J. Anim. Sci. 2003. 81:1823-1829
© 2003 American Society of Animal Science
Specific window of prolactin inhibition in late gestation decreases mammary parenchymal tissue development in gilts1,2
C. Farmer3 and
D. Petitclerc
Agriculture and Agri-Food Canada, Dairy and Swine Research and Development Centre, Lennoxville, Québec J1M 1Z3, Canada
3 Correspondence—phone:
819-565-9174, ext. 222; fax: 819-564-5507; E-mail:
farmerc{at}agr.gc.ca.
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Abstract
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Prolactin is required from d 70 to 110 of gestation for normal mammary development of gilts. The goal of the present study was to determine the effect of inhibiting prolactin with bromocriptine during specific time windows during the second half of gestation on mammary gland development in gilts. Crossbred primigravid gilts were assigned as controls (n = 12) or received 10 mg of bromocriptine orally three times daily from d 50 to 69 (BR50, n = 12), d 70 to 89 (BR70, n = 12), or d 90 to 109 (BR90, n = 12) of gestation. Jugular blood samples were collected on d 50, 70, 90, and 109 of gestation and assayed for prolactin and estradiol. Gilts were slaughtered on d 109 of gestation and fetuses were counted and weighed. One row of mammary glands was used for dissection of parenchymal and extraparenchymal tissues, and for biochemical analyses. Tissue from the other row was used for measures of prolactin receptor number and affinity. Concentrations of prolactin were decreased markedly (P < 0.001) at the end of each bromocriptine treatment period compared with controls, but there was no overall treatment effect (P > 0.1) on estradiol concentrations. Extraparenchymal tissue weight of the mammary glands was unaffected by treatments (P > 0.1), but weight of parenchymal tissue, total DNA, and total RNA were lower (P < 0.01) in BR90 than control gilts. The percentage of DM in parenchymal tissue was unaffected by treatments (P > 0.1), but percentage of fat was higher and percentage of protein lower (P < 0.01) in BR90 gilts compared with controls. Cell size, as estimated by the protein:DNA ratio, also was lower (P < 0.01) in the BR90 group. Number and affinity of prolactin receptors in parenchymal tissue were not significantly altered by treatments. In conclusion, there is a specific time period in the second half of gestation, from 90 to 109 d, during which prolactin is essential for normal mammary parenchymal tissue development.
Key Words: Bromocriptine • Mammary Development • Mammary Glands • Pregnancy • Prolactin • Sows
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Introduction
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Prolactin is one of the most versatile hormones of the pituitary gland in terms of biological actions. One of its major roles relates to mammary gland physiology. Indeed, it is well known that prolactin is a lactogenic hormone in various species and is also involved in stimulation of mammary growth (Tucker, 1985). A recent review by Horseman (1999) specifically covers the implication of prolactin in mammary gland development. It reports that prolactin regulates mammogenesis at three stages of reproduction in females, more specifically, during organogenesis that occurs around puberty, when lobuloalveolar expansion takes place during pregnancy, and for lactational differentiation and maintenance of milk secretion after parturition. In swine, the preparturient prolactin surge is essential for lactogenesis (Whitacre and Threlfall, 1981), and prolactin concentrations must be maintained throughout lactation to support galactopoiesis (Farmer et al., 1998). The specific role of prolactin for mammogenesis in pregnant gilts was only recently demonstrated in a study using prolactin inhibition via bromocriptine treatment during the last third of gestation (Farmer et al., 2000). Weight of parenchymal tissue and percentage of protein in parenchyma decreased, whereas percentages of fat and DM in parenchyma increased in response to bromocriptine treatment (Farmer et al., 2000). It is not known, however, if such an inhibition of prolactin over a shorter time period in gestation would also have a negative impact on mammary development. The present study was therefore carried out to determine the effect of bromocriptine treatment during three consecutive 20-d periods at the end of gestation on mammogenesis in gilts.
