Vitamin phosphate increased

Pyndoxal phosphate is also a cofactor for transamination reactions, In these reactions, an amino group is transferred from an amino acid to an or-keto acid, thus founing a new amino acid and a new or-keto acid, Transamination reactions are important for the synthesis of amino acids from non-protein metabolites and for the degradation of amino acids for energy production. Since pyridoxal phosphate is intimately involved ill amino add metabolism, the dietary requirement for vitamin B6 increases as the protein content of the diet increases. 

Tables 63-6.5 list some of the causes that affect plasma calcium, magnesium, and phosphate. Increased plasma calcium concentration may occur when the xeno-biotic specifically targets calcium metabolism, behaves similarly to vitamin D, and causes hyperparathyroidism or renal disease. Lead and cadmium enter bone and inhibit bone growth, increase calcium release from bone, and inhibit renal tubular reabsorption of calcium salts lead inhibits the renal bioactivation of 25-hydroxy-cholecaliciferol (Sauk and Somerman 1991). In longer-term studies, increased plasma calcium may be associated with tumor burden. Because roughly half of circulating calcium is bound to plasma albumin, hypercalcemia can also arise from dehydration. Hypoparathyroidism, pancreatitis, and renal disease can reduce plasma calcium. Acidosis increases plasma-ionized calcium concentrations, whereas alkalosis causes a decrease due to the effects of pH in the ECF or on protein binding.

Vitamin D increases serum calcium and phosphate, with calcitriol d.25rOH], vitamin D) being the major derivative responsible for promoting their intestinal absorption. Calciferol and calcitriol decrease renal excretion of calcium and phosphate. Parathyroid hormone, not vitamin D. acts via cAMP. The cause of Paget s disease is obscure. The answer is (C). 

It is well known that vitamin D increases serum phosphate levels of rachitic rats which is in turn responsible for the mineralization of bone The source of the phosphate has been examined in rats on extremely low phosphorus diets so that intestinal absorption would be a minor factor The response to 1, 25<0H)2D3 was found to the same extent in these animals as in those on a 0.1% phosphorus diet. Increased renal reabsorption of phosphate was excluded by direct examination ... 

It is no surprise that the interpretation of some of the early studies, e.g., that by Orr et al. (1923), was that vitamin D increases the absorption of calcium and phosphate. 

Most foods contain phosphorous thus there is usually no problem associated with an inadequate intake. In addition, the GI system is very efficient in the absorption of these mineral, usually absorbing two-thirds of the phosphorous ingested. Additionally, vitamin D increases phosphate absorption in the intestines. Foods that are highest in phosphorus include... 

If vitamin D has no effect on calcium absorption, it does affect calcium mobilization and thereby restores plasma concentrations of calcium. This finding explains why vitamin D deficiency was associated with hypocalcemia. The effect on the bone seems to require a synergetic action of vitamin D and parathormone. The 1,25-hydroxylated derivative seems to be the major active compound causing calcium release from the bone. The 25-hydroxyl derivative has, however, been shown to be active as well. Finally, vitamin D increases renal proximal tubular reabsorption of phosphate in normal and vitamin D deficient animals. Consequently phosphate excretion is decreased. Inasmuch as this effect occurs in parathyroidectomized animals, the effect of vitamin D or its metabolites must be direct. Again, the active metabolites are the 25 and 1,25-hydroxy derivatives. A calcium binding protein has been isolated from the kidney cortex, but its role in renal reabsorption is not known. 

Both are equally effective In man, and the latter Is often placed In the class of hormones since calciferol Is formed by the action of sunlight on 7-dehydrocholesterol In the skin (Frleden and Llpner, 1971) Vitamin D Increases bone sensitivity to parathyroid hormones and promotes Intestinal absorption of calcium and phosphate ... 

Mizumoto, Y., Liu, Z., and Klip, A., 1994, A long-lasting vitamin C derivative, ascorbic acid 2-phosphate increases myogenin gene expression and promotes differentiation in L6 muscle cells, Bio-chem. Biophys. Res. Commun. 199 394-402. 

