Role of 1,25-Dihydroxycholecalciferol in Calcification of Bone and Maintenance of Serum Calcium Concentration in the Rat

Tanaka, Yoko; Frank, Helen; DeLuca, Hector F.

doi:10.1093/jn/102.12.1569

Cited by 50 publications

(17 citation statements)

References 32 publications

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“…That such an action may be occurring is suggested by the results in Tables III and IV where after pretreatment of rats with 1,25-(OH)2D3, the concentration of 1,25-(OH)2D3 in the tissues due to the last administered dose is decreased and the amount of the metabolites of 1,25-(OH) 2D3 is increased when compared with rats given a single oral or intravenous dose. These data also explain the previous observation that vitamin D-deficient rats treated orally with 1,25-(OH)2D3 over a period of days behave in many respects like untreated vitamin D-deficient rats (23). In contrast to this, vitamin-D-deficient rats given daily oral doses of either vitamin D3 or 25-OHD3 show a marked stimulation in growth, serum calcium levels, and bone calcification.…”

Section: Resultssupporting

confidence: 85%

The Stimulation of 1,25-Dihydroxycholecalciferol Metabolism in Vitamin D-deficient Rats by 1,25-Dihydroxycholecalciferol Treatment

Frolik¹,

DeLuca²

1973

J. Clin. Invest.

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A B S T R A C r Daily oral administration of 1,25-dihvdroxycholecalciferol to vitamin D-deficient rats increases the rate of disappearance of [3H]1,25-dihydroxycholecalciferol and increases the rate of appearance of metabolites both less polar and more polar than 1,25-dihydroxycholecalciferol in the intestine, bone, liver, kidney, plasma, and muscle. Since 1,25-dihydroxycholecalciferol is believed to be the metabolically active form of vitamin D in the stimulation of intestinal calcium transport and bone calcium mobilization, these results provide an explanation for the fact that daily oral administration of 1,25-dihydroxycholecalciferol is relatively ineffective in the maintenance of serum calcium and in the calcification of bone in rats.

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Section: Resultssupporting

confidence: 85%

The Stimulation of 1,25-Dihydroxycholecalciferol Metabolism in Vitamin D-deficient Rats by 1,25-Dihydroxycholecalciferol Treatment

Frolik¹,

DeLuca²

1973

J. Clin. Invest.

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“…Addition of 1α-OH D 3 increased tibia Ca and P content. Tanaka et al (1971Tanaka et al ( , 1972 found the positive effects of 1α-OH D 3 on the absorption and retention of Ca in rats. These findings and our results suggest that the increase of the intestinal absorption of calcium by dietary 1α-OH D 3 improves tibia breaking-strength and calcium content in broiler chickens.…”

Section: Tibia Qualitymentioning

confidence: 98%

Dietary Calcium Levels Reduce the Efficacy of One Alpha-Hydroxycholecalciferol in Phosphorus-Deficient Diets of Broilers

et al. 2012

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One alpha-hydroxycholecalciferol (1α-OH D 3 ), an analog of cholecalciferol (vitamin D 3 ), improves growth performance and phosphorus retention in broilers. In the present study, we investigate the effects of dietary calcium (Ca) levels on the efficacy of 1α-OH D 3 in the phosphorus (P)-deficient corn-soybean meal diets of 1-to 21-d-old broilers. Four hundred female Ross 308 broilers, 1-d-old, were randomly allotted to 10 treatments with 4 cages of 10 birds each. A 5×2 factorial experiment was designed to test 0.40, 0.60, 0.80, 1.00, and 1.20% Ca combined with 0 and 5 μg/kg of 1α-OH D 3 in a basal diet (0.25% non-phytate phosphorus (NPP), 0.48% total phosphorus (tP)) without vitamin D 3 . The lowest levels of body weight gain (BWG), feed intake (FI), feed efficiency (FE), tibia quality (except of ash and P), as well as the highest value of mortality, were observed at 0.40% Ca. Additional Ca corrected the Ca deficiency and eventually 1.2% Ca caused a P deficiency. The addition of 1α-OH D 3 improved BWG, FI, FE, serum inorganic phosphate concentration, tP retention, tibia weight, length, breaking-strength, and content of ash, Ca, and P, and decreased mortality. However, 1α-OH D 3 efficacy responded negatively to dietary Ca level. These results indicate that 1α-OH D 3 exerts the highest activities at lower concentration of dietary Ca.

