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Impacts of dietary protein level and feed restriction during prepuberty on mammogenesis in gilts^1,2

C. Farmer^*,3, D. Petitclerc^*, M. T. Sorensen, M. Vignola and J. Y. Dourmad

^* Agriculture and Agri-Food Canada, Dairy and Swine R & D Centre, Lennoxville, Québec J1M 1Z3, Canada; and Danish Institute of Agricultural Sciences, Foulum Research Centre, Tjele, DK-8830 Denmark; and Shur-Gain, Brossard, J4W 3E7 Canada; and and INRA, Unité Mixte de Recherches sur le Veau et le Porc, 35590 Saint Gilles, France

	Abstract

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The possible roles of dietary protein level and feed restriction in regulating mammary development of prepubertal gilts were investigated. Crossbred gilts were fed a commercial diet until 90 d of age and then divided into four nutritional regimens based on two pelleted diets (as-fed basis): a high-protein diet (HP = 13.8 MJ of ME, 1.0% total lysine, 18.7% CP) and a low-protein diet (LP = 13.8 MJ of ME, 0.7% total lysine, 14.4% CP). Nutritional regimens were as follows: 1) HP ad libitum until slaughter (n = 22, T1); 2) HP ad libitum until 150 d of age followed by LP until slaughter (n = 20, T2); 3) LP ad libitum until slaughter (n = 21, T3); and 4) HP with a 20% feed restriction until slaughter (n = 19, T4). Gilts were weighed, their backfat thickness was measured, and jugular blood samples were obtained on d 90, 150, and at slaughter to determine concentrations of prolactin, IGF-I, leptin, and glucose. Gilts were slaughtered 8 ± 1 d after their first or second estrus (202.7 ± 14.5 d of age). Mammary glands were excised, parenchymal and extraparenchymal tissues were dissected, and composition of parenchymal tissue (protein, fat, DM, DNA, protein/DNA) was determined. The T4 gilts weighed less (P < 0.01) and had less backfat (P < 0.01) than did gilts on other treatments on d 150 and at slaughter. Treatments had no significant effects on prolactin, IGF-I, or glucose concentrations, but there was a treatment x day interaction (P < 0.01) for leptin, with concentrations being lower at slaughter in restricted-fed (T4) vs. LP (T3) gilts (P < 0.05). There was less extraparenchymal mammary tissue (P < 0.01) in T4 gilts than in gilts from the other groups and a tendency (P = 0.13) for the amount of parenchymal tissue to be lower in T4 gilts. In conclusion, a lower lysine intake during prepuberty did not hinder mammary development of gilts, but a 20% feed restriction decreased mass of parenchymal and extraparenchymal tissues. The effect of feed restriction on extraparenchymal tissue is most likely associated with the lower fat deposition.

Key Words: Mammary Development • Mammary Glands • Pigs • Prepubertal Females • Protein Intake • Restricted Feeding

	Introduction

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Sow milk yield is a major determinant of piglet growth and is largely affected by the number of milk secretory cells present at the onset of lactation (Head et al., 1991). There are two phases of rapid accretion of mammary cells in swine, namely, from 90 d of age until puberty and during the last third of gestation (Sorensen et al., 2002a). In heifers, it is well established that prepubertal nutrition affects mammogenesis (Petitclerc et al., 1983; Capuco et al., 1995; Dobos et al., 2000). In contrast, the effects of prepubertal feeding on mammary development in gilts are contradictory. This is especially true when possible effects of treatments on mammary development are evaluated by monitoring piglet performance. For example, variation in prepubertal feeding level had no effect on sow milk yield (Sorensen et al., 1998). In another trial (Kirchgessner et al., 1984), feed restriction from weaning to mating only altered piglet growth rate in the second lactation. Le Cozler et al. (1998, 1999) reported no effect of a 20% feed restriction during prepuberty on subsequent litter gain, and protein intake from 120 to 180 d of age had no effect on subsequent piglet growth (Stalder et al., 2000). Conversely, recent findings wherein mammary composition was measured, suggest that a period of ad libitum feeding before puberty is needed to maximize mammary growth in gilts (Sorensen et al., 2002b). Furthermore, Lyvers-Peffer and Rozeboom (2001) reported that decreasing energy intake of gilts at specific periods between 9 and 25 wk of age decreased the weight of parenchymal tissue and tended to lower parenchymal DNA at the end of gestation. The goal of the current study was to determine the effects of decreased protein and/or energy intake during the prepubertal period when rapid mammary development occurs, namely as of 90 d of age, on composition of mammary glands in gilts at 200 d of age.

