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  Impaired gastric acidification negatively affects calcium homeostasis and bone mass

Schinke, T., Schilling, A. F., Baranowsky, A., Seitz, S., Marshall, R. P., Linn, T., et al. (2009). Impaired gastric acidification negatively affects calcium homeostasis and bone mass. Nature Medicine, 15, 674-681. doi:10.1038/nm.1963.

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Genre: Journal Article
Alternative Title : Nature Med

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 Creators:
Schinke, Thorsten, Author
Schilling, Arndt F., Author
Baranowsky, Anke, Author
Seitz, Sebastian, Author
Marshall, Robert P., Author
Linn, Tilman, Author
Blaeker, Michael, Author
Huebner, Antje K., Author
Schulz, Ansgar, Author
Simon, Ronald, Author
Gebauer, Matthias, Author
Priemel, Matthias, Author
Kornak, Uwe1, Author           
Perkovic, Sandra, Author
Barvencik, Florian, Author
Beil, F. Timo, Author
Del Fattore, Andrea, Author
Frattini, Annalisa, Author
Streichert, Thomas, Author
Pueschel, Klaus, Author
Villa, Anna, AuthorDebatin, Klaus-Michael, AuthorRueger, Johannes M., AuthorTeti, Anna, AuthorZustin, Jozef, AuthorSauter, Guido, AuthorAmling, Michael, Author more..
Affiliations:
1Research Group Development & Disease (Head: Stefan Mundlos), Max Planck Institute for Molecular Genetics, Max Planck Society, ou_1433557              

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 Abstract: Activation of osteoclasts and their acidification-dependent resorption of bone is thought to maintain proper serum calcium levels. Here we show that osteoclast dysfunction alone does not generally affect calcium homeostasis. Indeed, mice deficient in Src, encoding a tyrosine kinase critical for osteoclast activity, show signs of osteopetrosis, but without hypocalcemia or defects in bone mineralization. Mice deficient in Cckbr, encoding a gastrin receptor that affects acid secretion by parietal cells, have the expected defects in gastric acidification but also secondary hyperparathyroidism and osteoporosis and modest hypocalcemia. These results suggest that alterations in calcium homeostasis can be driven by defects in gastric acidification, especially given that calcium gluconate supplementation fully rescues the phenotype of the Cckbr-mutant mice. Finally, mice deficient in Tcirg1, encoding a subunit of the vacuolar proton pump specifically expressed in both osteoclasts and parietal cells, show hypocalcemia and osteopetrorickets. Although neither Src- nor Cckbr-deficient mice have this latter phenotype, the combined deficiency of both genes results in osteopetrorickets. Thus, we find that osteopetrosis and osteopetrorickets are distinct phenotypes, depending on the site or sites of defective acidification (pages 610–612).

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Language(s): eng - English
 Dates: 2009-06
 Publication Status: Published in print
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Title: Nature Medicine
  Alternative Title : Nature Med
Source Genre: Journal
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Pages: - Volume / Issue: 15 Sequence Number: - Start / End Page: 674 - 681 Identifier: ISSN: 1078-8956