Patients With High-Bone-Mass Phenotype Owing to Lrp5-T253I Mutation Have Low Plasma Levels of Serotonin

被引:49
作者
Frost, Morten [1 ]
Andersen, Tom Erenskjold [1 ]
Yadav, Vijay [2 ]
Brixen, Kim [1 ]
Karsenty, Gerard [2 ]
Kassem, Moustapha [1 ,3 ]
机构
[1] Univ So Denmark, Ctr Med Biotechnol, Lab Mol Endocrinol KMEB, Dept Endocrinol & Metab, Odense, Denmark
[2] Columbia Univ, Dept Genet & Dev, New York, NY USA
[3] King Saud Univ, Coll Med, Dept Anat, Stem Cell Unit, Riyadh 11461, Saudi Arabia
关键词
SEROTONIN; LRP5; HIGH BONE MASS; T2531; BONE FORMATION; REUPTAKE INHIBITORS; DENSITY; RISK;
D O I
10.1002/jbmr.44
中图分类号
R5 [内科学];
学科分类号
100201 [内科学];
摘要
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 (T2531). 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.
引用
收藏
页码:673 / 675
页数:3
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