio BevilacquaVelella RighiniG. BaldiRosanna ToscanoLigia J. Dominguezsubject
Calcitoninmedicine.medical_specialtyEndocrinology Diabetes and MetabolismClinical BiochemistryThyroid GlandAdministration Oralchemistry.chemical_element.CalciumBiochemistryKidney CalculiEndocrinologyOral administrationCalcium Metabolism DisordersInternal medicineGastrinsmedicineHumansGastrin-Secreting CellsHypercalciuriaAgedGastrinBiochemistry (medical)Middle AgedCalcitonin secretionmedicine.diseaseCalcium GluconateEndocrinologychemistryGastrointestinal hormoneParathyroid HormoneCalcitoninPeptonesFemaleCalcium-sensing receptorReceptors Calcium-Sensinghormones hormone substitutes and hormone antagonistsdescription
The calcium-sensing receptor (CaSR) has been detected in human antral gastrin-secreting cells, where, upon calcium and/or amino acid allosteric activation, it stimulates gastrin secretion. Patients with absorptive hypercalciuria (AH) display an enhanced gastric acid output; therefore, we evaluated the secretion of gastrin in subjects with AH ( 30 subjects vs. 30 healthy female controls, all postmenopausal) after oral calcium administration ( 1 g calcium gluconate) and, on a separate occasion, after peptone loading test ( protein hydrolyzed, 10 g). Gastrin and monomeric calcitonin responses were higher in AH after both oral calcium administration ( P < 0.01) and peptone loading ( P< 0.01). Because the activation of CaSR by oral calcium and peptones directly induces gastrin release, the higher gastrin responses to these stimuli suggest an increased sensitivity of gastrin-secreting cells CaSR in patients with AH. A similar alteration in thyroid C cells might explain the enhanced calcitonin responses to both calcium and peptones. If the same alterations should in addition be present in the distal tubule ( where CaSR is expressed as well), then a possible explanation for amino acid-induced hypercalciuria in AH would have been identified
year | journal | country | edition | language |
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2005-03-01 | The Journal of Clinical Endocrinology & Metabolism |