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|Title:||Calcitonin receptor plays a physiological role to protect against hypercalcemia in mice.|
|Authors:||Davey, Rachel A;Turner, Andrew G;McManus, Julie F;Chiu, W S Maria;Tjahyono, Francisca;Moore, Alison J;Atkins, Gerald J;Anderson, Paul H;Ma, Cathy;Glatt, Vaida;MacLean, Helen E;Vincent, Cristina;Bouxsein, Mary L;Morris, Howard A;Findlay, David M;Zajac, Jeffrey D|
|Affiliation:||Department of Medicine, Austin Health, University of Melbourne, Heidelberg, Victoria, Australia. firstname.lastname@example.org|
|Citation:||Journal of Bone and Mineral Research : the Official Journal of the American Society For Bone and Mineral Research; 23(8): 1182-93|
|Abstract:||It is well established that calcitonin is a potent inhibitor of bone resorption; however, a physiological role for calcitonin acting through its cognate receptor, the calcitonin receptor (CTR), has not been identified. Data from previous genetically modified animal models have recognized a possible role for calcitonin and the CTR in controlling bone formation; however, interpretation of these data are complicated, in part because of their mixed genetic background. Therefore, to elucidate the physiological role of the CTR in calcium and bone metabolism, we generated a viable global CTR knockout (KO) mouse model using the Cre/loxP system, in which the CTR is globally deleted by >94% but <100%. Global CTRKOs displayed normal serum ultrafiltrable calcium levels and a mild increase in bone formation in males, showing that the CTR plays a modest physiological role in the regulation of bone and calcium homeostasis in the basal state in mice. Furthermore, the peak in serum total calcium after calcitriol [1,25(OH)(2)D(3)]-induced hypercalcemia was substantially greater in global CTRKOs compared with controls. These data provide strong evidence for a biological role of the CTR in regulating calcium homeostasis in states of calcium stress.|
|Internal ID Number:||18627265|
Femur.anatomy & histology.pathology
Hypercalcemia.metabolism.prevention & control
Mice, Inbred C57BL
|Appears in Collections:||Journal articles|
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