Sclerostin and DKK1 levels during 14 and 21 days of bed rest in healthy young men

J Musculoskelet Neuronal Interact. 2013 Mar;13(1):45-52.

Abstract

Objectives: Wnt signaling pathway may be crucial in the pathogenesis of disuse-induced bone loss. Sclerostin and DKK1, antagonists of the Wnt signaling pathway, were assessed during immobilization by bed rest in young, healthy people.

Methods: Two bed rest studies were conducted at the German Aerospace Center in Cologne. 14 days of 6° head-down-tilt bed rest were applied to eight healthy young male test subjects in study 1 and 21 days of head-down-tilt bed rest to seven healthy male subjects in study 2.

Results: Sclerostin levels increased in both studies during bed rest (study 1, 0.64±0.05 ng/ml to 0.69±0.04 ng/ml, P=0.014; study 2, 0.42±0.04 ng/ml to 0.47±0.04 ng/ml, P=0.008) and they declined at the end of the 14- and 21-day bed rest periods. DKK1 decreased during the bed rest period in study 1 (P<0.001) but increased during bed rest in study 2 (P=0.006). As expected, bone formation marker PINP decreased (study 1, P=0.013; study 2, P<0.001) and bone resorption marker NTX increased during bed rest (P<0.001).

Conclusion: Data suggest that the Wnt signaling pathway is involved in disuse-induced bone loss in young, healthy humans.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adaptor Proteins, Signal Transducing
  • Adult
  • Bed Rest / adverse effects
  • Bed Rest / methods*
  • Biomarkers / blood
  • Bone Morphogenetic Proteins / blood*
  • Bone Resorption / blood
  • Cross-Over Studies
  • Down-Regulation / physiology
  • Genetic Markers
  • Head-Down Tilt / adverse effects
  • Head-Down Tilt / physiology*
  • Humans
  • Intercellular Signaling Peptides and Proteins / blood*
  • Male
  • Up-Regulation / physiology
  • Young Adult

Substances

  • Adaptor Proteins, Signal Transducing
  • Biomarkers
  • Bone Morphogenetic Proteins
  • DKK1 protein, human
  • Genetic Markers
  • Intercellular Signaling Peptides and Proteins
  • SOST protein, human