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ARS Home » Southeast Area » Little Rock, Arkansas » Microbiome and Metabolism Research Unit » Research » Publications at this Location » Publication #217092
Title: Chronic Ethanol Consumption Inhibits Postlactational Anabolic Rebuilding in Female Rats

Author
item SHANKAR, KARTIK - ACNC/UAMS
item HIDESTRAND, MATS - UAMS
item LIU, XIAOLI - ACNC/UAMS
item CHEN, JINRAN - ACNC/UAMS
item HALEY, RANI - ACNC/UAMS
item PERRIEN, DANIEL - UAMS
item SKINNER, ROBERT - UAMS
item LUMPKIN, CHARLES - UAMS
item BADGER, THOMAS - ACNC/UAMS
item RONIS, MARTIN - ACNC/UAMS

Submitted to: Journal of Bone and Mineral Research
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 10/11/2007
Publication Date: 3/3/2008
Citation: Shankar, K., Hidestrand, M., Liu, X., Chen, J., Haley, R., Perrien, D., Skinner, R.A., Lumpkin, C.A., Badger, T.M., Ronis, M.J. 2008. Chronic ethanol consumption inhibits postlactational anabolic rebuilding in female rats. Journal of Bone and Mineral Research. 23(3):338-349.

Interpretive Summary: Consumption of alcohol (ethanol) during pregnancy remains an important public health issue, primarily due to the effects on the growing baby. However, the harmful effects of alcohol on the mother, especially on the maternal skeleton, remain unclear. Specifically, the post-lactation period when active rebuilding of the skeleton in the mother is occurring is a period susceptible to the detrimental effects of alcohol. To examine this issue we have undertaken studies using post-weaning rats and fed them nutritionally sufficient diets either with or without alcohol. The studies show that consumption of alcohol is harmful to the bones, as both the density and mineral content of the bones (and hence strength) were decreased in rats consuming alcohol. Further, the way alcohol causes this decrease in bone health appears to be related to the ability of alcohol to produce harmful reactive intermediates in the bone, called reactive oxygen species. These appear to activate chemical signals called cytokines (like TNF-alpha) and halt the formation/maturation of new bone forming cells (osteoblasts). These effects of alcohol can be reversed by antioxidants like N-acetyl cysteine. Further, our studies also indicate that consumption of alcohol diverts the new bone-forming oteoblasts to become fat-laden adipocytes, hence decreasing the strength and density of the bone. These findings may have important implications for the long-term health consequences of post-weaning mothers consuming alcohol.

Technical Abstract: Despite significant loss of bone during lactation, bone mineral density (BMD) is restored by a powerful anabolic rebuilding process following weaning. A significant number of women resume alcohol consumption after weaning their offspring from breast feeding. The objectives of the present study were to examine the consequences of chronic EtOH consumption on the post-lactational rebuilding process and to investigate the underlying mechanisms by which EtOH mediates its detrimental effects. Female Sprague-Dawley rats (n = 7-9 per group) were fed EtOH-containing diets (13 g/kg/d) for 1, 2, or 4 wk following weaning of their offspring. Skeletal parameters in the proximal tibia were examined using pQCT, Mu CT, and histomorphometric techniques, and interventional studies were performed on the mechanistic roles of EtOH-induced oxidative stress and TNF-alpha. EtOH consumption completely abolished the anabolic bone rebuilding that occurred following lactation. Decreased BMD and BMC were associated with decreased bone formation and not with increased osteoclast activity. Further, EtOH-fed rats showed greater proportion of fat volume/BV and expression of adipocyte-specific genes. EtOH-induced skeletal effects were mitigated by the dietary antioxidant, N-acetyl cysteine (NAC) or by blocking TNF-alpha signaling. These data suggest EtOH consumption in the period immediately post-weaning may significantly impair the mother's skeletal health and lead to long-term osteopenia.