Oxytocin deficiency impairs maternal skeletal remodeling

Biochem Biophys Res Commun. 2009 Oct 9;388(1):161-6. doi: 10.1016/j.bbrc.2009.07.148. Epub 2009 Aug 3.

Abstract

We have reported that the posterior pituitary hormone, oxytocin (OT), known for its effects in inducing parturition, lactation and social bonding, is also a skeletal hormone. Here, we demonstrate that OT plays a key role in enabling maternal skeletal mobilization during pregnancy by enhancing the formation of bone resorbing osteoclasts. Osteoclast formation ex vivo is thus diminished in pregnant mothers with genetic OT-deficiency. OT(-/-) pups at day E20 also show a defect in trabecular bone. microCT measurements reveal normal bone volume, but increased trabecular numbers, suggesting that trabeculae in OT(-/-) pups are hypomineralized. We suggest that OT facilitates intergenerational transfer of calcium ions from a pregnant mother to the pups.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Bone and Bones / embryology*
  • Bone and Bones / metabolism
  • Calcification, Physiologic / genetics
  • Calcification, Physiologic / physiology*
  • Calcium Signaling
  • Female
  • Mice
  • Mice, Mutant Strains
  • Osteoclasts / metabolism
  • Osteoclasts / physiology*
  • Oxytocin / genetics
  • Oxytocin / physiology*
  • Pregnancy

Substances

  • Oxytocin