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Inhibition of bone mineral loss during lactation by Cl2MBP
1Department of Physiology, Chicago College of Osteopathic Medicine, Downers Grove, Illinois.
Pregnant rats were injected subcutaneously with either saline or the bisphosphonate Cl2MBP (dichloromethylenebisphosphonic acid) at a daily dose of 15 mg P/kg body weight on days 1 through 16 of gestation. Cl2MBP treatment did not influence maternal body weight nor the number of pups born. When analyzed 1 day after birth, pups from Cl2MBP-treated rats had a normal body weight but a 10% reduction in carcass calcium (Ca) content. The Cl2MBP injections were resumed on day 1 postpartum and led to a 10% reduction in pup body weight gain and carcass Ca content at 16 days of age. In saline-injected rats, lactation resulted in slight hypocalcemia, greatly elevated serum levels of 1,25(OH)2D3, and loss of bone mineral, as indicated by a reduction in femur ash weight. In non-lactating rats, Cl2MBP treatment produced slight hypercalcemia but had no effect on serum 1,25(OH)2D3 levels or bone mineral content. Compared to lactating rats receiving saline, Cl2MBP-treated lactating rats were more hypocalcemic and had higher serum 1,25(OH)2D3 levels. However, the lactation-induced loss of bone mineral was completely inhibited by Cl2MBP treatment.
Pregnant rats were injected subcutaneously with either saline or the bisphosphonate Cl2MBP (dichloromethylenebisphosphonic acid) at a daily dose of 15 mg P/kg body weight on days 1 through 16 of gestation. Cl2MBP treatment did not influence maternal body weight nor the number of pups born. When analyzed 1 day after birth, pups from Cl2MBP-treated rats had a normal body weight but a 10% reduction in carcass calcium (Ca) content. The Cl2MBP injections were resumed on day 1 postpartum and led to a 10% reduction in pup body weight gain and carcass Ca content at 16 days of age. In saline-injected rats, lactation resulted in slight hypocalcemia, greatly elevated serum levels of 1,25(OH)2D3, and loss of bone mineral, as indicated by a reduction in femur ash weight. In non-lactating rats, Cl2MBP treatment produced slight hypercalcemia but had no effect on serum 1,25(OH)2D3 levels or bone mineral content. Compared to lactating rats receiving saline, Cl2MBP-treated lactating rats were more hypocalcemic and had higher serum 1,25(OH)2D3 levels. However, the lactation-induced loss of bone mineral was completely inhibited by Cl2MBP treatment.