Regulation of bone mass by serotonin: molecular biology and therapeutic implications

Annu Rev Med. 2011:62:323-31. doi: 10.1146/annurev-med-090710-133426.

Abstract

The molecular elucidation of two human skeletal dysplasias revealed that they are caused by an increase or a decrease in the synthesis of serotonin by enterochromaffin cells of the gut. This observation revealed a novel and powerful endocrine means to regulate bone mass. Exploiting these findings in the pharmacological arena led to the demonstration that inhibiting synthesis of gut-derived serotonin could be an effective means to treat low-bone-mass diseases such as osteoporosis.

Publication types

  • Review

MeSH terms

  • Animals
  • Bone Density / drug effects*
  • Clinical Trials as Topic
  • Duodenum / drug effects*
  • Duodenum / metabolism
  • Female
  • Humans
  • LDL-Receptor Related Proteins / genetics
  • Low Density Lipoprotein Receptor-Related Protein-5
  • Mice
  • Osteogenesis Imperfecta / genetics
  • Osteoporosis / drug therapy*
  • Osteoporosis / genetics
  • Pyrimidines / therapeutic use*
  • Rats
  • Serotonin / blood
  • Serotonin / metabolism*
  • Serotonin Antagonists / therapeutic use*
  • Tryptophan Hydroxylase / antagonists & inhibitors*

Substances

  • LDL-Receptor Related Proteins
  • LP533401
  • LRP5 protein, human
  • Low Density Lipoprotein Receptor-Related Protein-5
  • Lrp5 protein, mouse
  • Pyrimidines
  • Serotonin Antagonists
  • Serotonin
  • TPH1 protein, human
  • Tryptophan Hydroxylase

Supplementary concepts

  • Osteoporosis-pseudoglioma syndrome