Parathyroid glands hormones produced

Vitamin D deficiency in young children causes rickets. As a child becomes vitamin D deficient, this results in a decrease in the efficiency of intestinal calcium absorption. There is a decline in blood-ionized calcium, which causes the parathyroid glands to produce and secrete more parathyroid hormone (PTH). PTH tries to conserve calcium by enhancing tubular reabsorption of calcium in the kidney. However, in the face of developing hypocalcemia, which could disturb neuromuscular function and a wide variety of metabolic and cellular processes, the body calls upon l,25(OH)2D and PTH to mobilize stem cells to become functional osteoclasts, which, in turn, mobilize calcium from the skeleton. In addition, PTH causes a loss of phosphorus into the urine causing hypophosphatemia. Thus, in early vitamin D deficiency the serum calcium is normal it is the low serum phosphorus that causes the extracellular CaXP04 to be too low for normal mineralization of... 

Parathyroid hormone, a polypeptide of 83 amino acid residues, mol wt 9500, is produced by the parathyroid glands. Release of PTH is activated by a decrease of blood Ca " to below normal levels. PTH increases blood Ca " concentration by increasing resorption of bone, renal reabsorption of calcium, and absorption of calcium from the intestine. A cAMP mechanism is also involved in the action of PTH. Parathyroid hormone induces formation of 1-hydroxylase in the kidney, requited in formation of the active metabolite of vitamin D (see Vitamins, vitamin d). 

There are four parathyroid glands, which are situated behind the thyroid. They produce parathyroid hormone (PTH), a peptide which interacts with vitamin D to control the level of calcium in the blood. PTH stimulates release of calcium from bone and increases the uptake of calcium by the kidney tubules from the glomerular hltrate. 

The peptide hormone parathyrin (PTH), which is produced by the parathyroid gland, stimulates Ca "" resorption in the kidneys and at the same time inhibits the resorption of phosphate. In conjunction with the effects of this hormone in the bones and intestines (see p. 344), this leads to an increase in the plasma level of Ca and a reduction in the level of phosphate ions. 

Parathyroid hormone is a single-chain polypeptide of 84 amino acids which is produced in the parathyroid glands. It increases serum calcium and decreases serum phosphate. In bone it promotes resorption of calcium. It indirectly increases osteoclastic activity by promoting the action of osteoblasts. It has been shown that in low doses PTH may even increase bone formation without stimulating bone resorption. In the kidney PTH increases resorption of calcium and it increases excretion of phosphate. An other important activity in the kidney is the enhanced synthesis of 1,25-dihydroxyvitamin D. An increased serum calcium level inhibits PTH secretion and increased serum phosphate decreases free serum calcium and thus stimulates PTH secretion. 

The active forms of the D vitamins are la,25-dihydroxy-vitamin Dj and 25-hydroxy-vitamin Dj. They are formed by enzymatic hydroxylation in the liver microsomes and then in the kidney mitochondria by a ferredoxin flavoprotein and cytochrome P-450. The 1,25-dihydroxy vitamin is then transported to the bone, intestine, and other target organs (kidneys, parathyroid gland). Consequently, it can be considered a hormone since it is produced in one organ but used elsewhere. It mobilizes calcium and phosphate and also influences the absorption of these ions in the intestine, thus promoting bone mineralization. The hormone is also active in relieving hypoparathyroidism and postmenopausal osteoporosis, which, for example, results in the brittle bones of elderly women. 

Vitamin D3 is a precursor of the hormone 1,25-dihy-droxyvitamin D3. Vitamin D3 is essential for normal calcium and phosphorus metabolism. It is formed from 7-dehydrocholesterol by ultraviolet photolysis in the skin. Insufficient exposure to sunlight and absence of vitamin D3 in the diet leads to rickets, a condition characterized by weak, malformed bones. Vitamin D3 is inactive, but it is converted into an active compound by two hydroxylation reactions that occur in different organs. The first hydroxylation occurs in the liver, which produces 25-hydroxyvita-min D3, abbreviated 25(OH)D3 the second hydroxylation occurs in the kidney and gives rise to the active product 1,25-dihydroxy vitamin D3 24,25 (OH)2D3 (fig. 24.13). The hydroxylation at position 1 that occurs in the kidney is stimulated by parathyroid hormone (PTH), which is secreted from the parathyroid gland in response to low circulating levels of calcium. In the presence of adequate calcium, 25(OH)D3 is converted into an inactive metabolite, 24,25 (OH)2D3. The active derivative of vitamin D3 is considered a hormone because it is transported from the kidneys to target cells, where it binds to nuclear receptors that are analogous to those of typical steroid hormones. l,25(OH)2D3 stimulates calcium transport by intestinal cells and increases calcium uptake by osteoblasts (precursors of bone cells). 

Q2 The hormones that are normally involved in the control of calcium balance are parathyroid hormone (PTH) from the parathyroid gland calcitonin, which is secreted by the thyroid gland and 1,25-dihydroxycholecalciferol (1,25-DHCC, or calcitriol), which is produced in the kidneys. Calcitonin reduces the level of plasma calcium by attenuating its release from bone and by increasing its excretion. The PTH and 1,25-DHCC increase the level of plasma calcium by two mechanisms (1) a combination of an increase in calcium absorption by the gut and an increase in the release of calcium from bone and (2) a reduction in both bone formation and calcium excretion. The three hormones act together to maintain the physiological level of calcium and normal bone turnover. Over 95% of body calcium is located in bone as hydroxyapatite. 

