Effect of prenatal ethanol exposure on fetal calcium metabolism.
Alcohol consumption has adverse effects on both adult and developing bone. The mechanisms by which alcohol affects bone, however, are unknown. This study examined the possibility that maternal alcohol consumption may affect fetal bone development by altering fetal levels of parathyroid hormone (PTH), 1,25(OH)2D, or calcitonin (hormones that regulate calcium (Ca) and bone metabolism in the adult animal). Female Sprague-Dawley rats were bred and divided into three groups: 1 group was fed lab chow ad libitum (Control; C) and the other 2 groups received a liquid diet with (Ethanol; E) or without (Pair-fed; PF) ethanol. Blood from dams and fetuses was collected on day 21 of gestation, and selected fetuses were stained for determination of the degree of bone ossification. Mean fetal body weight and fetal skeletal ossification were reduced in the E compared with PF and C groups. Total Ca levels in fetal serum, however, showed a trend to be increased in E compared with PF and C fetuses, and no significant group differences were found in fetal serum levels of albumin, PTH, or calcitonin. Serum levels of 25-OH-D and 1,25(OH)2D were significantly decreased in E and PF, compared with C fetuses. Total Ca levels in maternal serum did not vary with the group; however, serum albumin levels were higher in E, compared with PF and C dams, suggesting that serum ionic Ca levels may have been reduced in the E dams. Serum levels of 25-OH-D were reduced in the E, compared with PF and C dams, whereas levels of 1,25(OH)2D were elevated. PTH levels did not vary among groups. Interestingly, serum calcitonin levels were elevated in the E, compared with PF and C, dams. These results indicate that the effects of ethanol on fetal bone development do not appear to be related to alterations in fetal serum levels of PTH, 1,25(OH)2D, or calcitonin. Maternal ethanol consumption, however, results in reduced appetite and a decrease in dietary Ca intake. Despite the reduced Ca intake, the ability of the dam to maintain Ca homeostasis appeared intact, although this may be dependent on the duration of ethanol consumption.
Keiver
K
K
Department of Anatomy, University of British Columbia, Vancouver, Canada.
Ellis
L
L
Anzarut
A
A
Weinberg
J
J
D000428:Alcohol Drinking; D000818:Animals; D001835:Body Weight; D001846:Bone Development / Q000187:drug effects; D002116:Calcitonin / Q000097:blood / Q000378:metabolism; D002118:Calcium / Q000378:metabolism*; D005314:Embryonic and Fetal Development / Q000187:drug effects; D000431:Ethanol / Q000494:pharmacology* / Q000633:toxicity; D005260:Female; D063647:Fetal Alcohol Spectrum Disorders / Q000378:metabolism; D005312:Fetal Blood / Q000737:chemistry; D005333:Fetus / Q000187:drug effects* / Q000378:metabolism*; D006801:Humans; D008297:Male; D018811:Maternal Exposure; D008431:Maternal-Fetal Exchange; D010012:Osteogenesis / Q000187:drug effects; D010281:Parathyroid Hormone / Q000097:blood / Q000378:metabolism; D011247:Pregnancy; D051381:Rats; D017207:Rats, Sprague-Dawley; D014807:Vitamin D / Q000097:blood / Q000378:metabolism
D010281:Parathyroid Hormone; D014807:Vitamin D; D000431:Ethanol; D002116:Calcitonin; D002118:Calcium