The effect of vitamin D on the bones of young rats receiving diets low in calcium or phosphorus

Ferguson, H. W.; Hartles, R.L.

doi:10.1016/0003-9969(63)90031-1

Cited by 36 publications

(11 citation statements)

References 10 publications

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“…In the present study, calcium deficiency alone caused a decrease in bone ash of 9-10%. The decrease was not as great as those observed by Rasmussen [33] and Ferguson and Hartles [34] because a less extreme deficiency of shorter duration was employed here. The loss of bone mineral from the skeleton caused by lactation alone has been reported to be between 10 and 20% [2, 3,35], which is in good agreement with the value (17%) obtained in the present study.…”

Section: Discussionsupporting

confidence: 52%

Metabolic aspects of bone resorption in calcium-deficient lactating rats

1980

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Lactating female rats were fed diets containing 1.0, 0.1, or 0.04% Ca for 21 days. Fat-free dry weight, ash weight, calcium and phosphorus content of the humerus, plasma calcium levels, and bone acid and alkaline phosphatase activities were compared to those of nonlactating rats fed the same diets. Bone, plasma, and urinary cAMP levels were also studied. Dietary calcium deficiency and/or lactation caused significant loss of bone mass from experimental animals. Urinary cAMP levels reflecting increased parathyroid activity were elevated by the stresses of lactation and calcium deficiency over those of control animals. Plasma and bone levels of cAMP were not different. Bone alkaline and acid phosphatase activities were affected only by the most extreme stress. The results demonstrated that the calcium-deficient lactating rat is an excellent model for bone resorption studies.

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Section: Discussionsupporting

confidence: 52%

Metabolic aspects of bone resorption in calcium-deficient lactating rats

1980

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“…Work in the first half of this century documented that a lack of dietary phosphorus produced rickets in vitamin D-deficient rats. (57)(58)(59)(60)(61) The op/op mouse also followed this general rule in the development of the rickets phenotype, but the op/op mouse required more dietary calcium and phosphorus to relieve the rickets since mineral was not available from bone. We have noted that the op/op mouse required more dietary calcium to prevent hypocalcemic tetany.…”

Section: Discussionmentioning

confidence: 91%

“…From this correlation, we showed that in both normal and op/op mice, the severity of rickets was indirectly related to serum phosphorus. Work in the first half of this century documented that a lack of dietary phosphorus produced rickets in vitamin D–deficient rats 57–61 . The op/op mouse also followed this general rule in the development of the rickets phenotype, but the op/op mouse required more dietary calcium and phosphorus to relieve the rickets since mineral was not available from bone.…”

Section: Discussionmentioning

confidence: 95%

Hypophosphatemia and the Development of Rickets in Osteopetrotic (op/op) Mice

McCary

Smith

DeLuca

1997

Journal of Bone and Mineral Research

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Our previous work has shown that op/op mice hyperabsorb dietary calcium in the vitamin D-deficient state and shunt that calcium into bone. Under these conditions, the op/op mice are hypocalcemic. The purpose of this study was to examine calcium metabolism and bone mineralization in vitamin D-deficient op/op mice. First, the op/op mice and their normal littermates were placed on a vitamin D-deficient, low phosphorus diet to limit bone mineralization. Under these circumstances, op/op mice survived, even when calcium was also removed from the diet. If the diet contained phosphate, op/op mice died from hypocalcemic tetany when calcium was also removed from the diet. Furthermore, serum calcium levels became similar to wild type in the op/op mice administered the vitamin D-deficient, low phosphorus diet, and op/op mice were able to increase serum calcium in response to 1,25-dihydroxyvitamin D 3 . The op/op mice developed rickets when their serum phosphorus level was too low to support bone mineralization. The op/op mice became hypophosphatemic on regimens in which normal mice were able to maintain normal serum phosphorus levels. It appears that the op/op mouse simply requires a higher dietary calcium and phosphorus level to prevent rickets and hypocalcemic tetany since the bone is not available as a source of these minerals. However, the ability of the op/op mouse to mineralize bone at low serum calcium and phosphorus levels remains

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“…An increase in pNNP-ase, PPi-ase, Ca 2+ -ATPase activities [23], and protein synthesis of odontoblasts [22] are reported as a response to calcium and vitamin D deficiency. However, in the rat, calcium deficiency causes a condition that is, in bones, closer to osteoporosis than osteomalacia, whereas calcium and vitamin D deficiency together induce changes closer to osteomalacia than osteoporosis [24]. As dietary vitamin D deficiency was not present in our study (Table 1), we concluded that the only factor that could explain the response of odontoblasts in calcium-deficient animals was the lower level of calcium in the diet, which caused hypocalcemia ( Table 2) and in that way, decreased dentin apposition (Fig.…”

Section: Discussionmentioning

confidence: 97%

The Reducing Effects of a Calcium-Deficient Diet and High Sucrose Diet on Dentin Apposition of Rat Molars

et al. 2000

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A high sucrose diet reduces dentin apposition of growing rats. The mechanisms of reduction are unclear, but disturbances in calcium balance or in mineralization of predentin may explain them. In this experiment, 29 Sprague-Dawley rats, 21 days old, were weaned and randomized into calcium-deficient, high-sucrose or standard-diet groups for 3 weeks. They were given food and water ad libitum. During the experiment, animals were individually housed in metabolic cages where urine samples were collected. At ages of 21 and 40 days mineralizing dentin was marked using I.P. injections of oxytetracycline hydrochloride. At 42 days of age, the animals were anesthetized and their blood was collected by cardiac puncture. Right hemimandibles were sectioned sagittally and left hemimandibles were fixed, decalcified, and cut into histological sections. Dentin appositions were measured planimetrically, predentin width, from histological sections. Ca, K, and Na levels of serum and urine were measured flame photimetrically and P levels were measured by the UV method. Statistical analyses were done using one-way analysis of variation (ANOVA) Tuckey's HSD t test. In the calcium-deficient group, hypocalcemia, reduced dentin apposition, and increased predentin width were noticed when compared with the control group (P<0.05). Also, the increase in predentin width, caused by calcium deficiency, was significant compared with sucrose-fed animals (P<0.05). Sucrose diet reduced dentinogenesis, increased Ca excretion to urine, but also reduced urinary levels of P, K, and Na, and the differences were significant for the controls (P<0.05). In conclusion, despite the same kind of reduced dentinogenesis in calcium-deficient and high-sucrose groups, calcium imbalance or reduced mineralization of predentin does not explain reduced dentinogenesis in sucrose-fed animals.

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The effect of vitamin D on the bones of young rats receiving diets low in calcium or phosphorus

Cited by 36 publications

References 10 publications

Metabolic aspects of bone resorption in calcium-deficient lactating rats

Metabolic aspects of bone resorption in calcium-deficient lactating rats

Hypophosphatemia and the Development of Rickets in Osteopetrotic (op/op) Mice

The Reducing Effects of a Calcium-Deficient Diet and High Sucrose Diet on Dentin Apposition of Rat Molars

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