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Materials and Methods
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Animals and Treatments
Crossbred (F2) primigravid gilts, from a cross between Large White x Landrace sows and Large White boars, were assigned as controls (n = 12) or received bromocriptine from d 50 to 69 (BR50, n = 12), d 70 to 89 (BR70, n = 12), or d 90 to 109 (BR90, n = 12) of gestation. Ten milligrams of bromocriptine (CB-154, Novartis, Basel, Switzerland) was given orally at 0730, 1530, and 2330 daily during the treatment period. This dose and frequency of treatment were previously demonstrated to be effective in inhibiting prolactin concentrations in sows (Farmer et al. 1998). The bromocriptine was inserted into a capsule, which was mixed in a ball of precreep feed (22% CP). All animals were previously trained to receive an empty capsule (within a ball of feed), starting 2 d prior to the onset of their respective treatments. All sows, including controls, received a ball of feed containing an empty capsule on the days between d 50 and 109 of gestation during which they were not scheduled to receive bromocriptine. Sows were fed 2.3 kg daily of a commercial feed (13% CP, 3,200 kcal/kg DE, 0.52% lysine) throughout gestation. Water intake was measured daily from d 50 to 109 of gestation using water-flow meters and water bowls with a float. Backfat thickness (measured ultrasonically at the last rib; Scanmatic SM-1, Medimatic, Hellerup, Denmark) and BW of sows were recorded at mating, and on d 48, 70, 90, and 109 of gestation. Gilts were housed in individual stalls (0.6 x 2.1 m). The trial took place between August and December 1999. Animals were cared for according to a recommended code of practice (Agriculture and Agri-Food Canada, 1993).
Jugular blood samples (20 mL) were collected from gilts by venipuncture before the morning meal on d 50, 70, 90, and 109 of gestation. Samples collected were left at room temperature for 4 h, stored overnight at 4°C, centrifuged the following day, and serum was then immediately frozen at -20°C until assayed for prolactin and estradiol.
Mammary Gland Measurements
All gilts were slaughtered on d 109 of gestation and the number of corpora lutea and fetuses were counted. Mammary glands were excised from the abdominal wall, separated in halves along the medial suspensory ligament, and stored at -20°C until dissection and analyses for tissue composition. Mammary glands from the side of the udder with the largest number of productive teats were used for determination of composition by biochemical analysis. Frozen mammary glands were sawed into 2-cm slices and trimmed of skin and teats according to the procedure of Petitclerc et al. (1984). All glands from one side of the udder were homogenized and a representative sample was used for determination of composition by biochemical analysis. Mammary parenchymal tissue from each slice was dissected from surrounding adipose (i.e., extraparenchymal tissue) at 4°C, and both parenchymal and extraparenchymal tissue weights were recorded. Mammary parenchyma was defined as the tissue that contains duct and alveolar cells; obviously, it also contained stromal cells because boundaries between parenchymal and extraparenchymal tissues are not well defined. The RNA content of parenchymal tissue was measured by UV spectrophotometry at 260 nm (Voldin and Cahn, 1954) and the DNA content was evaluated using a method based on fluorescence (Labarca and Paigen, 1980). Dry matter, protein, and lipid contents were also measured (AOAC, 1998). Number and weights of fetuses as well as number of corpus luteum were recorded.
A 30-g sample of mammary parenchymal tissue was obtained from the side of the udder not used for biochemical analyses. It was immediately frozen in liquid nitrogen and stored at -80°C until used for measurements of number and affinity of prolactin receptors. The methodology used for preparation of membranes was as described by Plaut et al. (1989), with a few modifications (Farmer et al., 1999). Prolactin binding studies were also done essentially as described by Plaut et al. (1989), but 200 ng of unlabelled ovine prolactin per tube was used to calculate nonspecific binding. In order to calculate receptor affinity, unlabelled ovine prolactin was used at concentrations varying from 0.008 to 0.5 ng/tube. The EBDA (equilibrium binding data analysis) program (Biosoft, Cambridge, U.K.) was used to estimate receptor affinity, expressed as the dissociation constant, and LIGAND (Biosoft, Cambridge, U.K) was used to estimate receptor number, defined as maximum population density of binding sites.
Hormone Assays
Concentrations of estradiol were established using a validated assay that was a modification (Guilbault et al., 1988) of the procedure described by Bélanger et al. (1980). Concentrations of prolactin were determined with a previously described RIA (Robert et al., 1989). The radioinert prolactin was donated by A.F. Parlow (U.S. National Hormone and Pituitary Program, National Institute of Diabetes and Digestive and Kidney Diseases, Torrance, CA), and the first antibody to prolactin was purchased from Research Products Int. Corp., (Mt. Prospect, IL). Parallelism of a serum pool from gestating sows was demonstrated in 50 to 200 µL of sample for both assays. Average recoveries, calculated by addition of various doses of radioinert hormone to 50 µL of a pooled serum sample, were 99.9 and 98.9% for prolactin and estradiol, respectively. Sensitivity of the assays were 0.1 ng per tube for prolactin and 2.5 pg/mL for estradiol. Six samples of a representative pool of serum were included in duplicates in all assays in order to calculate CV. The intraassay CV were calculated from the mean values of the pools within each assay and were 6.2 and 5.1% for prolactin and estradiol, respectively. The interassay CV were calculated from the mean values of the pools obtained for each assay and were 8.9 and 8.6% for prolactin and estradiol, respectively.