	Materials and Methods

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Animals and Treatments

Eighty-two crossbred (F2) gilts, from a cross between Large White x Landrace sows and Hamline boars, were fed a standard diet until 90 d of age. They were then divided into four nutritional regimens based on two pelleted diets (as-fed basis): a high-protein diet (HP = 13.8 MJ of ME, 1.0% total lysine, 18.7% CP) and a low-protein diet (LP = 13.8 MJ of ME, 0.7% total lysine, 14.4% CP). Formulation of these diets is shown in Table 1. These four strategies were chosen to induce differences in body protein and body fat depositions. Nutritional regimens were as follows: 1) HP ad libitum until slaughter (n = 22, T1); 2) HP ad libitum until 150 d of age followed by LP until slaughter (n = 20, T2); 3) LP ad libitum until slaughter (n = 21, T3); and 4) HP until slaughter with a 20% feed restriction relative to ad libitum intake of gilts from T1 at the same body weight (n = 19, T4). These four strategies corresponded to the practical situation of feeding replacement gilts ad libitum or restrictively either with a growing or gestation diet. Gilts came from 22 different litters and, whenever possible, four animals per litter were each assigned to a different treatment. Feed samples from experimental diets were taken twice weekly for compositional analyses (shown in Table 1). Fresh feed was given twice daily, at 1000 and 1500, and individual feed consumption was recorded daily. Gilts were weighed, and their backfat thickness measured ultrasonically at the last rib (Scanmatic SM-1, Medimatic, Hellerup, Denmark) on d 90, 150, at the first standing heat, and the day before slaughter. Gilts were housed in individual pens (1.5 x 2.4 m) from d 90 to 150, and then transferred to individual stalls (0.6 x 2.1 m) with a boar being present in the room. Estrus was detected daily by allowing physical contact between gilts and a mature boar. Gilts were slaughtered 8 ± 1 d after their first or second estrus (202.7 ± 14.5 d of age). Animals not exhibiting estrus (n = 26; namely, 7, 4, 6 and 9 for T1 through T4, respectively) were slaughtered at 199.7 ± 5.5 d of age. The trial took place between October 2001 and March 2002. Animals were cared for according to a recommended code of practice (Agriculture and Agri-Food Canada, 1993).

Mammary Gland Measurements

At slaughter, mammary glands were excised from the abdominal wall and stored at –20°C until dissection and analyses for tissue composition. 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 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 containing duct and alveolar tissue, but it also contained a large amount of adipose tissue because duct and alveolar tissues are embedded in adipose tissue in gilts of such young age. The DNA content of parenchymal tissue was evaluated using a method based on fluorescence (Labarca and Paigen, 1980). Dry matter, protein, and lipid contents were also measured (AOAC, 1998). Ovaries also were collected and the number of corpus lutea counted.

Hormone Assays

Concentrations of IGF-I (Abribat et al., 1993) and prolactin (Robert et al., 1989) were determined with previously described RIA. The IGF-I was extracted using the formic acid-acetone method. The first antibody in the IGF-I assay and the radioinert prolactin were donated by A. F. Parlow (U.S. National Hormone and Pituitary Program, National Institute of Diabetes and Digestive and Kidney Diseases, Torrence, CA). The radioinert IGF-I was purchased from GROPEP (Adelaide, SA, Australia), and the first antibody to prolactin was purchased from Research Products International (Mt. Prospect, IL). Parallelism of a plasma (for IGF-I) or serum (for prolactin) pool from lactating sows was demonstrated. Average recovery, calculated by addition of various doses of radioinert hormone to 50 µL of a pooled sample, was 105.1% for IGF-I and 104.3% for prolactin. Sensitivities of the IGF-I and prolactin assays were 62.5 pg/mL and 1.5 ng/mL, respectively. Six samples of a representative pool of plasma (for IGF-I) or serum (for prolactin) were carried out in duplicate in all assays in order to calculate CV. The intraassay CV were calculated from the mean values of the pools within each assay: values were 10.17 and 4.89% for IGF-I and prolactin, respectively. The interassay CV were calculated from the mean values of the pools obtained for each assay: values were 5.99 and 5.55% for IGF-I and prolactin, respectively.

