Chronic ethanol consumption inhibits postlactational anabolic bone rebuilding in female rats.

Shankar K, Hidestrand M, Liu X, Chen JR, Haley R, Perrien DS, Skinner RA, Lumpkin CK, Badger TM, Ronis MJ
J Bone Miner Res. 2008 23 (3): 338-49

PMID: 17967133 · DOI:10.1359/jbmr.071023

UNLABELLED - EtOH consumption significantly impaired anabolic rebuilding of bone after lactation. Lower BMD and BMC in EtOH-fed rats were associated with decreased bone formation in the proximal tibia, increased proportion of adipocytes, and increased expression of TNF-alpha. EtOH-induced skeletal deficits were prevented by treatment with either NAC or sTNFR1. These data suggest that postlactational anabolic rebuilding is influenced by EtOH consumption and may affect the long-term risk of osteopenia.

INTRODUCTION - Despite significant loss of bone during lactation, BMD is restored by a powerful anabolic rebuilding process after weaning. A significant number of women resume alcohol consumption after weaning their offspring from breast feeding. The objectives of this study were to examine the consequences of chronic ethanol (EtOH) consumption on the postlactational rebuilding process and to investigate the underlying mechanisms by which EtOH mediates its detrimental effects.

MATERIALS AND METHODS - Female Sprague-Dawley rats (n = 7-9 per group) were fed EtOH-containing diets (13 g/kg/d) for 1, 2, or 4 wk after weaning of their offspring. Skeletal parameters in the proximal tibia were examined using pQCT, microCT, and histomorphometric techniques, and interventional studies were performed on the mechanistic roles of EtOH-induced oxidative stress and TNF-alpha.

RESULTS AND CONCLUSIONS - EtOH consumption completely abolished the anabolic bone rebuilding that occurred after lactation. Decreased BMD and BMC were associated with decreased bone formation and not with increased osteoclast activity. Furthermore, EtOH-fed rats showed greater proportion of fat volume/bone volume and expression of adipocyte-specific genes. EtOH-induced skeletal effects were mitigated by the dietary antioxidant, N-acetyl cysteine or by blocking TNF-alpha signaling. These data suggest EtOH consumption in the period immediately postweaning may significantly impair the mother's skeletal health and lead to long-term osteopenia.

MeSH Terms (22)

Acetylcysteine Adipocytes Alcoholism Animals Bone Density Bone Diseases, Metabolic Bone Resorption Central Nervous System Depressants Ethanol Female Free Radical Scavengers Lactation Osteogenesis Oxidative Stress Pregnancy Rats Rats, Sprague-Dawley Risk Factors Signal Transduction Tibia Time Factors Tumor Necrosis Factor-alpha

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