The influence of prolactin on bone mineral density (BMD) and some biochemical markers of ovariectomized rats

Abstract

ABSTRACT:A model of postmenopausal osteoporosis was used in the study. 107 days after ovariectomy the animals were subcutaneously applied 1.0 IU PRL/kg BM or 1.0 IU calcitonin/kg BM for 7 days in single doses. The application of the preparations started again 80 days after the first application. After 194 days the animals were narcotized, blood was collected, and lumbar (L2-L4) and femoral bones were prepared. The material obtained was subjected to densitometric analysis of bone mineral density (BMD). In ovariectomized rats the loss of osseous tissue was observed only in the lumbar bone. The application of prolactin to ovariectomized rats caused an increase in the mineral density of the lumbar bone up to a BMD value equal to that of the control group which had not been subjected to ovariectomy (control healthy group -SHAM). Similar results were obtained in the case of calcitonin. An increase in osteocalcin concentration and activity of isoenzyme alkaline phosphatase (BAL), with a decrease in the activity of isoenzyme acid phosphatase (TRAP) was observed in experimental groups compared to control ones.

Influence of Prolactin and Calcium Gluconate Concentration on Permeation and Intestinal Absorption of Ca(II) Ions

“…The model applied in this in vitro study is an excellent confirmation of recent reports about the regulating function of PRL on systemic calcium balance. The obtained results demonstrate that this hormone specifically regulates the systemic calcium The data here presented has been confirmed by recent research on a osteoporosis female rat model, where the protecting action of prolactin, estradiol and calcitonin on calcium balance was demonstrated [17].…”

Osteogenic differentiation of adipose tissue-derived mesenchymal stem cells cultured with different concentrations of prolactin

“…The addition of prolactin in concentrations of 100 and 300ng increased cellularity, but did not promote significant changes of the parameters that allow us to evaluate the osteogenic differentiation of MSC, which suggests that the prolactin perhaps stimulates more the proliferative activity than the osteogenic differentiation of MSC. However, it cannot be ruled out that the reduction of osteogenic differentiation of the MSC is one of the mechanisms responsible for bone mass reduction observed in periods of hyperprolactinemia of gestation and lactation, since that in vivo, the hyperprolactinemia may have an indirect effect on the osteogenic differentiation of MSC for reducing concentrations of estrogen, progesterone and gonadotropin hormones these that have direct action and positive about the osteogenic differentiation of MSC (Qu et al, 1998;Dolinska et al, 2010;Grachev et al, 2015).…”

“…The physiological hyperprolactinemia that occurs during pregnancy and lactation has been associated to bone loss in women and animals (Zuni et al, 1999;Coss et al, 2000;Dolinska et al, 2010), with significant reduction of bone mineral density. The bone mass reduction observed in pregnant women varies from 2.1% to 9.4% in backbone; 0.9% to 3.9% in hip and approximately 2% to 4% in the radius (Karlsson et al, 2001).…”