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ANIMAL GROWTH, PHYSIOLOGY, AND REPRODUCTION |
,2
,3,4
* Department of Physiology and
and
Department of Obstetrics and Gynaecology, University of Adelaide, Adelaide 5005, Australia, and
and
Research and Development Unit, QAF Meat Industries, Ltd., Redlands Road, Corowa 2646, Australia
Abstract
Treatment of pigs with porcine ST (pST) in early to mid-pregnancy increases body weight and length of their fetuses by mid-pregnancy, but this increased weight may not persist to birth. We investigated the effects of short- (25 d) and long-term (75 d) treatment with pST, and interactions between long-term pST treatment and crude protein content of diet, in restricted-fed gilts. In both experiments, Large White x Landrace gilts were bred at first estrus to Large White x Duroc boars and allowed to farrow naturally. In the first experiment, gilts were fed 1.8 kg/d of a diet containing 13.5 MJ DE/kg of DM and 15.05% CP (as-fed basis) throughout pregnancy, and were injected daily with 0, 2, or 4 mg pST from d 25 to 50 of pregnancy. Maternal treatment with pST from d 25 to 50 of pregnancy did not affect the number of piglets born per litter or progeny size at birth. In the second experiment, gilts were injected daily with 0 or 2 mg of pST and fed 2.2 kg/d of a diet containing 14.5 MJ DE/kg and either (as-fed basis) 16.6% (0.81% lysine) or 22.2% CP (1.16% lysine) from d 25 to 100 of pregnancy. All gilts were then fed 3.0 kg/d of the lower protein diet from d 100 of pregnancy to farrowing. Treatment with 2 mg pST/d from d 25 to 100 of pregnancy increased live weight of all gilts during the treatment period (P = 0.016), but the change in maternal live weight from d 25 to 100 of pregnancy was only increased (P = 0.001) by pST in gilts fed the higher protein diet. Live weight of gilts 1 d after farrowing was increased by pST treatment (P = 0.007), but was not altered by protein content of diet during pregnancy. In gilts fed the lower protein diet, but not in those fed the higher protein diet, pST treatment decreased maternal backfat depth during treatment (P < 0.020) and 1 d after farrowing (P = 0.002). Treatment with pST during pregnancy did not affect the number of piglets born per litter but independently increased body weight by 11.6% (P < 0.001) and length by 3.4% (P = 0.005) of progeny at birth and decreased (P < 0.01) the negative effect of litter size on body weight at birth. We conclude that in feed-restricted gilts, fetal weight gains in response to 25 d of pST treatment before mid-pregnancy are not maintained to term but that treatment with pST during most of pregnancy increases progeny size at birth and reduces maternal constraint of fetal growth.
Key Words: Birth Weight • Dietary Protein • Pig • Pregnancy • Somatotropin
Introduction
In well-fed and feed-restricted gilts, treatment with porcine ST (pST) during early to mid-pregnancy promotes the growth of their placentae and/or fetuses (Kelley et al., 1995
; Sterle et al., 1995; Gatford et al., 2000). The increase in progeny size following maternal pST treatment in early to mid-pregnancy is not maintained until term in well-fed or feed-restricted gilts, however (Kelley et al., 1995; Gatford et al., 2003). The mechanisms that underlie increased fetal growth in response to maternal pST treatment have not yet been established. Metabolic responses to pST are unlikely to persist beyond 24 h after pST treatment (Schneider et al., 2002), although changes in placental structure may be long lasting (Sterle et al., 2003). We therefore tested the hypotheses that increased fetal size would not be maintained to term in feed-restricted gilts treated with pST from d 25 to 50 of pregnancy (Exp. 1), but that extending the period of pST treatment until d 100 of pregnancy would increase progeny size at birth (Exp. 2).
