A Role for Ethanol-Induced Oxidative Stress in Controlling Lineage Commitment of Mesenchymal Stromal Cells Through Inhibition of Wnt/β-Catenin Signaling
2010

Ethanol's Impact on Bone Health in Female Rats

Sample size: 28 publication 10 minutes Evidence: moderate

Author Information

Author(s): Chen Jin-Ran, Lazarenko Oxana P, Shankar Kartik, Blackburn Michael L, Badger Thomas M, Ronis Martin J

Primary Institution: University of Arkansas for Medical Sciences

Hypothesis

Ethanol inhibits bone formation through stimulation of oxidative stress to suppress Wnt signaling.

Conclusion

Chronic ethanol consumption reduces bone mineral density and disrupts bone rebuilding in postlactational female rats, but these effects can be blocked by the antioxidant N-acetylcysteine.

Supporting Evidence

  • Ethanol consumption decreased bone mineral density compared to control animals.
  • N-acetylcysteine blocked bone loss and downregulation of bone-formation markers.
  • Ethanol treatment inactivated TCF/LEF gene transcription in osteoblasts.
  • Ethanol increased adipogenesis while suppressing osteoblastogenesis.

Takeaway

Drinking alcohol can hurt your bones, especially after having babies, but taking a special vitamin can help protect them.

Methodology

Postlactational female Sprague-Dawley rats were fed ethanol-containing diets for 4 weeks, and bone mineral density and gene expression were measured.

Potential Biases

Potential bias in animal model selection and dietary control.

Limitations

The study was conducted on rats, which may not fully represent human physiology.

Participant Demographics

Postlactational female Sprague-Dawley rats.

Statistical Information

P-Value

p<0.05

Statistical Significance

p<0.05

Digital Object Identifier (DOI)

10.1002/jbmr.7

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