Panan Suntornsaratoon. Prolactin-induced alterations in the microarchitecture of trabecular bones in pregnant and lactating rats. Master's Degree(Physiology). Mahidol University. Mahidol University Library and Knowledge Center. : Mahidol University, 2009.
Prolactin-induced alterations in the microarchitecture of trabecular bones in pregnant and lactating rats
Abstract:
During pregnancy and lactation, bone resorption is enhanced to supply
calcium for fetal growth and milk production. Since hyperprolactinemia in nonmated
female rats can induce high bone turnover and trabecular bone loss,
prolactin (PRL) may be an important regulator of bone resorption during these
reproductive periods. The aims of this study were (i) to investigate normal changes
in the trabecular microarchitecture in pregnant and lactating rats by using dual
energy X-ray absorptiometry (DXA) and bone histomorphometry, and (ii) to
investigate whether PRL is involved in the changes in bone remodeling during
pregnancy and lactation. Pregnant and lactating Sprague-Dawley rats were treated
for 7 days with bromocriptine (Bromo) to suppress pituitary PRL secretion or
Bromo+PRL (0.4 or 0.6 mg/kg for pregnant and lactating rats, respectively). Agematched
control rats, non-suckling lactating rats and 15-day post-weaning rats
were injected with normal saline. After the rats were sacrificed, the left femur and
lumbar vertebra 5 (L5) were removed for measurement of bone mineral density
(BMD) and content (BMC) by DXA, and the left tibia was removed for bone
histomorphometric analysis.
The results showed that, during pregnancy, femoral and L5 BMD/BMC
were higher when compared to age-matched controls and became lower during
lactation only at the metaphysis (trabecular bone). Bone histomorphometry
showed that, on pregnant day 14 and lactating day 21, there was an increase in
bone turnover in the secondary spongiosa of the rat tibia. However, pregnancy did
not induce significant bone loss, whereas lactation led to a net bone loss, especially
on day 21 of lactation. The lactation-induced bone loss was partially restored
post-weaning. Elevated bone turnover during lactation, but not pregnancy, was
abolished in Bromo-treated rats. Exogenous PRL administration increased bone
turnover in Bromo-treated lactating rats, similar to lactation.
In conclusion, pituitary PRL secretion was responsible for the enhanced
bone turnover and trabecular bone loss during lactation, but not during pregnancy.