Statistical Analyses
The GLM procedure of SAS (SAS Inst., Inc., Cary, NC) was used for statistical analyses, using a one-way ANOVA. Individual analyses for each stage of observation were done for backfat, BW, water intake, litter size, fetal weight, embryonic mortality (based on number of corpora lutea; Ashworth and Pickard, 1998), and mammary gland composition of gilts, as well as for hormonal and receptor measurements. The model included the effect of treatment (the residual error being the error term used to test main effects of treatment) with contrasts comparing the controls to each of the treatments (Dunnett’s test). Repeated measures ANOVA with the factors treatment (the error term being sow within treatment) and day (the residual error being the error term) as well as the treatment x day interaction were also carried out on hormonal data of gilts. When the treatment x time interaction was significant, contrasts were used to compare the differences between two successive times for each treatment relative to the controls. Data were corrected with a logarithmic transformation (using natural logarithms) when variances were not homogeneous. Data in Tables and Figures are presented as arithmetic means ± SEM.
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Results
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Animal Performance
Body weights of gilts were similar (P > 0.1) across treatments at mating (138.8 ± 2.7 kg), as well as on d 48 (168.0 ± 2.6 kg), 70 (181.2 ± 2.6 kg), 90 (193.8 ± 2.9 kg), and 109 of gestation (207.2 ± 3.1 kg). Backfat of gilts was also similar (P > 0.1) among treatments at mating (18.4 ± 1.1 mm) and on d 48 (22.3 ± 1.2 mm), 70 (23.6 ± 1.2 mm), 90 (24.7 ± 1.4 mm), and 109 of gestation (25.2 ± 1.3 mm). The number of fetuses (10.8 ± 2.8) and average weight of fetuses on d 109 (1.1 ± 0.05 kg) were not altered (P > 0.1) by treatments. There was a treatment effect (P < 0.05) on the percentage of embryonic mortality (control = 35.8, BR50 = 22.4, BR70 = 20.5, BR90 = 34.3); however, none of the comparisons between each treatment and the control group reached significance (P > 0.05). Water intake results are presented in Table 1
. There was no effect (P > 0.1) of treatments on water intake in the period from 50 to 69 d of gestation or from 90 to 109 d of gestation. There was a tendency for water intake to be reduced (P = 0.06) in BR70 gilts during this period of treatment, although values for BR70 gilts were numerically lower than those for gilts from the other groups even prior to their treatment (i.e. from d 50 to 69).
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Table 1. Average daily water intake of sows receiving an empty capsule (Control) or 10 mg of bromocriptine orally three times daily from d 50 to 69 (BR50), 70 to 89 (BR70), or 90 to 109 (BR90) of gestation
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Hormonal Data
Prolactin concentrations at mating and on d 50 of gestation were not (P > 0.1) affected by treatments, but values on d 70, 90 and 109 of gestation were significantly decreased (P < 0.05), compared to controls, in the BR50, BR70 and BR90 groups, respectively (Figure 1). Concentrations of prolactin at the end of a 2-wk treatment period with bromocriptine were therefore decreased as of d 50 of gestation. There was a time x treatment interaction (P < 0.0001) on prolactin concentrations as well as an effect of time (P < 0.0001), with increasing values as gestation advanced. When comparing differences in prolactin concentrations between d 50 and 70 (P = 0.01), 70 and 90 (P < 0.0001), and 90 and 109 of gestation (P < 0.0001) for treated and control gilts, treatment variations were present. Concentrations of estradiol were not affected (P > 0.1) by bromocriptine at any of the sampling times and there was also no (P > 0.1) overall effect of treatment when all samples were considered. Average values (± SEM) at mating and on d 50, 70, 90 and 109 of gestation were 3.42 ± 0.45, 5.97 ± 0.68, 21.84 ± 2.3, 133.40 ± 14.1, and 323.45 ± 32.2 pg/mL, respectively. There was an effect (P < 0.0001) of time on estradiol concentrations and a tendency for a time x treatment interaction. Values of estradiol increased (P = 0.08) with advancing gestation, and the increase between d 90 and 109 was less (P = 0.01) for BR70 than for the other groups (Figure 2).