Leptin was measured with a multispecies commercial RIA kit (Linco, St-Charles, MO), which was validated for gilt serum in our laboratory. Parallelism for samples from 200 to 300 µL was demonstrated (99.4%) and average recovery was 93.3%. Sensitivity of the assay was 1.0 ng/mL, and intra- and interassay CV were 2.83 and 1.58%, respectively. Glucose was measured by an enzymatic colorimetric method with a commercial kit (Boehringer Mannheim, Laval, QC, Canada). Intra- and interassay CV were 1.79 and 1.78%, respectively.

Statistical Analyses

The MIXED procedure of SAS (SAS Inst., Inc., Cary, NC) was used for statistical analyses. The univariate model used for mammary gland and ovarian variables included the effect of nutritional treatment, with the residual error being the error term used to test main effects of treatment. This model was also used to evaluate possible treatment effects on age at first estrus. An ANOVA using weight at slaughter as a covariate was also performed on mammary data. Repeated-measures ANOVA with the factors treatment (the error term being gilt within treatment) and day of age (the residual error being the error term), as well as the treatment x day of age interaction were carried out on backfat thickness, BW, feed intake (from 90 to 150 d of age, and from 150 d to slaughter), and hormone data. These analyses were also carried out separately for cycling and noncycling gilts and, due to differences related to onset of puberty, a model including the effect of puberty was also used to analyze mammary gland data. When the treatment x day interaction was significant, individual ANOVA were done for each day. Multiple mean comparisons between nutritional regimens were performed with Tukey’s test. A ² test was used to determine whether there was an association between treatments and the percentage of gilts coming into estrus. Data were corrected with a logarithmic transformation (using natural logarithms) when variances were not homogeneous. Data in tables and figures are presented as least squares means ± maximal SEM. A statistical tendency was defined as 0.05 P 0.10. Pearson correlation coefficients between weight at slaughter, backfat at slaughter, ADG, increase in backfat from d 90 to slaughter, and age at puberty were also done with all measured mammary variables, using the PROC CORR procedure of SAS (SAS Inst., Inc., Cary, NC).

	Results

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Performance and Hormonal Data

There was a treatment x day effect (P < 0.01) on both BW and backfat thickness of gilts. Feed-restricted gilts (T4) were lighter (P < 0.01) and had less backfat (P < 0.01) than did gilts from other treatments at 150 d of age and at slaughter (Table 2). These effects were similar whether considering all gilts or only cycling gilts. In both the 90-to-150 d period and the 150 d-to-slaughter period, feed-restricted gilts consumed less feed (P = 0.01) and had a lower daily weight gain (P < 0.01) than did gilts from other treatments, whereas rates of feed conversion were similar across treatments (Table 3). There was a treatment x day interaction (P < 0.01) on feed consumption in the first period, demonstrating a slower increase in feed intake for feed-restricted gilts than for gilts from other treatments.

View larger version (13K): [in this window] [in a new window]   Figure 1. Leptin concentrations in the blood of gilts fed different diets from 90 d of age until slaughter, at 202.7 ± 14.5 d of age. Treatments were: T1 = high-protein (HP) diet ad libitum, n = 22; T2 = HP ad libitum until 150 d of age then low-protein (LP), n = 20; T3 = LP ad libitum, n = 21; and T4 = HP with a 20% feed restriction, n = 19. *T4 differed from T3, P < 0.05.

