Format

Send to

Choose Destination
J Bone Miner Res. 2010 Mar;25(3):673-5. doi: 10.1002/jbmr.44.

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

Author information

1
Department of Endocrinology and Metabolism, Laboratory for Molecular Endocrinology (KMEB), Medical Biotechnology Centre, University of Southern Denmark, Odense, Denmark.

Erratum in

  • J Bone Miner Res. 2010 Aug;25(8):1896.

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.

PMID:
20200960
DOI:
10.1002/jbmr.44
[Indexed for MEDLINE]
Free full text

Supplemental Content

Full text links

Icon for Wiley
Loading ...
Support Center