Danijela Radojkovic1,2, Milica Pesic3,4, Milan Radojkovic3,5, Dragan Dimic3,4, Marija Vukelic Nikolic3, Tatjana Jevtovic Stoimenov3, Sasa Radenkovic3,4, Milena Velojic Golubovic3,4, Tatjana Radjenovic Petkovic6, Slobodan Antic3,4. 1. Medical Faculty, University of Nis, Blvd.dr Zoran Djindjic 81, 18000, Nis, Serbia. dr.danijela3@gmail.com. 2. Clinic of Endocrinology, Diabetes and Metabolic disorders, Clinical Center Nis, Serbia Vojislav Ilic bb, 18000, Nis, Serbia. dr.danijela3@gmail.com. 3. Medical Faculty, University of Nis, Blvd.dr Zoran Djindjic 81, 18000, Nis, Serbia. 4. Clinic of Endocrinology, Diabetes and Metabolic disorders, Clinical Center Nis, Serbia Vojislav Ilic bb, 18000, Nis, Serbia. 5. Surgery Clinic, Clinical Center Nis, Vojislav Ilic bb, 18000, Nis, Serbia. 6. Center for Medical Biochemistry, Clinical Center, Nis, Blvd.dr Zoran Djindjic 48, 18000, Nis, Serbia.
Abstract
INTRODUCTION AND AIM: Hyperprolactinaemia in pregnancy leads to mild and reversible changes in the maternal skeletal system, and medicamentous hyperprolactinemia causes more detrimental effects. We conducted an experimental study to evaluate differences between Prlr gene expression in the duodenum, vertebrae and kidneys during physiological and medicamentous hyperprolactinaemia, which could influence calcium homeostasis. METHODS: Experimental animals (18 weeks old, Wistar female rats) were divided as follows: group P (nine rats that were 3 weeks pregnant), group M (ten rats that were intramuscularly administrated sulpiride (10 mg/kg) twice daily for 3 weeks), and the control group (C, ten age-matched nulliparous rats, 18-week-old). Laboratory investigations included measurements of serum ionized calcium, phosphorus, urinary calcium and phosphorus excretion, osteocalcin (OC), serum procollagen type 1 N-terminal propeptide (P1NP), vitamin D, parathyroid hormone (PTH) and prolactin (PRL). Relative quantification of gene expression for prolactin receptors in the duodenum, vertebrae and kidneys was determined using real-time PCR. RESULTS: Expression of the Prlr gene was significantly higher in the duodenum (p < 0.001) and lower in vertebrae (p < 0.001) and kidneys (p < 0.01) in rats with physiological hyperprolactinaemia (PHP) than in the control group. Significantly lower Prlr expression in the duodenum was verified (p < 0.001), along with increased Prlr gene expression in vertebrae (p < 0.001) and kidneys (p < 0.01), in rats with medicamentous hyperprolactinaemia (MHP) than in the C group. CONCLUSIONS: Downregulation of Prlr gene expression in the duodenum may explain the diminished intestinal calcium absorption in medicamentous hyperprolactinaemia. Prolactin takes calcium from the skeletal system following increased Prlr gene expression in the vertebrae to maintain calcium homeostasis, which increases the harmful effect on bone metabolism compared to that of physiological hyperprolactinaemia.
INTRODUCTION AND AIM: Hyperprolactinaemia in pregnancy leads to mild and reversible changes in the maternal skeletal system, and medicamentous hyperprolactinemia causes more detrimental effects. We conducted an experimental study to evaluate differences between Prlr gene expression in the duodenum, vertebrae and kidneys during physiological and medicamentous hyperprolactinaemia, which could influence calcium homeostasis. METHODS: Experimental animals (18 weeks old, Wistar female rats) were divided as follows: group P (nine rats that were 3 weeks pregnant), group M (ten rats that were intramuscularly administrated sulpiride (10 mg/kg) twice daily for 3 weeks), and the control group (C, ten age-matched nulliparous rats, 18-week-old). Laboratory investigations included measurements of serum ionizedcalcium, phosphorus, urinary calcium and phosphorus excretion, osteocalcin (OC), serum procollagen type 1 N-terminal propeptide (P1NP), vitamin D, parathyroid hormone (PTH) and prolactin (PRL). Relative quantification of gene expression for prolactin receptors in the duodenum, vertebrae and kidneys was determined using real-time PCR. RESULTS: Expression of the Prlr gene was significantly higher in the duodenum (p < 0.001) and lower in vertebrae (p < 0.001) and kidneys (p < 0.01) in rats with physiological hyperprolactinaemia (PHP) than in the control group. Significantly lower Prlr expression in the duodenum was verified (p < 0.001), along with increased Prlr gene expression in vertebrae (p < 0.001) and kidneys (p < 0.01), in rats with medicamentous hyperprolactinaemia (MHP) than in the C group. CONCLUSIONS: Downregulation of Prlr gene expression in the duodenum may explain the diminished intestinal calcium absorption in medicamentous hyperprolactinaemia. Prolactin takes calcium from the skeletal system following increased Prlr gene expression in the vertebrae to maintain calcium homeostasis, which increases the harmful effect on bone metabolism compared to that of physiological hyperprolactinaemia.
Entities:
Keywords:
Calcium homeostasis; Duodenum; Kidney; Prolactin receptors; Skeletal system
Authors: Flávia F Bezerra; Laura Mc Mendonça; Erika C Lobato; Kimberly O O'Brien; Carmen M Donangelo Journal: Am J Clin Nutr Date: 2004-11 Impact factor: 7.045
Authors: D E Cole; C M Gundberg; L J Stirk; S A Atkinson; D A Hanley; L M Ayer; L S Baldwin Journal: J Clin Endocrinol Metab Date: 1987-08 Impact factor: 5.958