Maternal responses to daily maternal porcine somatotropin injections during early-mid pregnancy or...

Nottle, K. L. Kind and J. A. OwensK. L. Gatford, R. J. Smits, C. L. Collins, C. Argent, M. J. De Blasio, C. T. Roberts, M. B.

early-mid or early-late pregnancy in sows and giltsMaternal responses to daily maternal porcine somatotropin injections during

published online December 18, 2009J ANIM SCI

http://jas.fass.org/content/early/2009/12/18/jas.2009-2265the World Wide Web at:

The online version of this article, along with updated information and services, is located on

www.asas.org

by guest on May 18, 2011jas.fass.orgDownloaded from

http://jas.fass.org/

1

Responses to pST in pregnant gilts and sows

Maternal responses to daily maternal porcine somatotropin injections during early-mid or

early-late pregnancy in sows and gilts1

K. L. Gatford*‡, R. J. Smits¶, C. L. Collins¶, C. Argent¶, M. J. De Blasio*‡, C. T. Roberts†‡,

M. B. Nottle₤‡, K. L. Kind†#, and J. A. Owens*‡

*Research Centre for Early Origins of Health and Disease, Robinson Institute, University of

Adelaide SA 5005, Australia; †Research Centre for Reproductive Health, Robinson Institute,

University of Adelaide SA 5005, Australia; ₤Stem Cell Research Centre, Robinson Institute,

University of Adelaide SA 5005, Australia; ‡Discipline of Obstetrics and Gynaecology, School

of Paediatrics and Reproductive Health, University of Adelaide SA 5005, Australia; ¶Research

and Innovation Unit, Rivalea Australia Pty Ltd., Redlands Rd, Corowa NSW 2646, Australia;

and #Animal Science, School of Agriculture, Food and Wine, University of Adelaide,

Roseworthy SA 5371, Australia

The authors wish to thank the staff of the Research and Innovation Unit at Rivalea Australia Pty

Ltd, for their excellent animal management, performing treatments and assistance with

measurements. We thank OzBioPharm Pty Ltd for their donation of porcine growth hormone

(Reporcin) used in this study. This study was supported by the Australian Cooperative Research

Centre for an Internationally Competitive Pork Industry (project 2F-103).

2Corresponding author: [email protected].

Published Online First on December 18, 2009 as doi:10.2527/jas.2009-2265 by guest on May 18, 2011jas.fass.orgDownloaded from


2

ABSTRACT: Piglet neonatal survival and postnatal growth and efficiency are positively related

to birth weight. In gilts, daily maternal porcine somatotropin (pST) injections from d 25 to 100

(term ~d 115), but not d 25 to 50 of pregnancy, increase progeny birth weight. Daily maternal

pST injections from d 25 to 50 increase fetal weight at d 50 in gilts and sows. We therefore

hypothesised that daily pST injections from d 25 to 100, but not d 25 to 50 of pregnancy, would

increase birth weight similarly in both parities. Landrace x Large White gilts and sows were

uninjected (controls), or injected daily with pST (gilts: 2.5 mg.d-1, sows: 4.0 mg.d-1, each ~15 g

pST.kg-1.d-1) from d 25 to 50 or 100 of pregnancy. Litter size and weights were recorded at birth,

mid-lactation, and weaning. Dams were followed through their subsequent mating and

pregnancy. Maternal pST injections from d 25 to 100, but not d 25 to 50, increased average

piglet birth weight by 11.6% in sows (P ≤ 0.001) and 5.6% in gilts (P = 0.008). Both pST

treatments decreased litter size by ~0.6 live-born piglets (each P ≤ 0.025). In sows, maternal pST

treatment from d 25 to 100 increased culls at weaning (P = 0.037). In remated dams, prior

treatments did not affect weaning-remating interval, conception rates, or subsequent litter size.

Greater pST-induced birth weight increases in sows than gilts may mean that underlying

metabolic or placental mechanisms for pST action are constrained by maternal competition for

nutrients in rapidly-growing gilts.

