Abstract
The goal of this project was to determine whether recombinant porcine (rp) prolactin (PRL) can enhance mammary development when given to pre-pubertal gilts and/or modify the expression of PRL-related genes. Crossbred gilts were injected s.c. twice daily with saline (CTRL; n = 13), 2 mg of rpPRL (4PRL; n = 13), or 4 mg of rpPRL (8PRL; n = 13) in a 2.0-mL volume for a period of 29 d, starting at 75.1 +/- 0.5 kg BW. Jugular blood samples were collected before the first injection, as well as 14 and 28 d later, and were assayed for PRL, IGF-I, and leptin. Gilts were slaughtered on d 29 of treatment, and mammary glands were collected for dissection of parenchymal and extraparenchymal tissues, and for determination of parenchymal DNA, DM, protein, and fat contents. Levels of mRNA for PRL, PRL receptor (PRL-R), and signal transducers and activators of transcription (STAT5A and STAT5B) were determined via real-time PCR in the mammary parenchyma, as well as levels for PRL and PRL-R in the pituitaries. Treatments did not alter plasma (P = 0.48) IGF-I. Serum concentrations of PRL at slaughter were greater (P < 0.01) in both 4PRL and 8PRL compared with CTRL, whereas at mid-treatment, they were greater (P < 0.05) only in 8PRL gilts. Parenchymal tissue weight and parenchymal DNA concentrations increased with exogenous rpPRL (P < 0.001). The percentage of protein in parenchyma increased (P < 0.001), whereas that of DM (P < 0.001), fat (P < 0.001), and the protein:DNA ratio (P < 0.05) decreased with exogenous rpPRL. Treatment differences were always observed between the 4 mg dose and CTRL, and no further differences were noted when the dose was increased to 8 mg daily. Expression levels of PRL, but not PRL-R, were decreased (P < 0.05) in anterior pituitary glands and mammary glands of treated gilts. The mRNA levels of STAT5A and STAT5B increased (P < 0.05) with exogenous rpPRL. It is evident from these data that rpPRL can stimulate mammogenesis in prepubertal gilts through hyperplasia and increased expression of PRL-related genes.
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