PTH is a polypeptide produced and secreted by parathyroid cells in response to certain secretagogue stimuli, the most potent of which is ionized calcium. PTH is formed by 84 amino acids and, like all secretion proteins, is synthesized from a larger precursor. This pre-pro-parathormone is cleaved in the wrinkled endoplasmic reticulum forming the pro-parathormone, a compound of reduced size that finally will be converted, in the Golgi apparatus, in the mature metabolite, the parathormone. The hormone’s biological activity lies in the amino acid sequence 1-34, which forms the amino-terminal fragment of PTH (Fig.1).

Fig1. Biosynthesis of parathyroid hormone. (Copyright EDISES 2021. Reproduced with permission)

PTH synthesis, not its secretion, strictly depends on intra cellular calcium concentration.

Immediately after synthesis, PTH is stored in dense cytoplasmic granules from which it is secreted and in amino- and carboxy-terminal fragments. The half-life of PTH is 5–10 minutes; approximately 70% is metabolized in the liver and the remaining 30% in the kidney. A negative feedback mechanism regulates PTH secretion by plasma ionized calcium concentrations. Because plasma calcium concentrations must be maintained within very narrow limits, PTH is extremely sensitive to changes in its concentrations. Therefore, the relationship between the hormone and the cat ion is sigmoidal and represents a high-gain system since significant changes follow small changes in plasma ionized calcium in PTH secretion.

The sensitivity to changes in serum calcium concentration by PTH, and therefore its ability to promptly correct abrupt changes in calcemia, is due to the presence of a receptor on the membrane of the parathyroid cell (Ca2+ sensing Receptor [CaR]). The PTH/CaR interaction activates the adenylate cyclase and phospholipase C signal transduction systems. Via a CaR-coupled G protein, the hormone-receptor com plex forms second messengers (cAMP, inositol triphosphate and diacylglycerol), responsible for intracellular biochemical signals transduction.

The pattern of PTH secretion has a circadian rhythm (with a peak around midnight) and an episodic rhythm (with fluctuations at intervals of about 60 minutes).

Although serum calcium is the primary regulator of PTH secretion, other secretagogue agents include magnesium, lithium, hyperphosphatemia, catecholamines, cortisol, histamine, dopamine, and alcohol.

In contrast, somatostatin, thyroid hormones excess, vita min D3, FGF23 (fibroblast growth factor 23), calcium channel blocker antihypertensive drugs, and aluminum intoxication, inhibit PTH secretion.

FGF23 is a phosphoglycoprotein secreted by osteoblasts and osteocytes in response to hyperphosphatemia and vita min D3. Noteworthy, parathyroid cell possesses the vitamin D3 receptor (VDR) and Klotho, which are sensitive to vita min D3 and FGF23, respectively.

The role of magnesium is not fully known. It is a less potent secretagogue than serum calcium, and under physio logical conditions, its influence on PTH secretion is negligible.

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مواضيع ذات صلة

 Regulation of Calcemia and Calcium- Phosphorus Homeostasis

Biological Actions of Parathormone (PTH)

Regulation of Thyroid Hormone Secretion and TSH

Biosynthesis and Secretion of Thyroid Hormones

العمل الجزيئي لهرمون الغدة الدرقية

الغدة الدرقية Thyroid gland

الغدة جار الدرقية The Parathyroid gland

الغدة الدرقية Thyroid gland

فيتامين د3 (Cholecalciferol Vit.D3)

الكالسيتونين (الثايروكالسيتونين) (Calctionine CT, Thyrocalcitonin TCT)

الإفراط في إفراز هرمون جار الدرقية Hyperparathyroidism

هرمون جار الدرقية أو الباراثورمون (Parathyroid H -PTH)