Phosphate level—Adequate vitamin D enhances the levels of phosphates in the body, because of (1) improved absorption of phosphorus through the intestinal wall, independent of calcium absorption and (2) increased resorption of phosphates from the kidney tubules. When sufficient vitamin D is not available, urinary excretion of phosphate increases and the blood level drops. 

Three hormones regulate turnover of calcium in the body (22). 1,25-Dihydroxycholecalciferol is a steroid derivative made by the combined action of the skin, Hver, and kidneys, or furnished by dietary factors with vitamin D activity. The apparent action of this compound is to promote the transcription of genes for proteins that faciUtate transport of calcium and phosphate ions through the plasma membrane. Parathormone (PTH) is a polypeptide hormone secreted by the parathyroid gland, in response to a fall in extracellular Ca(Il). It acts on bones and kidneys in concert with 1,25-dihydroxycholecalciferol to stimulate resorption of bone and reabsorption of calcium from the glomerular filtrate. Calcitonin, the third hormone, is a polypeptide secreted by the thyroid gland in response to a rise in blood Ca(Il) concentration. Its production leads to an increase in bone deposition, increased loss of calcium and phosphate in the urine, and inhibition of the synthesis of 1,25-dihydroxycholecalciferol. 

PTH is the most important regulator of bone remodelling and calcium homeostasis. PTH is an 84-amino acid polypeptide and is secreted by the parathyroid glands in response to reductions in blood levels of ionised calcium. The primary physiological effect of PTH is to increase serum calcium. To this aim, PTH acts on the kidney to decrease urine calcium, increase mine phosphate, and increase the conversion of 25-OH-vitamin D to l,25-(OH)2-vitamin D. PTH acts on bone acutely to increase bone resorption and thus release skeletal calcium into the circulation. However, due to the coupling of bone resorption and bone formation, the longer-term effect of increased PTH secretion is to increase both bone resorption and bone formation. 

PTH has a dual effect on bone cells, depending on the temporal mode of administration given intermittently, PTH stimulates osteoblast activity and leads to substantial increases in bone density. In contrast, when given (or secreted) continuously, PTH stimulates osteoclast-mediated bone resorption and suppresses osteoblast activity. Further to its direct effects on bone cells, PTH also enhances renal calcium re-absorption and phosphate clearance, as well as renal synthesis of 1,25-dihydroxy vitamin D. Both PTH and 1,25-dihydroxyvitamin D act synergistically on bone to increase serum calcium levels and are closely involved in the regulation of the calcium/phosphate balance. The anabolic effects of PTH on osteoblasts are probably both direct and indirect via growth factors such as IGF-1 and TGF 3. The multiple signal transduction... 

Six compounds have vitamin Bg activity (Figure 45-12) pyridoxine, pyridoxal, pyridoxamine, and their b -phosphates. The active coenzyme is pyridoxal 5 -phos-phate. Approximately 80% of the body s total vitamin Bg is present as pyridoxal phosphate in muscle, mostly associated with glycogen phosphorylase. This is not available in Bg deficiency but is released in starvation, when glycogen reserves become depleted, and is then available, especially in liver and kidney, to meet increased requirement for gluconeogenesis from amino acids. 

Pyridoxal phosphate is a coenzyme for many enzymes involved in amino acid metabolism, especially in transamination and decarboxylation. It is also the cofactor of glycogen phosphorylase, where the phosphate group is catalytically important. In addition, vitamin Bg is important in steroid hormone action where it removes the hormone-receptor complex from DNA binding, terminating the action of the hormones. In vitamin Bg deficiency, this results in increased sensitivity to the actions of low concentrations of estrogens, androgens, cortisol, and vitamin D. 

Check parathyroid hormone (PTH), vitamin D and precursors, magnesium, and phosphate levels ° Pharmacological causes of decreased ionized calcium may include excess infusions of citrate, EDTA, lactate, fluoride poisoning, foscarnet, cinacalcet, bisphosphates, or unrelated increase in serum phosphate or decrease in serum magnesium levels... 

