Licht-im-Terrarium: Literaturdatenbank
Licht-im-Terrarium: Literaturdatenbank |
|
 |
|
Lieben, L., Masuyama, R., Torrekens, S., Looveren, R. V., Schrooten, J., & Baatsen, P., et al. (2012). Normocalcemia is maintained in mice under conditions of calcium malabsorption by vitamin d–induced inhibition of bone mineralization. The Journal of Clinical Investigation, 122(5), 1803–1815. Added by: Sarina (2021-08-22 09:18:22) Last edited by: Sarina (2021-08-22 09:41:17) |
| Resource type: Journal Article DOI: 10.1172/JCI45890 BibTeX citation key: Lieben2012 View all bibliographic details  |
Categories: Englisch = English Keywords: Vitamin D = Vitamin D Creators: Baatsen, Bonewald, Bouillon, Carmeliet, Dresselaers, Feng, Lafage-Proust, Lieben, Looveren, Masuyama, Meyer, Pike, Schrooten, Torrekens Collection: The Journal of Clinical Investigation |
Views: 4/554 Views index: % Popularity index: 1.5% |
|
Meine Sichtweise (Keine vollständige Zusammenfassung des Artikels! Meine Meinung muss nicht mit der Meinung der Autoren übereinstimmen! Bitte lesen Sie auch die Originalarbeit!)
Mangelnde Kalziumaufnahme über die Nahrung bei gleichzeit ausreichend Vitamin-D3 führt dazu, dass Kalzium aus den Knochen entnommen wird. Added by: Sarina |
| Abstract |
|
Serum calcium levels are tightly controlled by an integrated hormone-controlled system that involves active vitamin D [1,25(OH)2D], which can elicit calcium mobilization from bone when intestinal calcium absorption is decreased. The skeletal adaptations, however, are still poorly characterized. To gain insight into these issues, we analyzed the consequences of specific vitamin D receptor (Vdr) inactivation in the intestine and in mature osteoblasts on calcium and bone homeostasis. We report here that decreased intestinal calcium absorption in intestine-specific Vdr knockout mice resulted in severely reduced skeletal calcium levels so as to ensure normal levels of calcium in the serum. Furthermore, increased 1,25(OH)2D levels not only stimulated bone turnover, leading to osteopenia, but also suppressed bone matrix mineralization. This resulted in extensive hyperosteoidosis, also surrounding the osteocytes, and hypomineralization of the entire bone cortex, which may have contributed to the increase in bone fractures. Mechanistically, osteoblastic VDR signaling suppressed calcium incorporation in bone by directly stimulating the transcription of genes encoding mineralization inhibitors. Ablation of skeletal Vdr signaling precluded this calcium transfer from bone to serum, leading to better preservation of bone mass and mineralization. These findings indicate that in mice, maintaining normocalcemia has priority over skeletal integrity, and that to minimize skeletal calcium storage, 1,25(OH)2D not only increases calcium release from bone, but also inhibits calcium incorporation in bone.
Added by: Sarina |