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Davey, Rachel A; Turner, Andrew G; McManus, Julie F; Chiu, WS Maria; Tjahyono, Francisca; Moore, Alison J; Atkins, Gerald J; Anderson, Paul H; Ma, Cathy; Glatt, Vaida; MacLean, Helen E; Vincent, Cristina; Bouxsein, Mary; Morris, Howard A; Findlay, David M; Zajac, Jeffrey D

Calcitonin Receptor Plays a Physiological Role to Protect Against Hypercalcemia in Mice

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  • Medientyp: E-Artikel
  • Titel: Calcitonin Receptor Plays a Physiological Role to Protect Against Hypercalcemia in Mice
  • Beteiligte: Davey, Rachel A; Turner, Andrew G; McManus, Julie F; Chiu, WS Maria; Tjahyono, Francisca; Moore, Alison J; Atkins, Gerald J; Anderson, Paul H; Ma, Cathy; Glatt, Vaida; MacLean, Helen E; Vincent, Cristina; Bouxsein, Mary; Morris, Howard A; Findlay, David M; Zajac, Jeffrey D
  • Erschienen: Oxford University Press (OUP), 2008
  • Erschienen in: Journal of Bone and Mineral Research
  • Sprache: Englisch
  • DOI: 10.1359/jbmr.080310
  • ISSN: 0884-0431; 1523-4681
  • Schlagwörter: Orthopedics and Sports Medicine ; Endocrinology, Diabetes and Metabolism
  • Entstehung:
  • Anmerkungen:
  • Beschreibung: <jats:title>Abstract</jats:title> <jats:p>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 &amp;gt;94% but &amp;lt;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)2D3]-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.</jats:p>
  • Zugangsstatus: Freier Zugang