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

Morten Frost, Tom E. Andersen, Vijay Yadav, Kim Brixen, Gerard Karsenty, Moustapha Kassem

Research output: Contribution to journalJournal articleResearchpeer-review

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. (c) 2010 American Society for Bone and Mineral Research.
Original languageEnglish
JournalJournal of Bone and Mineral Research
Volume25
Issue number3
Pages (from-to)673-675
Number of pages2
ISSN0884-0431
DOIs
Publication statusPublished - 29. Jan 2010

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