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During the reproductive cycle, the maternal loss of calcium to the foetus during pregnancy and to the newborn during lactation present a great challenge to the body calcium homeostasis. Maternal adaptations such as increases in intestinal calcium absorption and bone turnover were found to be unrelated to changes in levels of parathyroid hormone, calcitonin, and calcitriol. Due to its high plasma levels in pregnancy and lactation and its reported actions on electrolyte transport, we proposed that prolactin may have a role in the regulation of calcium metabolism.
We have previously shown that pharmacologic dose of 0.2 mg prolactin/kg bodyweight intraperitoneally administered, induced acute and significant increases in duodenal active and passive calcium absorption, the latter of which resulted from prolactin-stimulated Na+K+ATPase activity which in turn increased the solvent drag- induced calcium transport. The acute stimulatory effect of prolactin on net calcium absorption was also shown in the proximal jejunum and caecum but not in the ileum or colon. We further demonstrated that two weeks of daily subcutaneous administration of 2.5 mg prolactin/kg body weight increased bone formation in weaned rats, tibial calcium content in growing rats and fractional calcium absorption and calcium retention in mature rats. Administration of bromocriptine, a dopaminergic inhibitor of endogenous prolactin secretion, delayed peak-intestinal calcium absorption and lowered the vertebral calcium content after 8 weeks of daily treatment in weanling rats, and decreased food consumption, fractional calcium absorption and bone calcium turnover after 3 day treatment in pregnant and lactating rats. Hyperprolactinaemia from transplanted pituitaries in weaned rats, on the other hand, increased the fractional calcium absorption and femoral calcium content by 16%. Recently, we investigated the acute action of prolactin on the three components of active transport across the duodenal tissue mounted between two hemichambers. Duodenal segments directly exposed to 200, 400, and 800 ng prolactin/mL responded by increasing the transcellular and solvent drag-induced calcium transport, but not the voltage dependent component.
In conclusion, we have demonstrated the acute and long term stimulatory actions of prolactin on the intestinal calcium absorption, calcium retention, and bone turnover. The responses appear to vary with dosage of prolactin, intestinal segments and bone type. Different stages of development and reproductive status such as pregnancy or lactation also influence the actions of prolactin.
The investigations were supported by research grants from the Faculty of Science, Mahidol University and the Thailand Research Fund.