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

@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 G{\'e}rard Karsenty and Moustapha Kassem},
  journal={Journal of Bone and Mineral Research},
  year={2010},
  volume={25}
}
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… 
Patients with high‐bone‐mass phenotype owing to Lrp5‐T253I mutation have low plasma levels of serotonin
TLDR
An improved version of the image appears below and has also replaced the sub-standard version originally published in [1].
Levels of serotonin, sclerostin, bone turnover markers as well as bone density and microarchitecture in patients with high‐bone‐mass phenotype due to a mutation in Lrp5
TLDR
Increased bone mass in Lrp5‐HBM patients seems to be caused primarily by changes in trabecular and cortical bone mass and structure.
Measurement of Plasma, Serum, and Platelet Serotonin in Individuals With High Bone Mass and Mutations in LRP5
  • Grace S. Lee, C. Simpson, K. Insogna
  • Biology
    Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research
  • 2014
TLDR
There is no change in PPP serotonin in individuals with HBM‐causing mutations in LRP5, and levels of the hormone were measured in the platelet poor plasma, serum, and platelet pellet of 16 affected individuals and 16 age‐matched controls.
New Avenues in the LRP5-mediated Bone Mass Acquisition
TLDR
Key players for LRP5-mediated bone mass acquisition turn out to be different molecules with respect to the expressing tissue and action mode of these molecules, providing a chance to speculate new avenues in the LRP4-mediatedBone mass acquisition.
Genetic Analysis of Lrp5 Function in Osteoblast Progenitors
TLDR
It is shown that mice with a Dermo1-Cre-mediated disruption of Lrp5 in osteoblast progenitor cells have normal embryonic skeletogenesis and normal skeletal growth and development postnatally and add further support to the notion that dysregulation of serotonin synthesis is involved in bone mass abnormalities observed in OPPG patients.
Circulating serotonin and bone density, structure, and turnover in carcinoid syndrome.
TLDR
High circulating serotonin in carcinoid syndrome is not associated with clinically significant lower bone density, poorer bone structure, or lower bone formation markers.
LRP5, serotonin, and bone: Complexity, contradictions, and conundrums
  • D. Goltzman
  • Biology
    Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research
  • 2011
TLDR
A direct role for LRP5 in bone formation has been proposed based on studies in transgenic mice that express the Lrp5 HBM mutation in osteoblast-lineage cells, which could underlie the pathophysiology of sclerosteosis and van Buchem disease.
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