Restricted maternal nutrition during pregnancy constrains fetal growth and development (Dwyer et al., 1994; Gatford et al., 2003) and may limit responses to maternal pST treatment. The nutrients in maternal feed during pregnancy that are the major determinants of progeny growth and development are unknown. Restriction of dietary protein during the first third of pregnancy in gilts reduces progeny birth weight but not postnatal rates of live weight gain, whereas protein restriction throughout pregnancy reduces size at birth, postnatal rates of live weight gain, and subsequent muscle size of progeny (Pond et al., 1992; Schoknecht et al., 1993). In Exp. 2, we therefore also tested the hypothesis that increased dietary protein availability from d 25 to 100 of pregnancy would increase progeny size at birth and would also increase the effects of pST on progeny size at birth in the feed-restricted gilt.
Materials and Methods
Animals
Both studies were designed in accordance with the Australian Code of Practice for the Care and Use of Animals for Scientific Purposes (National Health and Medical Research Council of Australia, 1997) and approved by the Animal Experimentation Ethics Committee of QAF Meat Industries, Ltd. (formerly known as Bunge Meat Industries, Ltd.). In both studies, the gilts were individually housed and fed. During pregnancy, gilts were housed in individual, 2.1- x 0.6-m stalls. During farrowing, they were housed with their litters in 2.1- x 0.6-m farrowing crates.
Experiment 1—Short-Term (25-d) pST Treatment.
Ninety-two Large White x Landrace gilts were bred at first estrus to crossbred (Large White x Duroc) boars and were allocated to one of three treatment groups (n = 30 or 31 gilts/treatment) such that maternal body weight (139.7 ± 1.3 kg) and backfat depth (18.7 ± 0.4 mm) at mating did not differ between treatment groups. From d 25 to 50 of pregnancy, gilts were given a daily i.m. injection of sterile water (vehicle) containing either 0, 2, or 4 mg of recombinant pST (Southern Cross Biotech Pty., Ltd., Melbourne, Australia). Gilts were fed 1.8 kg/d of a diet containing 13.5 MJ DE/kg of DM and 15.05% CP (as-fed basis) throughout pregnancy. This level of nutrition in the pregnant gilt corresponds to approximately 30% of ad libitum feed intake and permits maintenance of pregnancy and limited maternal live weight gain during pregnancy, but restricts fetal growth (Noblet et al., 1985). Live weight and backfat depth of pregnant gilts, measured by real-time ultrasound 65 mm from the midline over the last rib (P2 backfat depth), were recorded at mating and on the day after farrowing. Seventeen gilts returned to estrus before d 25 of pregnancy. Three gilts were removed from the trial during the treatment period. One gilt from the vehicle-treated group returned to estrus 33 d after mating, one gilt from the group treated with 4 mg pST/d aborted at d 41 of pregnancy, and one gilt from the vehicle-treated group aborted at d 50 of pregnancy. Seventy-two gilts completed the injection protocol. Five gilts from each treatment group were killed on d 51 of pregnancy for analysis of fetal growth responses, as described previously (Gatford et al., 2000). One gilt was removed from the trial after d 51 of pregnancy and before farrowing due to illness. Fifty-six gilts (n = 18 to 19 gilts per group) farrowed naturally at term. Litter size and individual piglet body weight, crown–rump length, abdominal circumference, and skull width were measured within 12 h of birth (188 to 202 progeny/treatment, total of 582 newborn progeny).
Experiment 2—Long-Term (75-d) pST Treatment.
