Nature Medicine：胃酸过少会导致骨质疏松症
德国汉堡艾本德医学院的研究人员22日发表新闻公报说，他们通过研究发现，胃酸分泌过少会削弱人体从食物中摄取钙的能力，从而导致骨质疏松症。服用葡萄糖酸钙可以避免这种情况发生。

公报说，这一研究成果解释了服用抗酸药物的胃病患者更容易发生骨折的原因。研究人员还发现，在胃酸过少的情况下服用葡萄糖酸钙可以避免骨质疏松，因为人体吸收葡萄糖酸钙的能力与胃酸无关。

研究人员提醒说，目前德国市场销售的补钙药物中，95%以上的主要成分是碳酸钙，但汉堡埃彭多夫医学院的研究结果表明，碳酸钙不易被人体吸收。

这一研究成果已发表在新一期英国《自然－医学》杂志上。

生物谷推荐原始出处：

Nature Medicine 15, 674 - 681 (2009) 17 May 2009 | doi:10.1038/nm.1963

Impaired gastric acidification negatively affects calcium homeostasis and bone mass

Thorsten Schinke1,11, Arndt F Schilling1,11, Anke Baranowsky1, Sebastian Seitz1, Robert P Marshall1, Tilman Linn1, Michael Blaeker2, Antje K Huebner1, Ansgar Schulz3, Ronald Simon4, Matthias Gebauer1, Matthias Priemel1, Uwe Kornak5, Sandra Perkovic1, Florian Barvencik1, F Timo Beil1, Andrea Del Fattore6, Annalisa Frattini7,8, Thomas Streichert9, Klaus Pueschel10, Anna Villa7,8, Klaus-Michael Debatin3, Johannes M Rueger1, Anna Teti6, Jozef Zustin4, Guido Sauter4 & Michael Amling1

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).

1 Center for Biomechanics and Skeletal Biology, Department of Trauma, Hand, and Reconstructive Surgery, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
2 Department of Internal Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
3 Department of Pediatrics, University Medical Center Ulm, Ulm, Germany.
4 Institute of Pathology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
5 Institute of Medical Genetics, Charite University Medical Center, Berlin, Germany.
6 Department of Experimental Medicine, University of L'Aquila, L'Aquila, Italy.
7 Human Genome Department, Istituto di Tecnologie Biomediche, Italian National Research Council (CNR), Segrate, Italy.
8 Istituto Clinico Humanitas, IRCCS, Rozzano, Italy.
9 Institute of Clinical Chemistry, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
10 Institute of Forensic Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
11 These authors contributed equally to this work.