Quantitation of Calcium Metabolism. Theory*

Aubert, Jean-Paul; Bronner, Felix; Richelle, Laurence

doi:10.1172/jci104781

Cited by 113 publications

(53 citation statements)

References 21 publications

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“…According to this model the decrease in specific activity (R) in plasma or in urine, after the tracer has become distributed homogenously in the miscible pool, is described by a monoexponential curve R (t) = Aekt, where A and k are experimental constants, and t is time in days. In most studies performed on human subjects a monoexponential decrease of plasma and urine specific activity was indeed found to occur between about 36 and 146 hr after intravenous injection of radiocalcium (19,(21)(22)(23). Accordingly in our study the parameters A and k were derived from the linear portion of the semilogarithmic urine specific activity curve obtained from 34 hr to 106, 130, or 154 hr after injection of the isotope.…”

Section: Methodsmentioning

confidence: 86%

“…Kinetic calculations were carried out according to a simplified method (19)(20)(21) based upon the assumption of an open one compartmental homogenous miscible calcium pool (21,22). Calcium is removed from the pool via the plasma to the bone and is excreted in the urine and in the feces.…”

Section: Methodsmentioning

confidence: 99%

“…Calcium is removed from the pool via the plasma to the bone and is excreted in the urine and in the feces. It is further assumed that during the experimental period no labeled calcium is returned from the bone to the miscible calcium pool (21)(22)(23)(24). According to this model the decrease in specific activity (R) in plasma or in urine, after the tracer has become distributed homogenously in the miscible pool, is described by a monoexponential curve R (t) = Aekt, where A and k are experimental constants, and t is time in days.…”

Section: Methodsmentioning

confidence: 99%

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Metabolic and calcium kinetic studies in idiopathic hypercalciuria

Liberman¹,

Sperling²,

Atsmon³

et al. 1968

J. Clin. Invest.

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A B S T R A C T Calcium balances and calcium kinetic studies using 47Ca were performed in nine male patients with idiopathic hypercalciuria and in three normal male subjects. A sharp reduction in calcium intake in eight patients with idiopathic hypercalciuria caused a decrease in urinary calcium excretion, the latter remaining elevated above that reported for normal subjects on a low calcium diet. The hypercalciuric patients had an enlarged miscible calcium pool size, an increased calcium turnover rate, increased bone formation and bone resorption rates, and an elevated true intestinal calcium absorption rate, the increase of the latter three parameters being proportional to the increase of the turnover rate. The fraction of the calcium turnover rate excreted in the urine was elevated whereas that constituted by the endogenous fecal calcium excretion was decreased. Arguments are presented for the concept that the primary abnormality in idiopathic hypercalciuria is neither renal calcium hyperexcretion nor intestinal calcium hyperreabsorption, but a more fundamental disturbance in calcium metabolism of as yet unknown cause, leading to a high calcium turnover.

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Section: Methodsmentioning

confidence: 86%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

See 1 more Smart Citation

Metabolic and calcium kinetic studies in idiopathic hypercalciuria

Liberman¹,

Sperling²,

Atsmon³

et al. 1968

J. Clin. Invest.

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show abstract

“…Whereas in adults the primary regulatory response to an increase in intestinal calcium absorption is a decrease in bone resorption (3,5,6,9), VLBW infants respond largely by increasing the flow of calcium directed at bone. In both adults and VLBW infants, the effect of these responses is the same, i.e.…”