Large White x Landrace gilts (n = 100) were bred at first estrus to crossbred (Large White x Duroc) boars and randomly assigned to one of four treatment groups, in a 2 x 2 factorial arrangement of pST treatment and maternal diet. From estrus to d 24 of pregnancy, all animals were provided a diet containing 14.5 MJ DE/kg and 16.6% CP (0.81% lysine; as-fed basis) at 2.2 kg/d. Nine gilts returned to estrus following the allocation of gilts to treatment groups. From the 25th to the 100th day of pregnancy, 49 gilts were continued on the same diet and 42 were fed 2.2 kg/d of an isocaloric diet containing (as-fed basis) 22.2% CP (1.16% lysine). During this period, gilts on both diets were given a daily i.m. injection of sterile water (vehicle) containing either 0 (23 gilts on each diet) or 2 mg (26 gilts on the lower and 19 on the higher protein diet) recombinant pST (Southern Cross Biotech Pty., Ltd.). From d 100 of pregnancy until term, all gilts were fed 3.0 kg/d of the lower protein diet. The average dose rate for the pST-treated animals was 14.14 ± 0.15 µg/kg at d 25 of pregnancy, decreasing to 10.72 ± 0.12 µg/kg at d 100, and averaged 12.34 ± 0.13 µg/kg across the treatment period. Live weight and P2 backfat depth of pregnant gilts, measured by real-time ultrasound 65 mm from the midline over the last rib, were recorded 25, 50, 75, and 100 d after mating, and on the day after farrowing. Five gilts were removed from the experiment due to pregnancy loss, and the remaining gilts farrowed naturally at term. Litter size and individual piglet body weight, crown–rump length, abdominal circumference, and skull width were measured within 12 h of birth (164 to 235 progeny per treatment, total of 844 newborn progeny).
Statistical Analyses
Data are presented as arithmetic mean ± SEM (n = number of dams or progeny). Data were transformed where required to achieve equivalent variance and normal distribution before ANOVA. A probability of P < 0.05 was considered significant.
Experiment 1—Short-Term (25-d) pST Treatment.
The experimental unit for all measures was the gilt, with measures of individual progeny treated as repeated measures on their mother. Maternal live weight and backfat depth, litter size, and average and total litter weights were analyzed by one-way ANOVA for effects of maternal pST dose. Comparisons between different pST dose groups were made using the Tukey honest significant difference procedure. Measurements of progeny size at birth were fitted to a model in the linear mixed models procedure of the Statistical Package for the Social Sciences (SPSS) for Windows, Version 11.0 (SPSS, Inc., Chicago, IL), that included the effects of maternal pST dose, progeny sex and pST dose x sex interaction, total litter size as a covariate, and gilt nested within treatment, using a compound symmetry variance structure. In a further series of analyses, progeny in each litter were assigned to quartiles of birth weight within the litter and the birth weight data from each quartile was fitted to the above model to analyze effects of maternal pST dose, progeny sex and total litter size. Associations between measurements were identified by Pearson correlation.
Experiment 2—Long-Term (75-d) pST Treatment.
The experimental unit for all measures was the gilt, with measures of individual progeny treated as repeated measures on their mother. Change in maternal live weight and backfat depth between d 25 and 100 of pregnancy, maternal live weight and backfat depth 1 d after farrowing, litter size, and average and total litter weights were analyzed by two-way ANOVA for effects of maternal pST dose and maternal diet. Effects of maternal nutrition and maternal pST dose on measurements of gilts and progeny were assessed by two-way ANOVA using repeated measures and day of pregnancy (time) as a within factor where appropriate. Measurements of maternal live weight and maternal backfat depth during the treatment period were fitted to a model in the linear mixed models procedure of SPSS for Windows, Version 11.0, that included the effects of maternal pST dose, maternal diet, and day of pregnancy, with gilt nested within pST x diet, using a first-order autoregressive covariance structure for repeated measures across time. Measurements of progeny size at birth were fitted to a model in the linear mixed models procedure of SPSS for Windows, Version 11.0, that included the effects of maternal pST dose, maternal diet, progeny sex and full interactions, with total litter size as a covariate, and gilt nested within treatment, using a compound symmetry variance structure. In a further series of analyses, progeny in each litter were assigned to quartiles of birth weight within the litter and birth weight data from each quartile was fitted to the above model to analyze effects of maternal pST dose, maternal diet, progeny sex, and total litter size. Associations between measurements were identified by Pearson correlation. Differences between slopes of linear regressions were assessed using the method of Zar (1974).
Results
Experiment 1
Maternal Responses to Short-Term (25-d) pST Treatment.
