Enhanced parathyroid hormone absorption

The a ns wer is a. (Hardman, pp 1525-1528.) Pa r a thyroid ho r m o ne is synthesized by and released from the parathyroid gland increased synthesis of PTI1 is a response to low serum Ca concentrations. Resorption and mobilization of Ca and phosphate from bone are increased in response to elevated PTI1 concentrations. Replacement of body stores of Ca is enhanced by the capacity of PTH to promote increased absorption of Ca by the small intestine in concert with vitamin D, which is the primary factor that enhances intestinal Ca absorption. Parathyroid hormone also causes an increased renal tubular reabsorption of Ca and excretion of phosphate. As a consequence of these effects, the extracellular Ca concentration becomes elevated. 

High phosphate diets cause decreased Ca absorption, secondary hyperparathyroidism, accelerated bone resorption and soft tissue calcification in some animals, but not in normal humans. Although phosphates may decrease Ca absorption in man at very high (> 2000 mg/day) Ca intakes, they do not do so at more moderate Ca levels and enhance Ca absorption at very low levels (< 500 mg/day). Phosphates increase renal tubular reabsorption and net retention of Ca. At low Ca intakes, phosphates stimulate parathyroid hormone (PTH) secretion without causing net bone resorption. 

The major location of calcium in the body is in the skeleton, which contains more than 90% of the body calcium as phosphate and carbonate. Bone resorption and formation keeps this calcium in dynamic equilibrium with ionized and complexed calcium in blood, cellular fluids and membranes. Homeostasis is mainly regulated by the parathyroid hormone and vitamin D which lead to increased blood calcium levels, and by a thyroid hormone, calcitonin, which controls the plasma calcium concentration J5 Increasing the concentration of calcitonin decreases the blood calcium level, hence injections of calcitonin are used to treat severe hyperalcaemia arising from hyperparathyroidism, vitamin D intoxication or the injection of too high a level of parathyroid extract. High levels of calcitonin also decrease resorption of calcium from bone. Hypocalcaemia stimulates parathyroid activity, leading to increased release of calcium from bone, reduction in urinary excretion of calcium and increased absorption of calcium from the intestine. Urinary excretion of phosphate is enhanced. 

As discussed in Section 2.4.1, there are some data that suggest that aluminum absorption can be enhanced by parathyroid hormone and vitamin D, but the data are inconclusive. 

The physiological role of vitamin D is to maintain calcium homeostasis. Phosphate metabolism is also affected. Vitamin D accomplishes its role by enhancing the absorption of calcium and phosphate from tte small intestines, promoting their mobilization from bone, and decreasing their excretion by the kidney. Also involved are parathyroid hormone and edeitonin. 

The concentration of ionized calcium is closely regulated by the interactions of parathyroid hormone (PTH), phosphorus, vitamin D, and calcitonin (Fig. 49-9). Parathyroid hormone increases serum calcium concentrations by stimulating calcium release from bone, reducing renal excretion, and enhancing absorption in the gastrointestinal tract secondary to increased renal production of 1,25-... 

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. 

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... 

As RJ contains testosterone [24] and possesses steroid hormone-type activities [54—57], it was hypothesized that it may have beneficial effects on osteoporosis. In a recent study, both an ovariectomized rat model and a tissue culture model were used. The results of the study indicated that RJ was almost as effective as 17p-estradiol in preventing the development of bone loss induced by ovariectomy in rats. In tissue culture models, RJ increased calcium contents in femoral-diaphyseal and femoral-metaphyseal tissue cultures obtained from normal male rats however, in a mouse marrow culture model, it neither inhibited the parathyroid hormone (PTH)-induced calcium loss nor affected the formation of osteoclast-like cells induced by PTH. Therefore, these results suggested that RJ may prevent osteoporosis by enhancing intestinal calcium absorption, but not by directly antagonizing the action of PTH [60]. In a comparable study, it was investigated whether RJ and bee pollen reduce the bone loss due to osteoporosis in oophorectomized female rats model. It was concluded that RJ and bee pollen after a 12-week treatment decrease the bone loss due to osteoporosis, proposing that these results may contribute to the clinical practice [61]. 

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