Section: Discussionmentioning

confidence: 99%

Compartmental Analysis of Calcium Metabolism in Very-Low-Birth-Weight Infants

et al. 1994

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The calcium metabolism of 13 very-low-birth-weight infants fed a high-calcium diet was evaluated by means of stable isotope kinetic and balance studies. The studies used orally and i.v. administered stable isotopes, and the kinetic data were evaluated with the aid of a sequential, threecompartment model. The infants (postmenstrual age 33 a 1 wk, weight 1.34 -c 0.03 kg) had higher bone calcium deposition rates (160 2 7 mg-kg-'.d-' or 4.00 2 0.18 mmol-kgpt-d-I) than those previously reported for either older children or adults. Furthermore, when analyzed as a function of net calcium absorption, bone calcium deposition rates increased markedly and significantly as net calcium absorption increased (r = 0.70,~ < 0.01), whereas in older individuals, bone calcium deposition is a relatively invariant function of absorption. A relatively smaller response of bone calcium removal to calcium absorption was found for the Mathematical analysis of the time-dependent changes in the serum, urinary, and fecal levels of orally and i.v. administered calcium isotopes permits evaluation of the major components of calcium metabolism (1-10). A compartmental model has been used for these analyses, and its use allows the evaluation of the effects of variations in physiologic, nutritional, and endocrinologic status on cal- very-low-birth-weight infants in this study (r = -0.39, p = 0.18), whereas in adults, bone calcium removal constitutes the major regulatory response. It is suggested that the calcium kinetic results in the very-low-birth-weight infants reflect the high rate of bone growth typical of the third trirnester of gestation. VLBW, very low birth weight (< 1500 g) APA, serum alkaline phosphatase activity cium metabolism. Although the form of the model chosen will affect the precise numerical values for given parameters, fundamental relationships and characteristics including the bone calcium deposition and resorption rates are independent of model configuration (2, 6).The application of compartmental models to the study of calcium metabolism in small infants poses significant problems (11,12). Blood sampling must be minimized in infants and complete fecal and urine collections of adequate length are difficult to obtain. Because radioactive isotopes cannot ethically be used in small infants, stable Supported by the General Clinical Research Center. Baylor College of Medi-isotopes must be used at much greater expense. cium regulatory mechanisms that have been described for

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“…Radiocalcium kinetic data were analyzed according to the model of Aubert, Bronner, and Richelle (6). A tracer dose (usually 10 jCi) was given intravenously, and serum disappearance and urinary and fecal excretion were determined by radioassay using standard methods (7).…”

Section: Methodsmentioning

confidence: 99%

Short- and long-term effects of estrogen and synthetic anabolic hormone in postmenopausal osteoporosis

Riggs¹,

Jowsey²,

Goldsmith³

et al. 1972

J. Clin. Invest.

225

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A B S T R A C T In 29 women with postmenopausal osteoporosis, the proportion of total bone surface undergoing resorption or formation was evaluated by microradiography of iliac crest biopsy samples before and after shortterm (21-4 months) and long-term (26-42 months for estrogen and 9-15 months for anabolic hormone) treatment. After estrogen administration, values for boneresorbing surfaces decreased, although less prominently after long-term than after short-term therapy. The magnitude of this decrease was positively correlated with the pretreatment value for bone-resorbing surfaces (P < 0.001). When the pretreatment value for bone-resorbing surfaces was used as a covariable, estrogen and anabolic hormone appeared to be equally effective. For boneforming surfaces, short-term therapy with either hormone had no effect but long-term therapy significantly decreased the values. Serum immunoreactive parathyroid hormone (IPTH) increased significantly after estrogen therapy; the change in IPTH was inversely related to the change in serum calcium (P < 0.001, sign test). We conclude that the primary effect of sex hormones in postmenopausal osteoporosis is to decrease the increased level of bone resorption, perhaps by decreasing the responsiveness of bone to endogenous parathyroid hormone. However, this favorable effect, at least in part, is negated after long-term treatment by a secondary decrease in bone formation. Our data are consistent with the concept that the maximal benefit that can be derived from sex hormone therapy in postmenopausal osteoporosis is arrest or slowing of the progession of bone loss.

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Quantitation of Calcium Metabolism. Theory*

Cited by 113 publications

References 21 publications

Metabolic and calcium kinetic studies in idiopathic hypercalciuria

Metabolic and calcium kinetic studies in idiopathic hypercalciuria

Compartmental Analysis of Calcium Metabolism in Very-Low-Birth-Weight Infants

Short- and long-term effects of estrogen and synthetic anabolic hormone in postmenopausal osteoporosis

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