Gilt live weight at mating and 1 d after farrowing was not altered by maternal pST treatment from d 25 to 50 of pregnancy (Table 1). Maternal pST treatment altered the backfat depth of gilts after farrowing (P = 0.025), and the effect varied between pST doses such that gilts treated with 2 mg pST/d from d 25 to 50 of pregnancy were fatter (P < 0.05) after farrowing than gilts that were treated with 4 mg pST/d during the same period (Table 1). Gestation length (115.2 ± 0.2 d) was not affected by maternal pST treatment (P = 0.30).
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Experiment 2
Maternal Responses to Long-Term (75-d) pST Treatment.
Gilt live weight at d 25 of pregnancy did not differ between treatments (Figure 1a). Gilt live weight increased from d 25 to 100 of pregnancy (P < 0.001). Two-way interactions were identified between day of pregnancy and maternal diet (P = 0.038) and between day of pregnancy and maternal pST treatment (P < 0.001); therefore, maternal live weight at each day of pregnancy was analyzed by two-way ANOVA for effects of pST treatment and maternal diet. The interaction among day of pregnancy, maternal pST treatment, and maternal diet for live weight was also significant (P = 0.029), reflecting different rates of growth in the four treatment groups. Gilts fed the higher protein diet tended to have higher live weights (P = 0.053) at d 100 of pregnancy but not at other days of pregnancy. Treatment with pST increased gilt live weight at d 50 (P = 0.005), d 75 (P < 0.001), and d 100 (P = 0.001) of pregnancy (Figure 1a). There was a significant interaction between pST treatment and maternal pregnancy diet for the total live weight gain from d 25 to 100 of pregnancy (P = 0.039). The combination of pST treatment and a high-protein diet during this period produced a greater live weight gain between d 25 and 100 of pregnancy than for any other treatment combination (P < 0.004 for all comparisons), whereas live weight gain did not differ among the other treatment groups (Figure 1a). One day after farrowing, maternal live weight was higher in gilts that had been treated with pST during pregnancy (P = 0.008) and was not significantly affected by protein content of pregnancy diet or by an interaction between pST treatment and diet (Figure 1a). Nevertheless, maternal live weight 1 d after farrowing was 9.9 kg greater (P = 0.043) in gilts that had been treated with pST and fed the high-protein diet than in gilts treated with pST and fed the low-protein diet, 13.8 kg greater (P = 0.003) than in vehicle-treated gilts on the high-protein diet, and 14.1 kg greater (P = 0.002) than in vehicle-treated gilts on the low-protein diet.
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). Within the group of gilts allocated to the higher protein diet, however, gilt P2 backfat depth at d 25 of pregnancy was higher (P = 0.001) in gilts subsequently injected with 2 mg pST/d than those injected with vehicle. The depth of P2 backfat at d 25 of pregnancy did not differ significantly between pST treatment groups in gilts allocated to the low-protein diet. During the treatment period from d 25 to 100 of pregnancy, the P2 backfat depth of gilts changed with time (P = 0.001) (Figure 1b). Interactions were identified between day of pregnancy and maternal pST treatment (P < 0.001) and between maternal pST treatment and maternal diet (P = 0.050); therefore, maternal backfat depth at each day of pregnancy was analyzed by two-way ANOVA for effects of maternal pST and maternal diet. Interactions between treatment with pST and the protein content of diet were evident from d 50 of pregnancy (d 50: P = 0.031, d 75: P = 0.029, d 100: P = 0.010) so the two diet groups were analyzed separately for effects of maternal pST treatment. In gilts fed the lower protein diet, 2 mg pST/d reduced P2 backfat depth at d 50 (P = 0.020), 75 (P = 0.001), and 100 (P < 0.001) of pregnancy (Figure 1b). In gilts fed the higher protein diet, 2 mg pST/d had no significant effect on gilt P2 backfat depth at any stage of pregnancy examined. The change in P2 backfat depth between d 25 and 100 of pregnancy was altered by maternal pST treatment (P < 0.001) but not by maternal diet (for both diets combined, 2.9 ± 0.4 mm at 0 mg pST/d and -0.6 ± 0.4 mm at 2 mg pST/d). Maternal pST treatment decreased maternal P2 backfat depth 1 d after farrowing (Figure 1b) overall (P = 0.001) and in gilts fed the lower protein diet (P = 0.001) but not in those fed the higher protein diet during pregnancy (P = 0.20). Consequently, maternal backfat 1 d after farrowing was higher in gilts fed the low-protein diet witout pST treatment than in gilts treated with pST and fed either the low- (P = 0.001) or high-protein (P = 0.025) diet. Maternal backfat 1 d after farrowing was not different in gilts fed the high-protein diet without pST treatment than in other treatment groups.