Factors that can predispose patients to developing metabolic bone disease include deficiencies of phosphorus, calcium, and vitamin D vitamin D and/or aluminum toxicity amino acids and hypertonic dextrose infusions chronic metabolic acidosis corticosteroid therapy and lack of mobility.35,39 Calcium deficiency (due to decreased intake or increased urinary excretion) is one of the major causes of metabolic bone disease in patients receiving PN. Provide adequate calcium and phosphate with PN to improve bone mineralization and help to prevent metabolic bone disease. Administration of amino acids and chronic metabolic acidosis also appear to play an important role. Provide adequate amounts of acetate in PN admixtures to maintain acid-base balance. 

Decrease blood calcium Increase blood calcium decrease blood phosphate activation of vitamin D 3 "Fight-or-flight" response reinforces effects of the sympathetic nervous system Reabsorption of sodium excretion of potassium... 

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. 

Much discussion of vitamin D focuses on bone health, though this is by no means the only focus on vitamin D action. One result of l,25(OH)2D action is the upregulation of the synthesis of a calcium-binding protein whose function is to transport dietary calcium across the intestinal mucosa and into the systemic circulation. Phosphate accompanies the calcium. This has the effect of increasing the fraction of dietary calcium that is actually absorbed and is, therefore, potentially useful for bone formation. In addition, l,25(OH2)D has the effect of mobilizing calcium from bone. Both actions tend to raise the extracellular level of calcium. 

Excretion of Ca-r-r phosphates is significantly higher in leukemia patients in comparison with healthy controls. Vitamin D3 levels in patients with leukemia are significantly lower (18.8+0.5 vs 32.1+2.0). In acute leukemia changes are revealed in bone tissue collagen with an increase of oxyproline and asparaginic acid concentrations (fig. 5). 

Vitamin D hormone is derived from vitamin D (cholecalciferol). Vitamin D can also be produced in the body it is formed in the skin from dehydrocholesterol during irradiation with UV light. When there is lack of solar radiation, dietary intake becomes essential, cod liver oil being a rich source. Metaboli-cally active vitamin D hormone results from two successive hydroxylations in the liver at position 25 ( calcifediol) and in the kidney at position 1 ( calci-triol = vit. D hormone). 1-Hydroxylation depends on the level of calcium homeostasis and is stimulated by parathormone and a fall in plasma levels of Ca or phosphate. Vit D hormone promotes enteral absorption and renal reabsorption of Ca and phosphate. As a result of the increased Ca + and phosphate concentration in blood, there is an increased tendency for these ions to be deposited in bone in the form of hydroxyapatite crystals. In vit D deficiency, bone mineralization is inadequate (rickets, osteomalacia). Therapeutic Liillmann, Color Atlas of Pharmacology... 

The polypeptide parathormone is released from the parathyroid glands when plasma Ca + level falls. It stimulates osteoclasts to increase bone resorption in the kidneys, it promotes calcium reabsorption, while phosphate excretion is enhanced. As blood phosphate concentration diminishes, the tendency of calcium to precipitate as bone mineral decreases. By stimulating the formation of vit D hormone, parathormone has an indirect effect on the enteral uptake of Ca + and phosphate. In parathormone deficiency, vitamin D can be used as a substitute that unlike parathormone, is effective orally. 

PTH is secreted from the parathyroid glands in response to a low plasma concentration of ionized (free) calcium. PTH immediately causes the transfer of labile calcium stores from bone into the bloodstream. PTH increases rates of dietary calcium absorption by the intestine indirectly via the vitamin D3 system activation of enterocyte activity. Within the kidney, PTH directly stimulates calcium reabsorption and a phosphate diuresis. 

With the exception of the possible development of a hypervitaminosis associated with high-dose administration of vitamin D2 or D3, the compounds discussed in this chapter are relatively safe. Allergic reactions to the injection of calcitonin and PTH have occurred and chronic use of some bisphosphonates has been associated with the development of osteomalacia. The principal side effects of intravenous bisphosphonates are mild and include low-grade fever and transient increases in serum creatinine and phosphate levels. Oral bisphosphonates are poorly absorbed and can cause esophageal and gastric ulceration. They should be taken on an empty stomach the individual must remain upright for 30 minutes after ingestion. 

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