Resumé
| Originalsprog | Engelsk |
|---|---|
| Tidsskrift | Journal of Bone and Mineral Research |
| Vol/bind | 25 |
| Udgave nummer | 3 |
| Sider (fra-til) | 673-675 |
| Antal sider | 2 |
| ISSN | 0884-0431 |
| DOI | |
| Status | Udgivet - 29. jan. 2010 |
Fingeraftryk
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Patients with high-bone-mass phenotype owing to Lrp5-T253I mutation have low plasma levels of serotonin. / Frost, Morten; Andersen, Tom E.; Yadav, Vijay; Brixen, Kim; Karsenty, Gerard; Kassem, Moustapha.
I: Journal of Bone and Mineral Research, Bind 25, Nr. 3, 29.01.2010, s. 673-675.Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › peer review
TY - JOUR
T1 - Patients with high-bone-mass phenotype owing to Lrp5-T253I mutation have low plasma levels of serotonin
AU - Frost, Morten
AU - Andersen, Tom E.
AU - Yadav, Vijay
AU - Brixen, Kim
AU - Karsenty, Gerard
AU - Kassem, Moustapha
PY - 2010/1/29
Y1 - 2010/1/29
N2 - 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.
AB - 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.
U2 - 10.1002/jbmr.44
DO - 10.1002/jbmr.44
M3 - Journal article
C2 - 20200960
VL - 25
SP - 673
EP - 675
JO - Journal of Bone and Mineral Research
JF - Journal of Bone and Mineral Research
SN - 0884-0431
IS - 3
ER -