Birth Characteristics of Progeny Following Long-Term (75-d) Maternal pST Treatment.
Neither protein content of the pregnancy diet nor maternal treatment with pST significantly affected the number of piglets delivered per gilt (10.2 ± 0.3), the number of liveborn piglets per litter (9.6 ± 0.3) or the number of stillborn piglets/litter (0.5 ± 0.1). The body weight, crown–rump length, and abdominal circumference of individual progeny at birth were all negatively correlated with litter size, were increased by treatment with pST during pregnancy, were not significantly affected by protein content of diet during pregnancy, and were greater in male than in female progeny (Table 2). The skull width of individual progeny at birth was not significantly affected by litter size or by maternal treatments but was greater in male than in female progeny (Table 2). There were no significant interactions between the effects of different maternal treatments and/or progeny gender on progeny body size at birth. For all quartiles of piglet birth weights within their litter, individual birth weights were negatively correlated with total litter size (P < 0.002 for all). Maternal pST treatment increased progeny birth weight for piglets in the second, third, and fourth quartiles of birth weight within their litter (P < 0.02 for all). Maternal diet during pregnancy did not affect individual progeny birth weights for piglets in the second, third, and fourth quartiles of birth weight within their litter. For piglets in the lightest quartile of birth weight for their litter, maternal pST treatment increased birth weight in progeny of sows fed the high-protein diet (P = 0.049), but did not affect birth weight in progeny of sows fed the low-protein diet (P = 0.50).
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) with the total number born per litter. Maternal diet during pregnancy did not affect litter mean birth weight, and the progeny of gilts fed both pregnancy diets were grouped together for regression analysis. The slope of the linear regression of litter size vs. litter mean birth weight was also altered (P < 0.01) by treatment with pST. Average body weight per litter at birth (y) was reduced to a lesser extent as litter size (x) increased for gilts treated with 2 mg pST/d (y = 1.87 - 0.032x, r = 0.365, P = 0.016) than for those treated with 0 mg pST/d (y = 1.86 - 0.044x, r = 0.572, P < 0.001) from d 25 to 100 of pregnancy (Figure 2).
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The effects of maternal pST treatment on the progeny phenotype at birth depended on the duration of pST treatment but not on the protein content of maternal diet during pregnancy. In contrast to long-term treatment, maternal treatment with either 2 or 4 mg pST/d from early to mid-pregnancy did not alter the weight or size of piglets at birth in the present study, despite the fact that these treatments both increased fetal weight and size at the end of treatment (Gatford et al., 2000). We have previously reported that daily treatment with 4 or 8 mg pST during the second quarter of pregnancy in similarly fed gilts did not alter progeny weight and size at birth (Gatford et al., 2003). Even in gilts provided larger amounts of feed during pregnancy, maternal treatment with approximately 4 mg pST/d during early to mid-pregnancy produced only small increases in birth length and no increase in birth weight of progeny (Kelley et al., 1995). Previous studies have indicated that the effects of maternal pST treatment on fetal growth may be greatest in those piglets in each litter whose growth is restricted to the greatest extent. Rehfeldt et al. (2001) found that maternal treatment with 6 mg pST/d from d 10 to 27 of pregnancy in well-fed gilts increased birth weight only in those progeny in the lowest 25% of birth weight for their litter, although average fetal weight and birth weight across the litter were not altered by maternal pST