Department of Endocrinology and Metabolism, Laboratory for Molecular Endocrinology (KMEB), Medical Biotechnology Centre, University of Southern Denmark, Odense, Denmark.
J Bone Miner Res. 2010 Mar;25(3):673-5. doi: 10.1002/jbmr.44.
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.
Lrp5 基因是骨量积累的主要决定因素。最近的研究表明，它通过阻碍肠道衍生的 5-羟色胺的合成来实现这一功能，而 5-羟色胺是一种强大的骨形成抑制剂。在这项研究中，我们分析了 Lrp5（T253I）功能获得性突变导致高骨量（HBM）表型患者的血浆 5-羟色胺水平。共比较了 9 例 HBM 患者和 18 名性别和年龄匹配的对照。在 HBM 患者中，血小板少血浆中的 5-羟色胺浓度明显低于对照组（分别为 2.16 +/- 0.28ng/ml 和 3.51 +/- 0.49ng/ml，p <.05）。我们的数据支持这样一种假设，即循环 5-羟色胺水平介导了 Lrp5 功能获得性突变导致的人类骨量增加。
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