Endocrine Abstracts

Introduction: The aim of this study was to compare prolactin receptor gene (Prlr) expression in the duodenum, vertebra and kidney, during physiological and medicamentous hyperprolactinaemia.

Methods: Wistar female rats 18 weeks old were divided into: Group P: nine rats, 3 week pregnant; Group M: ten rats that were intramuscular administrated Sulpirid (10 mg/kg) twice daily for 3 weeks; and age matched nulliparous rats as a control group: ten rats, 18 weeks old (C). Laboratory analysis included: prolactin, serum ionized calcium, phosphorus, urinary calcium and phosphorous excretion, and serum procollagen type 1 N-terminal propeptide (P1NP). Relative quantification of Prlr gene expression in duodenum, vertebra and kidney was determined by quantitative real time polymerase chain reaction.

Results: PRL concentrations were significantly higher in group P and M, compared to C (P<0.001). In the pregnancy ionized calcium was significantly decreased compared to C and M (P<0.001); serum phosphorus was significantly increased compared to C (P<0.05); urinary calcium was increased compared to C (P<0.01) and lower compared to M (with no significance); urinary phosphorous was significantly increased compared to C and M (P<0.001) and P1NP was significantly increased compared to C and M (P<0.001). In the physiological hyperprolactinaemia expression of Prlr gene was significantly higher in the duodenum (P<0.001) and significantly lower in the vertebra (P<0.01). While down-regulation of Prlr gene was verified in the kidney, in both groups.

Conclusions: In medicamentous hyperprolactinaemia, down-regulation of Prlr gene expression in duodenum could be underlying reason for diminished intestinal calcium absorption. Increased calcium uresis could be partly due to down-regulated Prlr gene expression in the kidney. In order to maintain calcium homeostasis, since intestinal absorption is compromised and loosing via kidney elevated, prolactin will rapidly take calcium from skeletal system, thank to increased Prlr gene expression in the vertebra, leading to more harmful effect on bone metabolism compering to physiological hyperprolactinaemia.