Patients with high-bone-mass phenotype owing to Lrp5-T253I mutation have low plasma levels of serotonin

✍ Scribed by Morten Frost; Tom Erenskjold Andersen; Vijay Yadav; Kim Brixen; Gerard Karsenty; Moustapha Kassem

• Book ID: 102301382
• Publisher: American Society for Bone and Mineral Research
• Year: 2010
• Tongue: English
• Weight: 109 KB
• Volume: 25
• Category: Article
• ISSN: 0884-0431
• DOI: 10.1002/jbmr.44

✦ Synopsis

Abstract

The Lrp5 gene is a major determinant of bone mass accrual. It has been demonstrated recently to achieve this function by hampering the synthesis of gut‐derived serotonin, which is a powerful inhibitor of bone formation. In this study we analyzed plasma serotonin levels in patients with a high‐bone‐mass (HBM) phenotype owing to gain‐of‐function mutation of Lrp5 (T253I). A total of 9 HBM patients were compared with 18 sex‐ and age‐matched controls. In HBM patients, the serotonin concentrations in platelet‐poor plasma were significantly lower than in the controls (mean ± SEM: 2.16 ± 0.28 ng/mL versus 3.51 ± 0.49 ng/mL, respectively, p < .05). Our data support the hypothesis that circulating serotonin levels mediate the increased bone mass resulting from gain‐of‐function mutations in Lrp5 in humans. © 2010 American Society for Bone and Mineral Research.