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

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.

DOI: 10.1002/jbmr.44
05010020102011201220132014201520162017
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@article{Frost2010PatientsWH, title={Patients with high-bone-mass phenotype owing to Lrp5-T253I mutation have low plasma levels of serotonin.}, author={Morten Frost and Tom Erenskjold Andersen and Vijay K Yadav and Kim Brixen and Gerard Karsenty and Moustapha Kassem}, journal={Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research}, year={2010}, volume={25 3}, pages={673-5} }