Parathyroid hormone: Wikis


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Parathyroid hormone

PDB rendering based on 1bwx.
Available structures
1bwx, 1et1, 1fvy, 1hph, 1hpy, 1zwa, 1zwb, 1zwc, 1zwd, 1zwe, 1zwf, 1zwg
Symbols PTH;
External IDs OMIM168450 MGI97799 HomoloGene266 GeneCards: PTH Gene
RNA expression pattern
PBB GE PTH 206977 at tn.png
More reference expression data
Species Human Mouse
Entrez 5741 19226
Ensembl ENSG00000152266 ENSMUSG00000059077
UniProt P01270 n/a
RefSeq (mRNA) NM_000315 NM_020623
RefSeq (protein) NP_000306 NP_065648
Location (UCSC) Chr 11:
13.47 - 13.47 Mb
Chr 7:
113.18 - 113.18 Mb
PubMed search [1] [2]

Parathyroid hormone (PTH), parathormone or parathyrin, is secreted by the parathyroid glands as a polypeptide containing 84 amino acids. It acts to increase the concentration of calcium (Ca2+) in the blood, whereas calcitonin (a hormone produced by the parafollicular cells (C cells) of the thyroid gland) acts to decrease calcium concentration. PTH acts to increase the concentration of calcium in the blood by acting upon parathyroid hormone receptor in three parts of the body:[1] PTH half-life is approximately 4 minutes.[2] It has a molecular mass of 9.4 kDa.[3]




Regulation of serum calcium

Parathyroid hormone regulates serum calcium levels through its effects on the following tissues:[4]

Region Effect
bone It enhances the release of calcium from the large reservoir contained in the bones.[5] Bone resorption is the normal destruction of bone by osteoclasts, which are indirectly stimulated by PTH. Stimulation is indirect since osteoclasts do not have a receptor for PTH; rather, PTH binds to osteoblasts, the cells responsible for creating bone. Binding stimulates osteoblasts to increase their expression of RANKL, which can bind to osteoclast precursors containing RANK, a receptor for RANKL. The binding of RANKL to RANK stimulates these precursors to fuse, forming new osteoclasts which ultimately enhances bone resorption.
kidney It enhances active reabsorption of calcium and magnesium from distal tubules and the thick ascending limb. As bone is degraded both calcium and phosphate are released. It also greatly increases the excretion of phosphate, with a net loss in plasma phosphate concentration. By increasing the calcium:phosphate ratio more calcium is therefore free in the circulation. [6]
intestine via kidney It enhances the absorption of calcium in the intestine by increasing the production of activated vitamin D. Vitamin D activation occurs in the kidney. PTH up-regulates 25-hydroxyvitamin D3 1-alpha-hydroxylase, the enzyme responsible for 1-alpha hydroxylation of 25-hydroxy vitamin D, converting vitamin D to its active form (1,25-dihydroxy vitamin D). This activated form of vitamin D increases the absorption of calcium (as Ca2+ ions) by the intestine via calbindin.
Calcium regulation in the human body.[7] The role of parathyroid hormone is shown in blue.

PTH was one of the first hormones to be shown to use the G-protein, adenylyl cyclase second messenger system.

Normal total plasma calcium level ranges from 8.5 to 10.2 mg/dL (2.12 mmol/L to 2.55 mmol/L).[8]

Regulation of serum phosphate

PTH reduces the reabsorption of phosphate from the proximal tubule of the kidney[6] which means more phosphate is excreted through the urine.

However, PTH enhances the uptake of phosphate from the intestine and bones into the blood. In the bone, slightly more calcium than phosphate is released from the breakdown of bone. In the intestines, which is mediated by an increase in activated vitamin D, the absorption of phosphate is not as dependent on vitamin D as is that of calcium. The end result is a small net drop in the serum concentration of phosphate.

Vitamin D synthesis

PTH increases the activity of 1-α-hydroxylase enzyme, which converts 25-hydroxycholecalciferol to 1,25-dihydroxycholecalciferol, the active form of vitamin D.

