| First Author | Davey RA | Year | 2008 |
| Journal | J Bone Miner Res | Volume | 23 |
| Issue | 8 | Pages | 1182-93 |
| PubMed ID | 18627265 | Mgi Jnum | J:150982 |
| Mgi Id | MGI:3852612 | Doi | 10.1359/jbmr.080310 |
| Citation | Davey RA, et al. (2008) Calcitonin receptor plays a physiological role to protect against hypercalcemia in mice. J Bone Miner Res 23(8):1182-93 |
| abstractText | 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. |