treatment. In the present study, however, short-term maternal pST treatment did not affect the size at birth of piglets from any quartile of birth weight in their litter. These results support our initial hypothesis that increased progeny size is not maintained to term following maternal pST treatment from d 25 to d 50 of pregnancy. The lack of change in birth weight following pST treatment during the second quarter of pregnancy in restrictedly fed gilts suggests that maternal constraint of fetal growth is reimposed after pST treatment ceases at d 50 of pregnancy. Further, because progeny of mothers that received short-term pST treatment were heavier immediately following pST treatment (Gatford et al., 2000), their growth from mid-pregnancy to term must have been constrained to a greater extent than that of the progeny from mothers that did not receive pST treatment. Consistent with this hypothesis, Sterle et al. (2003) found that maternal treatment with 5 mg pST/d from d 0 to 30 of pregnancy in conditions of uterine crowding actually reduced fetal weight 35 d after pST treatment was completed. In contrast to maternal pST treatment during the second quarter of pregnancy only, daily maternal treatment with 2 mg of pST that was sustained from early to late pregnancy (d 25 to 100) increased the body weight (
12%), length (3%), and girth (5%) of piglets at birth without affecting litter size in feed-restricted gilts, which is consistent with our hypothesis that extending the period of pST-treatment until d 100 would increase progeny size at birth. Variation of the protein content of the diet throughout most of pregnancy did not affect fetal growth responses to long-term maternal pST treatment, which is contrary to our hypotheses that increased dietary protein availability from d 25 to 100 of pregnancy would increase progeny size at birth and would increase the effects of pST on progeny size at birth in the feed-restricted gilt. Maternal pST treatment in the latter part of pregnancy thus appears to be able to maintain the increases in fetal weight induced by pST treatment up to d 50 of pregnancy, resulting in larger piglets at term. Maternal pST treatment of shorter duration in late pregnancy has little or no effect on progeny weight at term, however. Progeny birth weight was increased by only 5% following maternal treatment with 6 mg pST/d from d 80 to 94 of pregnancy (Rehfeldt et al., 1993), and elevated maternal plasma GH in the last 2 or 3 wk of pregnancy did not increase progeny weight at term (Kveragas et al., 1986; Etienne et al., 1992). Contrary to suggestions that at least short-term maternal pST treatment has its greatest effects in the smallest piglets of each litter (Rehfeldt et al., 2001), in the present study, long-term pST treatment during pregnancy in restrictedly fed gilts increased birth weight in piglets in the second, third, and fourth quartile of birth weight for their litter but not in those of the lightest quartile of each litter. A novel finding of the present study was that the decrease in average progeny birth weight with increasing litter size was less in pST-treated gilts, indicating that maternal pST treatment increased progeny weight at birth most in the litters subjected to the greatest maternal constraint. Consistent with this result, Sterle et al. (1995) found that maternal treatment with 5 mg pST/d from d 30 to 43 of pregnancy in well-fed gilts increased fetal growth to the greatest extent in piglets whose placenta had a short implantation length. Because they subdivided fetuses into quartiles of placental implantation length across the entire study population, rather than within litters, differences in placental implantation length in that study may have reflected litter size as well as position in the uterus. However, maternal pST treatment was not able to increase fetal size in gilts where fetal growth was constrained by uterine crowding (Sterle et al., 2003).
