Parathyroid hormone

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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
Identifiers
Symbol(s)	PTH;
External IDs	OMIM: 168450 MGI: 97799 HomoloGene: 266
Gene ontology Molecular Function: • hormone activity Cellular Component: • extracellular region Biological Process: • skeletal development • cellular calcium ion homeostasis • G-protein coupled receptor protein signaling pathway • cell-cell signaling • lactation • induction of apoptosis by hormones • bone resorption • cAMP metabolic process
RNA expression pattern
More reference expression data
Orthologs
	Human	Mouse
Entrez	5741	19226
Ensembl	ENSG00000152266	ENSMUSG00000059077
Uniprot	P01270	n/a
Refseq	NM_000315 (mRNA) NP_000306 (protein)	NM_020623 (mRNA) NP_065648 (protein)
Location	Chr 11: 13.47 - 13.47 Mb	Chr 7: 113.18 - 113.18 Mb
Pubmed search	[1]	[2]

Parathyroid hormone (PTH), or parathormone, 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]

Contents 1 Functions 1.1 Effects on serum calcium (raising) 1.2 Effects on serum phosphate (decrease, with compensation) 2 Feedback regulation 3 Syndromes 4 Measurements 5 References 6 See also 7 Further reading

[edit] Functions

[edit] Effects on serum calcium (raising)

Region	Effect
bones	It enhances the release of calcium from the large reservoir contained in the bones.[2] 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 the resorption of bone.
kidney	It enhances active reabsorption of calcium from distal tubules[3] and the thick ascending limb.
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 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 affects the absorption of calcium (as Ca2+ ions) by the intestine via calbindin.

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 is 9.4mg/dl(8-11) or 2.4mmol/L^{[4] [5]} .

[edit] Effects on serum phosphate (decrease, with compensation)

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.

[edit] Feedback regulation

Increased calcium concentration in the blood acts (via feedback inhibition) to decrease PTH secretion by the parathyroid glands.

This is achieved by the activation of calcium-sensing receptors located on parathyroid cells.^[7]

[edit] Syndromes

• 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.

• A low level of PTH in the blood is known as hypoparathyroidism. Causes include surgical misadventure (eg inadvertent removal during routine thyroid surgery), autoimmune disorder, and inborn errors of metabolism.

[edit] Measurements

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.

[edit] References

[edit] See also

• Calcium metabolism
• Disorders of calcium metabolism
• Parathyroid hormone-related protein

[edit] Further reading

v • d • e Endocrine system: hormones/endocrine glands (Peptide hormones, Steroid hormones) Hypothalamic-pituitary Hypothalamus: TRH, CRH , GnRH, GHRH, somatostatin, dopamine - Posterior pituitary: vasopressin, oxytocin - Anterior pituitary: α (FSH, LH, TSH), GH, prolactin, POMC (ACTH, MSH, endorphins, lipotropin) Adrenal axis Adrenal medulla: epinephrine, norepinephrine - Adrenal cortex: aldosterone, cortisol, DHEA Thyroid axis Thyroid: thyroid hormone (T3 and T4) - calcitonin - Parathyroid: PTH Gonadal axis Testis: testosterone, AMH, inhibin - Ovary: estradiol, progesterone, inhibin/activin, relaxin (pregnancy) Other end. glands Pancreas: glucagon, insulin, somatostatin - Pineal gland: melatonin Non-end. glands Placenta: hCG, HPL, estrogen, progesterone - Kidney: renin, EPO, calcitriol, prostaglandin - Heart atrium: ANP - Stomach: gastrin, ghrelin - Duodenum: CCK, GIP, secretin, motilin, VIP - Ileum: enteroglucagon - Adipose tissue: leptin, adiponectin, resistin - Thymus: Thymosin - Thymopoietin - Thymulin - Skeleton: Osteocalcin - Liver/other: Insulin-like growth factor (IGF-1, IGF-2) Target-derived NGF, BDNF, NT-3