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This version published online on October 20, 2005
Endocrinology, doi:10.1210/en.2005-0529
A more recent version of this article appeared on January 1, 2006
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*Compound via MeSH
*Substance via MeSH
Hazardous Substances DB
*ETHANOL
Medline Plus Health Information
*High Risk Pregnancy

Submitted on May 3, 2005
Accepted on October 10, 2005

Different Molecular Mechanisms Underlie Ethanol-Induced Bone Loss in Cycling and Pregnant Rats

Kartik Shankar, Mats Hidestrand, Rani Haley, Robert A. Skinner, William Hogue, Chan-Hee Jo, Pippa Simpson, Charles K. Lumpkin Jr., James Aronson, Thomas M. Badger, and Martin J. J. Ronis*

Departments of Pharmacology and Toxicology (K.S., M.H., T.M.B., M.J.J.R), Physiology and Biophysics (T.M.B), Pediatrics (C.J, P.S, C.K.L), Orthopedics (J.A, R.A.S, W.H), College of Medicine, University of Arkansas for Medical Sciences, Little Rock, AR 72202, USA. Arkansas Children's Nutrition Center (K.S, M.H., R.H., T.M.B., M.J.J.R), Little Rock, AR, 72202, USA

* To whom correspondence should be addressed. E-mail: RonisMartinJ{at}uams.edu.

Chronic ethanol (EtOH) consumption can result in osteopenia. In the current study we examined the modulation of EtOH-induced bone-loss during pregnancy. Non-pregnant and pregnant dams were intragastrically infused either control or EtOH-containing diets throughout gestation (GD5 through 20 or an equivalent period of 15 days) by total enteral nutrition (TEN). The effects of EtOH (8.5 to 14 g/kg/d) on tibial bone mineral density (BMD), mineral content (BMC) and area (BMA) were assessed at GD20 via peripheral quantitative computerized tomography (pQCT). EtOH caused a dose-dependent decrease in BMD and BMC without affecting BMA. Trabecular BMD and BMC were significantly lower in EtOH-treated, non-pregnant dams compared with pregnant cohorts at the same infused dose of EtOH and UEC concentrations. Static histomorphometric analysis of tibiae from pregnant rats following EtOH treatment showed decreased osteoblast and osteoid surface indicating inhibited bone formation while EtOH treated cycling rats showed higher osteoclast and eroded surface indicative of increased bone resorption. Circulating osteocalcin and 1,25 (OH)2 vitamin D3 were lower in both EtOH-fed non-pregnant and pregnant rats. Gene expression of osteoclast markers, 70 kDa v-ATPase and tartrate resistant acid phosphatase were increased selectively in non-pregnant EtOH-treated rats, but not in pregnant rats. Moreover, only non-pregnant EtOH-fed rats showed induction in bone marrow RANK-L mRNA and decreased circulating 17-{beta}-estradiol levels. Our data suggest that EtOH-induced bone loss in pregnant rats is mainly due to inhibited bone formation, while in non-pregnant rats the data are consistent with increased osteoclast activation and bone resorption concomitant with decreased estradiol levels.
Key words: Ethanol • Pregnancy • Bone loss • Osteoporosis • pQCT




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