Endocrine Abstracts

Introduction: The aim of this study was to evaluate potential alterations in prolactin receptor gene expression (Prlr) in the duodenum, vertebra, and kidney - key organs in calcium metabolism, across the aging process.

Methods: Wistar female rats were divided into: Group A (10 rats, 5 weeks old), Group B (10 rats, 18 weeks old) and Group C (7 rats, 21 weeks old). Laboratory analysis included: prolactin, serum ionized calcium, phosphorus, urinary calcium and phosphorous excretion, alkaline phosphatase (ALP), osteocalcin (OC) and serum procollagen type 1 N-terminal propeptide (P1NP). Relative quantification of prolactin receptor (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 A compared to B and C (P<0,001). In the youngest rats (A) serum ionized calcium was significantly decreased compared to B (P<0,05) and C (P<0,01); serum phosphorus was significantly increased compared to B and C (P<0,001); urinary calcium was decreased compared to B and C (P<0,001); urinary phosphorous was significantly increased compared to B (P<0,05) and without significant changes compared to C. All bone turnover markers, ALP, OC and P1NP, were significantly increased in the Group A compared to B and C (P<0,001). In the youngest group of rats (A) expression of Prlr gene was higher in the duodenum comperd to the B and C, but without statistical significance. In the kidney there was significantly increased expression of Prlr gene in the A compared to C (P<0,05). While in the vertebra, significantly dicreased expression of Prlr gene was verified in the Group A compared to C (P<0,01).

Conclusions: Prlr gene expression undergoes significant changes during aging in tissues critical for calcium homeostasis, potentiall, contributing to adverse effects on bone metabolism. A considerable reduction in Prlr gene expression in the kidne, ma, explain the markedl, elevated calciumuresis in older experimental groups. To sustain normal calcium levels, the urinar, loss of calcium is compensated b, extracting calcium from the bones, facilitated b, the heightened expression of the Prlr gene, thereb, causing additional harm to the skeletal system in the aging process.