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“…The femurs were dried to constant weight and ashed in a muffle furnace at 650'C for 24 hours. The results are expressed as total weight of femur ash (15,16). RESULTS…”

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confidence: 99%

“…It has been reported that 1,25-(OH)2D3 has marked antirachitic activity when given each day intravenously or intraperitoneally (15,16). Results shown in Table 2 confirmed this finding and demonstrated that the daily parenteral administration of 1,25-(OH)2D3 resulted in a marked increase in the concentration of serum inorganic phosphorus, a slight increase in the level of serum calcium, and marked mineraliza- At the indicated time, the blood samples were obtained from the tail veins; intervals between sampling of blood from a single rat were not shorter than 24 hours.…”

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confidence: 99%

Role of 1,25-Dihydroxyvitamin D ₃ in Maintaining Serum Phosphorus and Curing Rickets

Tanaka

DeLuca

1974

Proc. Natl. Acad. Sci. U.S.A.

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130

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The intravenous injection of a single dose of 650 pmote of 1,25-dihydroxyvitamin D3 to rats fed a vitamin D-deticient, low-phosphorus diet caused an elevation of serum phosphorus within 5 hours which reached a maximum in about 10-12 hours. This elevated serum phosphorus returned to deficiency levels 2-3 days later. On the other hand, a single injection of 650 pmoles of 25-hydroxyvitamin D3 produced a significant rise at 12hours, reached a maximum in 24-36 hours, and was maintained for at least 7 days. before it can function (1). It generally has been assumed that this function involves (a) the stimulation of calcium absorption, and (b) the stimulation of calcium mobilization from bone, which in turn elevates serum calcium and phosphate levels. The elevation of these ions in the extracellular fluid is believed responsible for the well-known effect of vitamin D in the mineralization of bone (2-4). However, there are facts that are incompatible with such a simple explanation. Rickets in rats can be produced only with a diet deficient in both vitamin D and phosphorus (5), and is associated with low serum phosphorus and normal to slightly elevated serum calcium concentrations (5, 6). Although vitamin D-deficient rats fed low-phosphorus diets absorb adequate calcium to mineralize their bone (7), phosphorus is limiting. The development of rickets in man is in three phases, two of which are associated with a low serum phosphorus concentration (8).The present report shows that 1,25-(OH)2D3 dramatically and rapidly increases the concentration of phosphorus in the serum of rats on a low-phosphorus diet, and that this increase is independent of the well-known increases in intestinal calcium transport and bone calcium mobilization and may result from a specific effect of 1,25-(OH)2D3 in stimulating phosphate reabsorption in the kidney and possibly in stimulating phosphate absorption from the intestine. Additionally, evidence is offered that the mineralization of bone in rachitic rats is a response to increased levels of serum phosphorus induced by vitamin D3.MATERIALS AND METHODS Animals. Weanling male rats purchased from the Holtzman Co., Madison, Wis., were maintained in overhanging wire cages and fed a vitamin D-deflcient diet that contained either 1.2% calcium-0.1% phosphorus and 18% casein + 0.2% cystine (9), or 0.47% calcium-0.016% phosphorus and 18% egg white instead of casein (5). After the animals had been fed one of these diets for two weeks, they developed severe rickets, as evident in AgNO3-stained sections of radii and ulnae (10).

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Role of 1,25-Dihydroxycholecalciferol in Calcification of Bone and Maintenance of Serum Calcium Concentration in the Rat

Cited by 50 publications

References 32 publications

The Stimulation of 1,25-Dihydroxycholecalciferol Metabolism in Vitamin D-deficient Rats by 1,25-Dihydroxycholecalciferol Treatment

The Stimulation of 1,25-Dihydroxycholecalciferol Metabolism in Vitamin D-deficient Rats by 1,25-Dihydroxycholecalciferol Treatment

Dietary Calcium Levels Reduce the Efficacy of One Alpha-Hydroxycholecalciferol in Phosphorus-Deficient Diets of Broilers

Role of 1,25-Dihydroxyvitamin D ₃ in Maintaining Serum Phosphorus and Curing Rickets

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Role of 1,25-Dihydroxycholecalciferol in Calcification of Bone and Maintenance of Serum Calcium Concentration in the Rat

Cited by 50 publications

References 32 publications

The Stimulation of 1,25-Dihydroxycholecalciferol Metabolism in Vitamin D-deficient Rats by 1,25-Dihydroxycholecalciferol Treatment

The Stimulation of 1,25-Dihydroxycholecalciferol Metabolism in Vitamin D-deficient Rats by 1,25-Dihydroxycholecalciferol Treatment

Dietary Calcium Levels Reduce the Efficacy of One Alpha-Hydroxycholecalciferol in Phosphorus-Deficient Diets of Broilers

Role of 1,25-Dihydroxyvitamin D 3 in Maintaining Serum Phosphorus and Curing Rickets

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Role of 1,25-Dihydroxyvitamin D ₃ in Maintaining Serum Phosphorus and Curing Rickets