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Control of parathyroid hormone synthesis or secretion

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Parathyroid hormone (PTH) synthesis or secretion can be decreased in the chief cell of the parathyroid gland by different mechanisms: (1) increased extracellular calcium concentrations by activation of the calcium-sensing receptor (CaSR); (2) activation of the fibroblast growth factor (FGF)/alpha-Klotho receptor complex by FGF23; and (3) activation of the retinoid X receptor (RXR)/vitamin-D-receptor complex by 1,25-dihydroxyvitamin D. In bone, PTH acts on osteoblasts to secrete receptor activator of nuclear factor kappa-B ligand (RANKL), which acts on osteocytes to release calcium, thereby increasing extracellular calcium. FGF23 is released by the osteocytes in response to increased extracellular phosphate concentration, which acts on the FGF/alpha-Klotho receptor complex in the parathyroid gland and decreases synthesis of PTH mRNA and PTH secretion. PTH acts on the kidney to decrease the reabsorption of phosphate and increase the absorption of calcium, thereby increasing serum calcium and decreasing serum phosphate concentrations. PTH acts on 1-alpha-hydroxylase in the kidney to convert 25-hydroxyvitamin D to active 1,25-dihydroxyvitamin D, which increases both calcium and phosphate absorption and interacts with the RXR/vitamin-D-receptor complex in the parathyroid gland to suppress PTH mRNA. (Source: English KA, Lines KE, Thakker RV. Genetics of hereditary forms of primary hyperparathyroidism. Hormones [Athens] 2024;23[1]:3-14. Creative Commons Attribution 4.0 International [CC BY 4.0] license, creativecommons.org/licenses/by/4.0.)