The only mammary gland variable significantly affected by nutritional regimens was the extraparenchymal tissue mass, which was lighter (P < 0.01) in feed-restricted (T4) gilts than in gilts from the other treatments (Table 5). However, there was also a tendency (P = 0.13) for the amount of mammary parenchymal tissue to be lower in T4 gilts, and this represented a 26.3% decrease between values for control and T4 gilts (Table 5). When weight of the gilts at slaughter was used as a covariate, there was no significant treatment effect on extraparenchymal tissue, but a treatment effect (P < 0.05) was observed for total protein content, with values for T4 gilts being lower than those for T2 and T3 gilts. There was also a tendency (P = 0.05) for these same treatment effects to be seen on total parenchymal DNA, when the covariate weight at slaughter was used in the analysis. Mammary development was affected by the onset of puberty as the 26 gilts that had not started cycling by at 200 d of age, had more extraparenchymal tissue (P < 0.05) and less parenchymal tissue (P < 0.01) than did gilts that had shown heat (Table 6). Parenchymal tissue composition was also affected by the onset of puberty (Table 6). There was more total fat, total protein, and total DNA in the parenchyma of cycling vs. noncycling gilts (P < 0.01). There was no significant interaction between the onset of puberty and the nutritional regimens used on any of the mammary gland variables measured. The numbers of gilts that had not cycled in each treatment group were 7, 4, 6, and 9, representing 31.8, 20.0, 28.6, and 47.4% for T1, T2, T3, and T4, respectively. There was no association between the percentage of gilts reaching puberty and the nutritional regimen (P = 0.32). There were no significant treatment effects on age at first estrus (mean values of 176.2, 174.6, 176.5, and 176.1 d for T1 through T4, respectively) or at slaughter (mean values of 203.3, 203.9, 200.5, and 198.9 d for T1 through T4, respectively).

	Discussion

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Our findings of a negative effect with 20% feed restriction on mammary development in gilts are in agreement with data from Sorensen et al. (2002b). Previous reports using subsequent milk production as an indicator of mammary development showed no apparent effect of feed restriction on mammogenesis, but this conclusion was confounded by the experimental protocol. Specifically, effects on mammogenesis were indirectly measured by monitoring subsequent milk yield. Sorensen et al. (1998) restricted feeding level (semi ad libitum and approximately 85 or 62% of semi ad libitum) of gilts from 6 wk of age to mating, at approximately 220 d of age, and subsequent milk yield in four successive lactations was not altered. However, sows were fed restrictively according to litter size during lactation, which may have limited milk production. Kirchgessner et al. (1984) fed gilts either ad libitum (ADG of 592 g from 5 to 95 kg BW) or restricted (ADG of 432 g from 5 to 95 kg BW) from weaning to mating. Piglets from sows that were restricted-fed had the highest growth rate in parity two (but not in parity one and three). However, a different age at first pregnancy (239 d for ad libitum group vs. 284 d for restricted-fed) may have confounded the results. When gilts were fed either ad libitum or at 80% of ad libitum from approximately 73 d of age to either 180 d of age (Le Cozler et al., 1999) or mating (Le Cozler et al., 1998), no effects on subsequent litter weight gain were observed. The fact that using weight of gilts at slaughter abolished the effect of feed restriction on extraparenchymal tissue suggests that the decreased extraparenchymal tissue weight seen in restricted-fed gilts is solely due to the difference in BW. Conversely, the analysis with the covariate demonstrated that taking BW into account increased the effect of feed restriction on total protein and on total DNA in mammary parenchymal tissue. The effects of feed restriction on extraparenchymal and parenchymal tissues therefore do not seem to be exerted via similar mechanisms.

Decreasing protein (and lysine) supply over the entire experimental period (T3) did not affect average growth rate or body composition at slaughter, although BW at 150 d tended to be lighter in T4 than in T1. This suggests that dietary protein restriction was not severe enough to impair protein retention and consequently increase fat deposition. Indeed, digestible lysine content of the LP diet (0.63%) was only slightly below the requirement calculated from NRC (1998) for such animals (0.67%). The same observation was made when distribution of the LP diet started after 150 d of age (T2). Feed restriction (T4) resulted in a significant decrease in ADG compared with the other treatments; consequently, BW of these gilts at 150 d of age or at slaughter was significantly less. Feed restriction also affected body composition. Gilts from T4 had less backfat (15.5 vs. 22.7 mm) and a lower backfat:BW ratio (0.117 vs. 0.142 mm/kg). These results are in agreement with previous findings of Den Hartog (1984), Simmins et al. (1994), and Le Cozler et al. (1998).

