Métabolisme minéral osseux: données récentes et perspectives relatives à l’ostéogenèse

Gennero, Isabelle; Moulin, P.; Edouard, Thomas; Conte-Auriol, F.; Tauber, Maïté; Salles, Jean Pierre

doi:10.1016/j.arcped.2004.08.006

Cited by 5 publications

(1 citation statement)

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“…We assume that resorption is activated by (saturating levels of) PTH and D3 (42,54), and that resorption increases sixfold when stimulation by PTH and vitamin D3 is maximal; that is, ⌫ res min ϩ ␦ res max ϭ 6⌫ res min . The kidney compartment.…”

Section: Calcium Exchanges Between Organsmentioning

confidence: 99%

A model of calcium homeostasis in the rat

Granjon

Bonny

Edwards

2016

American Journal of Physiology-Renal Physiology

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We developed a model of calcium homeostasis in the rat to better understand the impact of dysfunctions such as primary hyperparathyroidism and vitamin D deficiency on calcium balance. The model accounts for the regulation of calcium intestinal uptake, bone resorption, and renal reabsorption by parathyroid hormone (PTH), vitamin D, and Ca itself. It is the first such model to incorporate recent findings regarding the role of the calcium-sensing receptor (CaSR) in the kidney, the presence of a rapidly exchangeable pool in bone, and the delayed response of vitamin D synthesis. Accounting for two (fast and slow) calcium storage compartments in bone allows the model to properly predict the effects of bisphophonates on the plasma levels of Ca ([Ca]), PTH, and vitamin D Our model also suggests that Ca exchange rates between plasma and the fast pool vary with both sex and age, allowing [Ca] to remain constant in spite of sex- and age-based hormonal and other differences. Our results suggest that the inconstant hypercalciuria that is observed in primary hyperparathyroidism can be attributed in part to counterbalancing effects of PTH and CaSR in the kidney. Our model also correctly predicts that calcimimetic agents such as cinacalcet bring down [Ca] to within its normal range in primary hyperparathyroidism. In addition, the model provides a simulation of CYP24A1 inactivation that leads to a situation reminiscent of infantile hypercalcemia. In summary, our model of calcium handling can be used to decipher the complex regulation of calcium homeostasis.

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Section: Calcium Exchanges Between Organsmentioning

confidence: 99%