Tissues that produce hormones include the hypothalamus, anterior and posterior pituitary, adrenal cortex and medulla, gonads, thyroid and parathyroid glands, heart, brain, cells of the gastrointestinal tract, and the pancreas. 

A hormone is a messenger that causes tissue, organ, and cellular activities to increase or decrease tissue equal to the amount of the hormones in the blood. Disease and aging cause inappropriate secretion of hormones, resulting in abnormal tissue, organ, and cellular activities. Hormonal therapy is used for hormones produced by the pituitary, thyroid, parathyroid, and adrenal glands and restores hormonal balance by either ... 

Figure 49-12 Secretion, metabolism, clearance, and circulating forms of PTH. Both intact PTH and inactive fragments containing the middle and carboxyl (C)-terminal amino acids are secreted by the parathyroid glands.These inactive fragments are also produced by peripheral metabolism of intact PTH by the liver and kidneys. Carboxyl fragments are cleared by the kidneys by glomerular filtration.The half-life and concentration of intact hormone are small compared with those of inactive fragments. (From Endres DB, Villanueva R, Sharp CF jr. Singer FR. Measurement of parathyroid hormone. Endocrinol Metab Clin North Am 1989 18 611-29.)...

Parathyroid implantation (B2) and tissue culture experiments (Gl, G2) have shown that the secretion of the parathyroid glands exerts a direct action on bone which results in resorption and destruction. Injection of the hormone produces definite cellular changes within a few hours in the osteoblasts and osteocytes (H3). There is also an increase in the number of osteoclasts. It is impossible to say, however, whether bone mineral or organic matrix is primarily affected, as they appear to be mobilized simultaneously (C6, M5). 

The pituitary does not control the endocrine pancreas or the parathyroid glands. The endocrine pancreas produces insulin, which regulates serum glucose levels. Pancreatic hormones are discussed on pages 154-155. 

Parathormone, parathyrin a hormone produced by the parathyroid gland, which influences the metabolism of calcium and phosphate. It is a single chain proteohormone with 84 amino acid residues of known primary structure [R.T. Sauer etal. Biochemistry 13 (1974), 1994-1999]. M, 9,402 (porcine). P. influences the cells that degrade bone (osteoclasts) by activation of membrane-bound adenylate cyelase and by increasing the entry of Ca into these cells. The resulting mobilization of Ca causes an increase in blood ealcium. This is necessarily accompanied by the release of free phosphate which is excreted via the kidneys. Thus P. favors phosphate secretion in the distal part of the kidney tubule, and inhibits phosphate resorption in the proximal tubule. P. promotes calcium absorption by the intestine. The action of P. is therefore opposite to that of Calcitonin (see). P. is degraded by the liver, and some is excreted in the urine. Absence of P. leads to a decrease of blood calcium, accompanied by neuromuscular overexcitability (tetany). 

When the calcium concentration drops below normal, the parathyroid gland secretes parathyroid hormone (PTH). This hormone stimulates bone-reabsorbing cells (i.e., osteocytes and osteoblasts), which cause an increase in calcium and phosphate ions in the extracellular fluid. PTH in association with vitamin D also can stimulate the absorption of calcium indirectly from the intestine and cause the kidney to conserve calcium ions and excrete phosphate ions. Therefore, any damage to the parathyroid gland or the kidneys or failure of the body to produce 1,25-dihydroxy vitamin D will prevent mobilization of calcium from the bones and intestine to the blood plasma. This will lead to hypocalcemia. 3... 

The amount of 1,25-dihydroxycholecalciferol produced by the kidney is controlled by parathyroid hormone. When the level of calcium in the blood is low (hypocalcaemia), the parathyroid gland is stimulated to secrete more parathyroid hormone, which induces the kidney to produce more 1,25-dihydroxycholecalciferol, which in turn enhances the intestinal absorption of calcium. 

The skeleton is not a stable unit in the chemical sense, since large amounts of the calcium and phosphorus in bone can be liberated by reabsorption. This takes place particularly during lactation and egg production, although the exchange of calcium and phosphorus between bones and soft tissue is always a continuous process. Resorption of calcium is controlled by the action of the parathyroid gland. If animals are fed on a low-calcium diet, the ionic calcium concentration in the extracellular fluid falls, the parathyroid gland is stimulated and the hormone produced causes resorption of bone, liberating calcium to meet the requirements of the animal. Since calcium is combined with phosphorus in bone, the phosphorus is also liberated and excreted by the animal. 

Parathyroid Glands Small glands, usually located within the thyroid gland, which produce parathyroid hormone this hormone regulates calcium levels in the bloodstream and bones. 

Although the thyroid gland is probably the most important source of calcitonin, the parathyroid glands and the thymus, which contain C cells as vestiges of the ultimobranchial body, also produce the hormone. 

Several years ago, it was discovered that the thyroid gland was also the source of a hypocalcemic hormone having effects in general opposition to those of the parathyroid hormone. This hormone is produced in mammals by the parafollicular C-ceUs and in other vertebrates by the ultimobrachial bodies (45). Originally called thyrocalcitonin, it is now referred to as calcitonin (CT). 

The hypothalamus-pituitary, thyroid, parathyroid, pancreas, adrenals, ovary, and testes are considered to be the principal endocrine glands producing hormones. A more complete list of the major endocrine hormones and their primary gland of origin is shown in Table 9.1. 

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