The mechanism(s) for promotion of fetal growth by pST treatment during pregnancy is not clear. It is possible that pST may promote the growth and functional development of the placenta. It is also possible that pST changes maternal metabolism in ways that support increased nutrient transfer to the fetus. Somatotropin-like peptides of placental origin, including placental growth hormone variant and placental lactogen (Southard and Talamantes, 1991; Walker et al., 1991; Wallis, 1996; Lacroix et al., 2002), are thought to play important roles in the maternal metabolic adaptations to pregnancy in many species, and their circulating levels are lower than normal in human pregnancies complicated by intrauterine growth retardation (Mirlesse et al., 1993; McIntyre et al., 2000). In contrast, the pig placenta is epitheliochorial and does not significantly invade the endometrium, and the pig lacks placental lactogen or placental growth hormone (Kelly et al., 1976). Circulating somatotropin does not rise (Sinha et al., 1990), and circulating levels of IGF-I fall during pregnancy in the pig (Farmer et al., 2000), implying that these hormones do not regulate maternal metabolic adaptations to pregnancy in this species, although there is some evidence for paracrine activity of this axis within the placenta (Farmer and Gaudreau, 1997). Nevertheless, changes in maternal metabolism probably account for much of the increase in fetal growth during maternal pST treatment in the pig. In the well-fed and in the feed-restricted pregnant gilt, pST treatment during early to mid-pregnancy enhances the deposition of lean tissue and reduces fat deposition, and it increases maternal plasma concentrations of IGF-I (Sterle et al., 1995; Gatford et al., 2000; Schneider et al., 2002). Because somatotropin has anti-insulin actions in the nonpregnant pig (Walton and Etherton, 1986; Magri et al., 1990), it may also enhance the normal maternal insulin resistance of pregnancy to increase glucose availability to the fetus. Consistent with enhanced maternal insulin resistance, treatment with pST during pregnancy in restrictedly fed gilts increases the concentrations of insulin and glucose in maternal blood during treatment (Gatford et al., 2003). Maternal pST treatment increased fetal plasma concentrations of glucose at d 51 of pregnancy in restrictedly fed gilts (Gatford et al., 2000), consistent with increased delivery of glucose to the fetus in response to elevated maternal glucose levels produced by pST treatment of pregnant mothers. Maternal pST treatment from d 10 to 27 of pregnancy in well-fed gilts increased maternal plasma concentrations of glucose and FFA (Schneider et al., 2002), and this was associated with increased glucose concentrations in allantoic and amniotic fluids at d 28 of pregnancy (Rehfeldt et al., 2001). Administration of pST to the mother is unlikely to have direct effects on fetal growth because somatotropin cannot cross the placenta, at least in rats (Fholenhag et al., 1994). In the pig, maternal pST treatment in early to mid-pregnancy increases placental RNA and protein content and/or weight (Sterle et al., 1995; Sterle et al., 2003; Rehfeldt et al., 2001) and also increases the area of uterine-placental interface (Sterle et al., 2003). Sterle et al. (1995) also reported that fetal growth was increased to the greatest extent in those fetuses whose placentas have the shortest implantation lengths. These results indicate that improved transfer of nutrients due to better placental function or increased circulating levels in maternal plasma, rather than increased placental size, may be the underlying mechanisms of action for maternal pST treatment to increase growth of the fetus in feed-restricted mothers. Effects of maternal pST treatment on placental function have not been assessed in pigs, but somatotropin increases placental capacity for transplacental diffusion of solutes in the late pregnant sheep (Harding et al., 1997). The increase in birth size following 75 d, but not 25 d, of maternal pST treatment in the present study suggests that somatotropin promotes fetal growth mainly via changes in maternal metabolism that increase nutrient availability to the fetus, and that any effects of pST to increase placental growth or function are not capable of sustaining increased fetal demand for nutrients if pST treatment ceases in mid-pregnancy. Although pST treatment from d 0 to 30 of pregnancy in gilts with uterine crowding caused an increase in uterine-placental contact area that was maintained at least to d 65 of pregnancy, fetal size at d 65 was reduced by this treatment (Sterle et al., 2003), also implying that altered placental structure is not the major mediator for the promotion of fetal growth by maternal pST.
