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ARS Home » Southeast Area » Little Rock, Arkansas » Arkansas Children's Nutrition Center » Research » Publications at this Location » Publication #149272
Title: ALCOHOL-INDUCED BONE LOSS IN PREGNANCY IS ASSOCIATED WITH INHIBITED BONE FORMATION AND DISRUPTED CALCIUM HOMEOSTASIS

Author
item Badger, Thomas
item Ronis, Martin
item LUMPKIN, CHARLES - UAMS
item HALEY, R - UAMS
item ZIPPERMAN, MICHELLE - ACNC
item GARDNER, WILLIAM - ACNC
item FERGUSON, MATTHEW - ACNC
item HALE, KIM - ACNC
item DALLARI, TAMMY - ACNC

Submitted to: Research Society on Alcoholism
Publication Type: Abstract Only
Publication Acceptance Date: 2/15/2003
Publication Date: 5/15/2003
Citation: BADGER, T.M., RONIS, M., LUMPKIN, C.K., HALEY, R., ZIPPERMAN, M., GARDNER, W., FERGUSON, M., HALE, K., DALLARI, T. ALCOHOL-INDUCED BONE LOSS IN PREGNANCY IS ASSOCIATED WITH INHIBITED BONE FORMATION AND DISRUPTED CALCIUM HOMEOSTASIS. Research Society on Alcoholism. 2003. v.27(5). p.60A. Abstract No. 326.

Interpretive Summary: The ACNC is interested in how dietary factors can promote bone growth and development, especially in children (fetal and postnatally). Bone turnover is accelerated in women during pregnancy and significant bone loss has been observed at the end of pregnancy and lactation. We have previously reported preliminary data demonstrating significant additional bone loss at the end of pregnancy following alcohol consumption even when optimal diets are infused intragastrically. In the current study, we extended these studies by examining serum osteocalcin (a marker of bone formation) and vitamin D status. Control and ethanol containing liquid diets were infused using an intragastric infusion model (total enteral nutrition, TEN) in pregnant Sprague-Dawley rats at a caloric intake of 220 kcal/kg3/4/d. The tibia and femur were studied by peripheral quantitative computerized tomography (pQCT). We found that trabecular bone mineral density (BMD) was significantly reduced in the proximal tibia from 353 + 8 to 298 + 10 and 293 + 10 respectively. In addition, cortical + subcortical BMD was significantly reduced in the distal tibia from 913 + 25 to 863 + 11 and 838 + 13, respectively. The loss of BMD was accompanied by a reduction in mean serum osteocalcin. In addition, the mean serum concentration of 25-hydroxy vitamin D3 was significantly elevated by ethanol treatment, while the mean serum level of 1,25 dihydroxy vitamin D3 were significantly reduced. These data suggest that ethanol exposure during pregnancy reduces bone formation at least in part through disruption of calcium homeostasis and suggests that ethanol acts to inhibit the 1-hydroxylation of 25-hydroxy vitamin D3. Our future studies will involve determining the long-term consequences of alcohol consumption during pregnancy on the mother's bone health and fetal bone development, and on mother's bone health during lactation.

Technical Abstract: We have previously reported preliminary data demonstrating significant bone loss at the end of gestation following alcohol consumption during pregnancy even when optimal diets are infused intragastrically (Ronis et al. Alc. Clin. Exp. Res. 26:142A, 2002). In the current study, we extended these studies to examine the effects of low and high ethanol doses; assessed serum osteocalcin and vitamin D status. Control and ethanol containing liquid diets were infused overnight (1800h to 0800 h) using an intragastric infusion model (total enteral nutrition, TEN). Time-impregnated Sprague-Dawley rats 220-250 g (N = 11) were infused with TEN diets at a caloric intake of 220 kcal/kg3/4/d from gestational (GE) d4 to GE d20. Two other groups of time-impregnated rats were infused with isocaloric TEN diets in which carbohydrate calories were substituted with ethanol to an average dose of 10 g/kg/d (N = 24) or 13 g/kg/d (N = 16). At sacrifice on GE d20, serum was collected. The tibia and femur were excised and scanned by peripheral quantitative computerized tomography (pQCT). In addition, urine was collected throughout the study. In both the 10 g/kg/d ethanol group (urine ethanol concentration (UEC) 109 + 13 mg/dl) and the 13 g/kg/d group (UEC 220 + 34 mg/dl), trabecular bone mineral density (BMD) was reduced in the proximal tibia from 353 + 8 to 298 + 10 and 293 + 10 respectively (p < 0.005). In addition, cortical + subcortical BMD was reduced in the distal tibia from 913 + 25 to 863 + 11 and 838 + 13, respectively (p < 0.05). The loss of BMD was accompanied by a reduction in mean serum osteocalcin (p < 0.05), a marker of bone formation. In addition, the mean serum concentration of 25-hydroxycholecalciferol was elevated by ethanol treatment (p < 0.05), while the mean serum level of 1,25 dihydroxycholecalciferol were significantly reduced (p < 0.05). These data suggest that ethanol exposure during pregnancy reduces bone formation at least in part through disruption of calcium homeostasis and suggests that ethanol acts to inhibit the 1-hydroxylation of 25-hydroxcholecalciferol.