Calcium, absorption binding proteins

Several other properties of selected dietary fibers may influence the bioavailability of calcium directly or indirectly. Those fibers which have cation exchange capabilities such as acid polysaccharides due to free carboxyl groups on the sugar residues may bind minerals such as calcium (3,17,33,36). Loss of calcium binding protein as a result of mucosa injury caused by the feeding of some kinds of dietary fiber was credited as being the partial cause of decreased calcium absorption in everted, rat gut sac studies by Oku et al. (16). 

CalcitrioPs action primary function is in regulating plasma calcium concentration. In health, the plasma total calcium concentration is tightly controlled at 2.35-2.55 mmol/1. Only the ionized or free fraction, amounting to about 50% of the total, is physiologically active in for example, maintenance of membrane electrical potential and bone formation. The hormone causes increased bone resorption via activation of osteoclasts (see Section 9.4) and increased intestinal absorption of calcium following the synthesis of a specific binding protein in mucosal cells. As described in Section 4.7, some... 

Further, fish protein hydrolysates contain hormone-like peptides and growth factors that accelerate calcium absorption (Fouchereau-Peron et ah, 1999). These peptides are capable of binding to the cell surface receptors on osteoclasts and have a role in calcium metabolism by decreasing the number of osteoclasts. Therefore, these peptides could be used in the treatment of osteoporosis and Paget s disease. Further,... 

Bonjour, J. P., Russell, R. G. G., Morgan, D. B., Fleisch, H. A. Intestinal calcium absorption, Ca-binding protein, and Ca-ATPase in diphosphonate-treated rats. Amer. J. 

Effect of vitamin D on the intestine 1,25-diOH D3 stimulates intestinal absorption of calcium and phosphate. 1,25-diOH D3 enters the intestinal cell and binds to a cytosolic receptor. The 1,25-diOH D3-receptor complex then moves to the nucleus where it selectively interacts with the cellular DNA. As a result, calcium uptake is enhanced by an increased synthesis of a specific calcium-binding protein. Thus, the mechanism of action of 1,25-diOH D3 is typical of steroid hormones (see p. 238). 

The next stage involves the synthesis of specific calcium-binding proteins, typified by the intestinal CaBP253 discussed in Section 62.1.3.4.5, which probably stimulates the transport of calcium. The role of the protein in vitamin D-dependent absorption of calcium is supported by the good correlation between the concentration of CaBP and the rate of calcium absorption. Under conditions of low calcium or phosphorus diets, chicks and other animals produce more intestinal CaBP to increase the efficiency of uptake of calcium. In general, adaptation to a low calcium diet involves increased synthesis of l,25-(OH)2D3 and the intestinal CaBP. Lowered requirements for calcium in old age are manifested by lower levels of both factors.449,450... 

Vitamin D-binding protein and its associated vitamin are lost in nephrotic urine. Biochemical abnormalities in nephrotic patients (children and adults) include hypocalcemia, both total (protein-bound) and ionized hypocalciuria, reduced intestinal calcium absorption and negative calcium balance reduced plasma 25-hydroxycholecalciferol and 24,25-dihydroxycholecalciferol and, surprisingly, also 1,25-dihydroxycholecalciferol and blunted response to parathormon (PTH) administration and increased PTH levels. Clinically, both osteomalacia and hyperparathyroidism have been described in nephrotic patients, more commonly in children than in adults, but bone biopsies are commonly normal, and clinically significant bone disease is very rare in nephrotic subjects. There is, however, evidence that patients with renal failure accompanied by nephrotic range proteinuria may be particularly prone to develop renal osteodystrophy. 

Vitamin D regulates calcium and phosphorus absorption and deposition and serum alkaline phosphatase levels. The recommended daily allowance is 5 /xg, increasing to 10 to 15 /xg in older age.109 Vitamin D3 is synthesized under UVB irradiation in the skin where it is stored and released into the circulation in a complex with the vitamin D binding protein. In liver it is hydroxylated to 25(OH)-cholecalciferol, the hormonal precursor, followed by another hydroxylation step in the... 

