Endocrine Abstracts

Introduction: During pregnancy (state with physiological hyperprolactinemia-HP) mothers require larger calcium amount for fetal growth. It has been shown that PRL stimulate intestinal calcium absorption in physiological HP, which can protect mother’s skeletal system from further mineral density loss. On the other hand, medicamentous-related hyperprolactinemia is more frequently associated with reduced BMD and increased fracture risk. We conducted the experimental study to evaluate if prolactin receptor (PRLR) gene expression in duodenum differs during physiological and medicamentous hyperprolactinemia.

Methods: Wistar female rats 18 weeks old were divided into: Group P: nine rats, 3 week pregnant; Group M3: ten rats that were i.m. administrated Sulpirid (10 mg/kg) twice daily for 3 weeks; and age matched nulliparous rats as a control group: ten rats, 18 weeks old (C1). Serum PRL concentration was measured using ELISA kit for PRL. Relative quantification of prolactin receptor gene expression in duodenum was determined by quantitative real time PCR.

Results: PRL concentrations were significantly higher in Group P, compared to C1 (181.80±29.65 vs 105.38±28.34; P<0.001). Significantly increased PRL levels in M3 compared to age matched control, confirmed the state of medicamentous HP (182.03±57.80 vs 105.38±28.34; P<0.001). There was no significant difference in PRL concentration between experimental Groups P and M3. Ratio between relative gene expression of PRLR in Groups P and C1 (log2 (P/C1) 10.02±1.41) was significantly higher in comparison with ratio between relative gene expression of PRLR in Groups M3 and C1 (log2 (M3/C1) 4.26±0.60) (P<0.001).

Conclusions: Significantly decreased PRLR gene expression in duodenum could be underlying reason for decreased intestinal calcium absorption in medicamentous HP. In order to maintain calcium homeostasis, when duodenal absorption is compromised, PRL in medicamentous HP will seek for another target organ, such as skeletal system, causing more detrimental effects on bone metabolism comparing to physiological HP.