Maternal responses to pST varied with treatment duration and dietary protein content during treatment. Short-term pST treatment in early to mid-pregnancy did not alter maternal weight at farrowing in the present study, although maternal weight gain during the treatment period increased with increasing pST dose (Gatford et al., 2000). Both doses of pST resulted in similar losses of backfat depth (~5 mm compared to 2 mm in controls) between d 25 and 50 of pregnancy (Gatford et al., 2000). The effects of short-term pST treatment on backfat in mothers at farrowing varied with pST dose, however. In the present study, backfat depth at farrowing was greater in dams that were treated with 2 mg/d pST from d 25 to 50 of pregnancy than in those treated with 4 mg/d during the same period, and backfat depth at farrowing was intermediate in control dams. Fat deposition from d 50 of pregnancy to term must therefore have been more rapid in mothers that were treated with 2 mg/d pST from d 25 to 50 of pregnancy than in the other groups. Maternal and fetal endocrine and metabolic responses to pST also differed between the two pST doses in the subset of animals killed at d 51 of pregnancy (Gatford et al., 2000), although the reasons for this are unclear. In contrast to the effects of short-term pST treatment, long-term pST treatment in the present study altered both maternal weight and backfat depth at farrowing. Maternal weight at farrowing was increased by long-term pST treatment during pregnancy, but was not altered by dietary protein content during pregnancy. However, interactions existed between diet and pST treatment for maternal weight gain and backfat loss during the treatment period. By itself, feeding a higher protein diet did not increase maternal weight gain, implying that a dietary protein content of 16.6% and a lysine content of 0.81% do not limit maternal weight gain in pregnant gilts. Lysine has been calculated to be the first-limiting amino acid in pregnancy diets for pigs (Pettigrew, 1993). Because the low- and high-protein diets in this study provide 173 and 247%, respectively, of the NRC (National Research Council [U.S.] Subcommittee on Swine Nutrition, 1998) estimated requirement for dietary lysine of 10.3 g of lysine/d for pregnant sows gaining 40 kg during their pregnancy, the protein contents of both diets should not limit maternal growth. Both pregnancy diets in this experiment also contained at least 150% of the NRC (National Research Council [U.S.] Subcommittee on Swine Nutrition, 1998) estimated requirements for all essential amino acids. Long-term pST treatment was only able to increase maternal weight gain during pregnancy in mothers that were fed the higher protein diet (22.2% CP and 1.16% lysine), however, implying that a dietary CP content of 16.6% and lysine content of 0.81% are not sufficient to meet maternal requirements for anabolic responses to exogenous pST in pregnancy. Conversely, pST reduced maternal backfat gain from d 25 to 100 of pregnancy, independent of dietary protein content, and reduced maternal backfat depth at farrowing overall and in dams that were fed the low-, but not the high-, protein diet in pregnancy. Long-term pST treatment may therefore increase maternal appetite during lactation because previous studies in gilts have shown a negative relationship between maternal fatness at farrowing and maternal appetite during lactation (Mullan and Williams, 1989; Dourmad, 1991; Revell et al., 1998).
In conclusion, maternal pST treatment in early to mid-pregnancy increases fetal growth but, unless pST treatment is continued, does not increase progeny size at birth. Maternal pST treatment that is continued from early to late pregnancy increases progeny size at birth and has the biggest effects in the largest litters.
Implications
Long-term treatment with porcine somatotropin, but not changes in diet during pregnancy, maintained gains in fetal growth in response to porcine somatotropin in pregnant gilts, and increased progeny size at birth. Conventional commercial gestation diets may not be adequate to meet maternal requirements for lean tissue deposition in gilts treated with porcine somatotropin for extended periods of pregnancy, and increased protein content in the diet seemed to overcome this problem.
Footnotes
1 This research was supported in part by Australian Pork Limited (formerly known as the Pig Research and Development Corporation of Australia); K. L. Gatford was supported initially by an Australian Pork Limited Scholarship and subsequently by a Peter Doherty Postdoctoral Fellowship from the National Health and Medical Research Council of Australia. The authors thank D. Harrison of QAF Meat Industries, Ltd., for assistance with animal studies and B. Willson, Dept. of Psychology, University of Adelaide, for assistance with statistical analyses. 
3 Current address: Tamworth Centre for Crop Improvement, NSW Agriculture, Tamworth NSW 2340, Australia.
4 Current address: Ausgene, P.O. Box 427, Gridley, IL 61744.
2 Correspondence: School of Molecular and Biomedical Science (phone: +61-8-8303-4158; fax: +61-8-8303-3356; e-mail: kathy.gatford{at}adelaide.edu.au).
Received for publication May 5, 2003. Accepted for publication September 3, 2003.
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