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Figure 1. Prolactin concentrations in the blood of gilts receiving an empty capsule (Control) or 10 mg of bromocriptine three times daily from d 50 to 69 (BR50), 70 to 89 (BR70), or 90 to 109 (BR90) of gestation. *Values differ from control, P < 0.05.
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Figure 2. Estradiol concentrations in the blood of gilts receiving an empty capsule (Control) or 10 mg of bromocriptine three times daily from d 50 to 69 (BR50), 70 to 89 (BR70), or 90 to 109 (BR90) of gestation. Values were not affected (P > 0.1) by treatments.
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Mammary Gland Development and Receptor Data
Mammary gland data are presented in Table 2 and typical transversal cuts of mammary glands from gilts of each treatment are shown in Figure 3. Weights of the halved mammary glands were affected (P < 0.001) by treatments, with mammary weight being lower (P < 0.01) in BR90 than in control gilts and BR50 gilts having a tendency (P < 0.1) for lower mammary weight than control gilts. Extraparenchymal tissue weight was similar (P > 0.1) among treatments, whereas amount of parenchymal tissue was lower (P < 0.01) in BR90 than in control gilts. Percentage of DM in parenchyma was unaffected (P > 0.1) by treatments, whereas percentage of fat was greater and percentage of protein lower (P < 0.01) in BR90 compared with control gilts. Total content of parenchymal RNA was lower (P < 0.01) in BR90 compared with control gilts, but RNA abundance (on a DM basis) was similar (P > 0.1) among treatments. Bromocriptine did not alter (P > 0.1) the number or the affinity of prolactin receptors (Table 2).
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Table 2. Mammary tissue composition on d 110 of gestation for gilts receiving an empty capsule (Control) or 10 mg of bromocriptine three times daily from d 50 to 69 (BR50), 70 to 89 (BR70), or 90 to 109 (BR90) of gestation
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Figure 3. Transversal cut from the mammary gland of a gilt receiving an empty capsule (C) or 10 mg of bromocriptine three times daily from d 50 to 69 (BR50), 70 to 89 (BR70), or 90 to 109 (BR90) of gestation.
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Discussion
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Previously, it was demonstrated that inhibition of prolactin using the dopamine agonist bromocriptine from d 70 to 110 of gestation inhibits mammary development of gilts (Farmer et al., 2000). The present results show that prolactin is not essential for development of the mammary glands throughout this whole period, but that it is specifically required during the latter part of gestation, namely, from d 90 to 109. Data from Sorensen et al. (2002) show that increases in accumulation of mammary tissue and DNA are most marked at the end of gestation, thereby supporting the importance of prolactin for mammogenesis during this period. Interestingly, when comparing their results on d 112 of gestation to those of Kim (1999) at 12 h postpartum, Sorensen et al. (2002) concluded that accumulation of mammary tissue and DNA probably continues until term. Earlier results from Kensinger et al. (1982) indicated no further increase in mammary DNA after d 90 of gestation, yet these were concentrations and not total amounts of mammary DNA. The present results do not exclude the fact that mammary development may have been affected by bromocriptine being given earlier in gestation if the gilts had been slaughtered immediately following treatments. However, gilts were slaughtered at the end of gestation because this is the time where mammary development should have most impact on future lactational performance.
Prolactin is known to be involved in osmoregulation (Nicoll, 1980). This was previously supported by the tendency for a greater water intake in lactating sows injected with recombinant porcine prolactin (Farmer et al., 1999) and by the reduction in water intake during each week of lactation when bromocriptine was given to sows (Farmer et al., 1998). An earlier study also showed lower water intake values for gilts receiving bromocriptine at the end of gestation (d 70 onward) (Farmer et al., 2000). The present findings again indicate a tendency for reduced water intake with bromocriptine treatment, but this only in the treatment period from 70 to 90 d of gestation. The reason for the lack of consistent effect is not known, but results do suggest that circulating prolactin concentrations may have an impact on water intake in gilts.