Correlations showed that growth and backfat thickness were highly associated with extraparenchymal tissue weight but had little association with weight or composition of parenchymal tissue. This, together with the fact that feed-restriction (T4) significantly decreased weight and backfat thickness of gilts without altering parenchymal fat content, suggests the presence of a "sparing mechanism" preserving parenchymal composition when gilts are in energetic defficiency. In contrast, feed restriction had a greater effect on weight of the mammary glands relative to BW. This is seen by the greater ratios of parenchymal or extraparenchymal weights over BW for gilts in T1 vs. T4. The absence of association between growth and backfat thickness with extraparenchymal tissue weight in T4 gilts is likely due to the much smaller variation in these variables within that treatment compared with the other treatments.

The fact that mammary development is significantly enhanced with the onset of puberty has not been previously shown in swine, but this is not surprising given the importance of estrogen for mammogenesis (Kensinger et al., 1986). Others (Sorensen et al., 2002a) have suggested that the shift in the rate of mammary development after 90 d of age in swine is likely linked with ovarian activity. Indeed, the negative correlation observed between age at puberty and concentration of DNA in parenchymal tissue in the current study suggests that early onset of puberty in gilts might be beneficial for mammogenesis. Prepubertal mammary development of heifers is also linked to the gradual maturation of the ovaries because ovariectomy abolishes mammary growth (Purup et al., 1993). The role of the GH/IGF-I axis for mammogenesis in the prepubertal period was studied extensively in cattle and rodents. It is now known that IGF-I must be present for pubertal mammary development to take place (Kleinberg et al., 2000). To the best of our knowledge, this was never investigated in swine, yet plasma IGF-I and IGFBP, as well as mammary development, seem to be altered by nutritional manipulation (Sorensen et al., 2002b). The current study shows that the negative effect of feed-restriction is not related to changes in plasma IGF-I concentrations. Lee et al. (2002) also reported no changes in concentrations of IGF-I or IGFBP-3 in barrows fed 80% of ad libitum.

Leptin is a protein-hormone secreted by adipose tissue, which is known to have an important role in feed regulation, as well as in reproductive and immune functions (Barb, 1999). In sows, serum concentrations of leptin are highest in animals with the greatest amount of backfat (Estienne et al., 2000, 2003), and feed restriction decreases leptin secretion in ovariectomized gilts (Whisnant and Harrell, 2002). Present results confirm these data and the lower leptin concentrations in T4 gilts therefore reflect their caloric deficit and signals insatiety. Leptin is also produced by epithelial cells of mammary tissue (Smith-Kirwin et al., 1998; Aoki et al., 1999), and its involvement in the regulation of mammary gland development was recently demonstrated in mice (Hu et al., 2002) and cattle (Smith and Sheffield, 2002). Leptin is thought to mediate the inhibitory effects of high-energy intake on mammary gland development in prepubertal heifers (Silva et al., 2003). The fact that leptin concentrations were unaltered in gilts fed standard (T1) or LP (T2 and T3) diets supports the lack of difference in mammary parenchyma between these nutritional regimens.

	Implications

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A lower protein intake during prepuberty (as of d 90 of age) did not hinder mammary development of gilts, but a 20% feed restriction during that period decreased extraparenchymal tissue mass by 42% and parenchymal tissue mass by 26%. The practice of feed restriction in growing gilts is therefore questionable, as it impairs some characteristics of mammary gland development. Conversely, ad libitum feeding of prepubertal gilts seems to be beneficial for mammary development. Replacement gilts could also be fed a low-protein diet at intakes of 2.5 and 3.3 kg/d from 90 to 150 d and 150 to 200 d of age, respectively. The possible effect of these nutritional strategies on other reproduction variables should be evaluated before they are adopted.

	Footnotes

 
¹ Lennoxville Dairy and Swine R & D Centre Contribution No. 826.

² The authors thank L. Thibault, L. Marier, and J. Brochu for their invaluable technical assistance; the staff of the Swine Complex, especially F. Phaneuf and M. Turcotte, for care of the animals, and S. Méthot for statistical analyses. This project was funded by the "Fédération des Producteurs de Porcs du Québec," and the feed was supplied by Shur-Gain (Brossard, Canada).

³ Correspondence: phone: 819-565-9174, ext. 222; fax: 819-564-5507; e-mail: farmerc{at}agr.gc.ca.

Received for publication December 3, 2003. Accepted for publication April 6, 2004.

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