Regulation of PTH secretion

Secretion of parathyroid hormone is controlled chiefly by serum [Ca2+] through negative feedback, which is achieved by the activation of calcium-sensing receptors located on parathyroid cells.[9] Calcium sensing receptors work by activating the phospholipase C pathway,[10][11] through a G type of G protein, which ultimately increases intracellular concentration of calcium, which triggers vesicle fusion and exocytosis of parathyroid hormone. It also inhibits (not stimulates, as some[12] sources state) the cAMP-dependent pathway.[11]


  • Decreased serum [Ca2+].
  • Mild decreases in serum [Mg2+].
  • An increase in serum phosphate (Since increased phosphate will complex with serum calcium to form calcium phosphate, which causes the Ca-sensitive receptors (CaSr) to think that serum Ca has decreased, as CaSR do not sense Calcium phosphate, thereby triggering an increase in PTH)


Clinical significance

  • A high level of PTH in the blood is known as hyperparathyroidism.
    • If the cause is in the parathyroid gland it is called primary hyperparathyroidism. The causes are parathyroid adenoma, parathyroid hyperplasia and parathyroid cancer.
    • If the cause is outside the gland, it is known as secondary hyperparathyroidism. This can occur in chronic renal failure. In secondary hyperparathyroidism, serum Calcium levels are decreased, which causes the hypersecretion of PTH from the parathyroid glands. PTH acts on the proximal tubules in the kidney to decrease reabsorption of Phosphate (increasing its excretion in urine, decreasing its serum concentration). NOTE: however, in chronic renal failure, because the kidneys are failing they are unable to excrete phosphate in the urine, so in this case of secondary hyperparathyroidism, serum calcium will be decreased, but serum phosphate will be increased.


PTH can be measured in the blood in several different forms: intact PTH; N-terminal PTH; mid-molecule PTH, and C-terminal PTH, and different tests are used in different clinical situations.

The average PTH level is 10-60 pg/ml.

See also


  1. ^ Physiology at MCG 5/5ch6/s5ch6_11
  2. ^ Bieglmayer C, Prager G, Niederle B (October 2002). "Kinetic analyses of parathyroid hormone clearance as measured by three rapid immunoassays during parathyroidectomy". Clin. Chem. 48 (10): 1731–8. PMID 12324490. 
  3. ^ Prahalad AK, Hickey RJ, Huang J, et al. (June 2006). "Serum proteome profiles identifies parathyroid hormone physiologic response". Proteomics 6 (12): 3482–93. doi:10.1002/pmic.200500929. PMID 16705755. 
  4. ^ Coetzee M, Kruger MC (May 2004). "Osteoprotegerin-receptor activator of nuclear factor-kappaB ligand ratio: a new approach to osteoporosis treatment?". South. Med. J. 97 (5): 506–11. doi:10.1097/00007611-200405000-00018. PMID 15180028. 
  5. ^ Poole K, Reeve J (2005). "Parathyroid hormone - a bone anabolic and catabolic agent". Curr Opin Pharmacol 5 (6): 612–7. doi:10.1016/j.coph.2005.07.004. PMID 16181808. 
  6. ^ a b
  7. ^ Page 1094 (The Parathyroid Glands and Vitamin D) in: Walter F., PhD. Boron (2003). Medical Physiology: A Cellular And Molecular Approaoch. Elsevier/Saunders. pp. 1300. ISBN 1-4160-2328-3. 
  8. ^ Zieve, MD, MHA, David. "MedlinePlus Medical Encyclopedia: Serum calcium". National Library of Medicine, National Institutes of Health. Retrieved 2009-02-01. 
  9. ^ Physiology at MCG 5/5ch6/s5ch6_9
  10. ^ InterPro: IPR000068 GPCR, family 3, extracellular calcium-sensing receptor-related Retrieved on June 2, 2009
  11. ^ a b Coburn JW, Elangovan L, Goodman WG, Frazaõ JM (December 1999). "Calcium-sensing receptor and calcimimetic agents". Kidney Int. Suppl. 73: S52–8. PMID 10633465. 
  12. ^ a b Costanzo, Linda S. (2007). BRS Physiology. Lippincott, Williams, & Wilkins. pp. 260. ISBN 978-0781773119. 

Further reading


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