Enhanced trabecular-bone calcium deposition in female rats with a high physiological dose of prolactin diminishes after ovariectomy

Abstract

Although an increase in trabecular-bone calcium deposition has been shown to be regulated by prolactin during lactation, the physiological significance of prolactin in bone calcium metabolism in nonlactating rats remains unclear. This investigation sought to demonstrate the effects of endogenous prolactin and a high physiological dose of exogenous prolactin on bone turnover and bone calcium deposition in normal female rats, using the45Ca-labeling technique. Our results showed that suppression of endogenous prolactin with 6 mg/kg bromocriptine for 15 days significantly enhanced bone formation, but not bone resorption, in primarily trabecular sites, resulting in a significant increase in calcium deposition in the sternum and vertebrae, from –0.20 ± 0.07 to 0.40 ± 0.09 (p < 0.05) and –0.07 ± 0.11 to 0.34 ± 0.06 (p < 0.05) mmol Ca·(g dry mass)–1, respectively. Similarly, 2.5 mg/kg prolactin, a high physiological dose, increased sternal and vertebral calcium deposition, from –0.20 ± 0.07 to 0.24 ± 0.09 (p < 0.05) and –0.07 ± 0.11 to 0.25 ± 0.18 (p < 0.05) mmol Ca·(g dry mass)–1, respectively, by increasing bone formation more than bone resorption. However, as expected, prolactin had no effect on the tibia or femur, which are primarily cortical sites. Because several actions of prolactin have been known to be estradiol-dependent, we further investigated the dependence of prolactin action on 17β-estradiol. We found that 2.5 mg/kg prolactin did not increase sternal calcium deposition in ovariectomized rats. However, 10 µg/kg 17β-estradiol supplementation restored the action of prolactin. Ovariectomized rats given 17β-estradiol plus prolactin also manifested slightly but significantly higher sternal total calcium content than sham-operated rats, (4.58 ± 0.12 vs. 4.36 ± 0.11 mmol Ca·(g dry mass)–1(p < 0.05)). We concluded that a high physiological dose of prolactin promoted calcium deposition in primarily trabecular sites of nonlactating rats. This effect was diminished after ovariectomy. In addition, we showed that basal endogenous prolactin played a role in the maintenance of normal trabecular-bone turnover.