The lower prolactin concentrations at the end of each treatment period in the present study demonstrated the effectiveness of the bromocriptine, whereas specificity of the treatment was indicated by the absence of effect on estradiol (present study), progesterone, and IGF-I (Farmer et al., 2000), as well as growth hormone and cortisol (Horth and Farmer, 2000) concentrations in pregnant gilts. These findings do not preclude the fact that bromocriptine may exert a direct effect on some other factor that could in turn impact on mammary development. However, to the best of our knowledge, such an effect was not reported. The absence of bromocriptine effect on estradiol concentrations is particularly important because previous findings showed that estradiol concentrations increased after 24 days of bromocriptine treatment in late-pregnant gilts (Farmer et al., 2000).
The fact that the number or affinity of prolactin receptors was not significantly altered by treatments in the present experiment was surprising because in an earlier study where bromocriptine was given from d 70 to 110 of gestation, there was a significant decrease in the number of prolactin receptors and a significant increase in their affinity (Farmer et al., 2000). Two possible explanations can be suggested for this discrepancy: first, the duration of treatment was shorter in the present study, and second, the state of differentation of the mammary cells throughout treatments differed. Indeed, it appears that bromocriptine must be given over a period of time covering a larger span of the developmental stages of the mammary cells in order for the incurring decrease in prolactin concentrations to alter receptor characteristics. Because the decrease in mammary development was almost similar when treatments were given from d 70 to 110 (Farmer et al., 2000) or from d 90 to 109 of gestation (present study), it also appears that the number or the affinity of prolactin receptors was not linked to the biological response to the treatments. In fact, circulating concentrations of prolactin seemed to be the key factor in elliciting a response. Indeed, the present finding that the specific period from d 90 to 109 of gestation is the period during which bromocriptine hinders mammary development could be due to the greater circulating concentrations of prolactin normally present in gilts at that time (Farmer et al., 2000).
The effects of prolactin on mammary development occur via a membrane receptor that, among other things, induces milk protein gene expression in the mammary gland. Analysis of prolactin-induced genes led to the identification of elements that bind members of the Stat (signal transducer and activation of trancription) family of transcription factors (Darnell et al., 1994). Two isoforms of Stat5 (a and b) appear to be the primary mediators of prolactin actions in mammals (Liu et al., 1996), and Stat5a was found to be mandatory for adult mammary gland development in rodents (Liu et al., 1997). A species difference seems to exist because in swine, expression levels of Stat5b mRNA, but not Stat5a, were associated with mammary gland development in late pregnancy (Palin et al., 2002). It is therefore apparent that even though the essential role of prolactin for mammogenesis in late gestation is now established, its specific modes of action still need to be clarified. Locally derived growth factors may be implicated in the mediation of prolactin-induced mammary gland development. Indeed in mice, several growth factors, such as epidermal growth factor, neuregulin, keratinocyte growth factor, hepatocyte growth factor, and IGF-I are known to play specific roles at different stages of mammary development (Horseman, 1999). Furthermore, IGF-II was recently shown to be a mediator of prolactin-induced alveologenesis in mammary epithelium of women (Brisken et al., 2002). The proper interplay between endocrine hormones and epithelial and stromal growth factors seems necessary for normal mammary development and studies designed to alter the normal function of these regulators need to be done in swine.
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Implications
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Mammary development in gilts can be influenced by various hormonal factors. In swine, there is a specific period in late gestation, from 90 to 110 d, during which prolactin plays an essential role for mammary parenchymal development. It is therefore during this period that attempts should be made to increase prolactin concentrations of pregnant sows in order to optimize mammary parenchymal growth and subsequent lactation performance. The inhibition of mammary development with bromocriptine was not related to changes in prolactin receptor number or affinity, suggesting that alterations in prolactin receptor characteristics at the end of gestation would not be a good avenue to explore in order to increase mammary development.
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Footnotes
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1 Lennoxville Dairy and Swine R & D Centre contribution No. 776. 
2 We wish to thank S. Horth, L. Thibault, and J. Brochu for their invaluable technical assistance; C. Mayrand, F. Phaneuf, E. Bérubé, F. Champagne, A. Marsh, J. Boudreau, and M. Turcotte for care and treatment of the animals, and R. Martineau and S. Méthot for statistical analyses. The bromocriptine was kindly donated by Novartis (Basel, Switzerland), and Genex Swine Group (Regina, SK, Canada) supplied the gilts.
Received for publication December 9, 2002.
Accepted for publication March 5, 2003.
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Abstract
Introduction