Q13 Osteomalacia and osteoporosis are complications of celiac disease. The mineral in bone is mainly calcium phosphate a supply of calcium is therefore needed for bone growth and replacement. Calcium is absorbed by active mechanisms in the duodenum and jejunum, facilitated by a metabolite of vitamin D. It is also passively absorbed in the ileum and specific calcium binding proteins are present in the intestinal epithelial cells. Loss of absorptive cells and calcium binding proteins markedly decreases calcium uptake and limits its availability for bone growth and repair. 

Early studies showed that, after the administration of [ H]cholecalciferol or ergocalciferol to vitamin D-deficient animals, there is marked accumulation of [ H] calcitriol in the nuclei of intestinal mucosal cells. Physiological doses of vitamin D cause an increase in the intestinal absorption of calcium in deficient animals the response is faster after the administration of calcidiol and faster stUl after calcitriol. There are two separate responses of intestinal mucosal cells to calcitriol a rapid increase in calcium uptake that is due to recruitment of calcium transporters to the cell surface (Section 3.3.2) and a later response from the induction of a calcium binding protein, calbindin-D. 

Due to the increased availability of calcium binding protein, the absorption of calcium is increased. 

Active calcitriol stimulates production of calcium binding protein in the mucosal cells of intestine, which helps absorption of more calcium. 

Chronic renal failure can result In the failure to synthesize i,25 OH)2D3and the consequent decrease in intestinal absorption of calcium (Pak, 1990). Genetic diseases can also result in the synthesis of defective l-hydrojcylase, as well as the synthesis of defective l,25(OH) D i-binding proteins. These proteins are involved in the regulation of specific genes. Each of these effects interrupts the normal action of vitamin D in maintaining plasma calcium levels. 

PTH also increases intestinal calcium absorption by increasing 1,25 (OH) 2D. PTH is a major trophic factor for renal 25(OH)t>-la-hydroxylase. It increases the conversion of 25(0H)D to the active vitamin D metabolite, l,25(OH)2D. Calcium is absorbed principally in the duodenum, although it can also be absorbed by the distal small bowel and colon. About 30% of a daily calcium intake of 1 g (25 mmo ) is absorbed. Approximately 100 mg (2.5 mmol) of calcium is secreted into gut lumen by intestinal secretion therefore net calcium absorption is 200 mg (5.0 mmol)/day. Calcium is absorbed by passive diffusion and by an active transport system. It is estimated that passive diffusion accounts for absorption of about 10% of ingested calcium per day. Active calcium absorption in the duodenum is under the control of l,25(OH)2D. This vitamin D metabolite increases the intestinal cell synthesis of a calcium-binding protein (CaBP), which enhances the net absorption of ingested calcium. 

DHCC acts like a steroidal hormone. It enters the small intestinal muscosal cell and binds to the nuclear membrane, stimulating the formation of a messenger RNA that diffuses back to the cytosol and directs the formation of several peptides. These are then assembled to form a calcium-binding protein that controls calcium absorption and transport by the small intestine (F5, H12). Besides its role in... 

Calcium Absorption. In animals, excess strontium indirectly suppresses the activation of vitamin D3 in the kidney, which severely reduces the expression of calbindin D mRNA and the translation of calbindin D protein in the duodenum (Armbrecht et al. 1979, 1998 Omdahl and DeLuca 1972). As a result, duodenal absorption of calcium is reduced. The reported inverse correlation between the amount of strontium that is absorbed and the levels of parathyroid hormone (Vezzoli et al. 1998) suggest that changes in parathyroid hormone levels mediate this effect. While there are no data on strontium-binding to the calcium receptor of the parathyroid gland, it is likely that strontium binds in place of calcium, mimicking calcium and thereby suppressing parathyroid hormone levels. A reduction in parathyroid hormone levels will decrease the level of 1-hydroxylase available to activate vitamin D3. 

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