Key words: birth weight, growth hormone, litter size, pig, pregnancy, subsequent reproduction

INTRODUCTION

Fetal growth and birth weight predict neonatal survival and postnatal growth rates and

efficiency in pigs, as in other species. Increased size at birth improves neonatal survival (Fahmy



3

and Bernard, 1971; van der Lende and de Jager, 1991; Roehe and Kalm, 2000), stimulates sow

milk production and growth of suckling piglets (Campbell and Dunkin, 1982; King et al., 1997),

and increases muscle fiber numbers and post-weaning growth (Wigmore and Stickland, 1983;

Dwyer et al., 1993; Gondret et al., 2005; Rehfeldt and Kuhn, 2006). In the pig, however, fetal

growth and birth weight are constrained by competing maternal demands in growing adolescent

animals, by large and variable litter size, and by restricted maternal nutrition used in commercial

pig production systems during pregnancy.

Daily maternal injections of gilts with porcine somatotropin (pST) during early-mid

pregnancy (d 30 to 43, 28 to 40, or 25 to 50) increase fetal growth, and progeny muscle size but

do not increase progeny birth weight (Kelley et al., 1995; Sterle et al., 1995; Sterle et al., 1998;

Gatford et al., 2000; Gatford et al., 2003; Gatford et al., 2004). More sustained pST treatment,

from d 25 to 100, increases progeny birth weight in gilts under commercial conditions (Gatford

et al., 2004). We recently reported that maternal pST injections from d 25 to 50 of pregnancy

increases fetal growth at d 50 to a similar extent in mature sows as in gilts (Gatford et al., 2009).

Whether sows are able to maintain increased fetal size to birth if maternal pST-treatment stops in

mid-pregnancy, the extent to which longer-term maternal pST treatment increases progeny size

at birth, and consequences for maternal and piglet outcomes, are not known. We therefore tested

the hypotheses that daily pST injections during early-mid pregnancy (d 25 to 50) or early-late

pregnancy (d 25 to 100) in gilts and sows increases progeny birth weight, lactation growth rates,

and neonatal survival, without adversely affecting subsequent reproductive performance.

MATERIALS AND METHODS



https://www.researchgate.net/publication/223099046_The_influence_of_piglet_body_weight_on_milk_production_of_sows?el=1_x_8&enrichId=rgreq-c9435377-4b73-4d2a-9d5b-88b2f29912c8&enrichSource=Y292ZXJQYWdlOzQwNzMwNjQxO0FTOjEwNDg4MzY1MDgyNjI1OEAxNDAyMDE3NjE5Nzc5

4

Animals

The study was 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, 2004) and approved by the University of Adelaide and the Rivalea Australia (formerly

QAF Meat Industries) Animal Ethics Committees. The in vivo studies were conducted under

commercial conditions at Rivalea Australia Corowa, NSW. Large White x Landrace (PrimeGro

Genetics) parity 0 sows (gilts) were mated at 23 wk of age, and mature Large White x Landrace

(PrimeGro Genetics) sows (2nd or 3rd parity at mating) were mated at the first post-weaning

estrus. The study was conducted over 12 wk, with 30 gilts and 30 sows allocated in equal

numbers to each treatment in each replicate wk of the study (2 x 2 factorial design, n = 120

dams/treatment and parity in total, 720 dams allocated to entire study). Gilts were mated 3 times

by artificial insemination using semen (3 x 109 sperm) from commercial hybrid boars in the

morning of detected estrus in the presence of a boar, followed by an afternoon mating and a third

the following morning. Sows were mated on the morning of detected estrus and 24 h later by

artificial insemination as above. The day of first insemination was taken as d 1 of pregnancy.

Pregnancy was confirmed by ultrasound scanning at d 23 to 24 after mating. Gilts were

individually housed in stalls from mating for 6 wk, then housed in groups of 8 to 12 at 1.8

m2/gilt, until entry to the farrowing house after 15 wk of pregnancy at d 108 to 110, when they

were transferred to individual farrowing crates for farrowing and lactation. Sows were housed

individually throughout pregnancy and were transferred to the same farrowing house as the

pregnant gilts after 15 wk of pregnancy. After weaning, all sows were returned to individual

stalls for approximately 1 wk for mating, and were then transferred to ecoshelters (Croft) where



5

animals were housed in groups of approximately 80 mixed parity sows (2.5 m2/sow) for the

subsequent pregnancy, before entering the farrowing house again at ~d 109 of pregnancy.

Nutrition and treatments

From mating until entry to the farrowing shed, gilts were fed 2.2 kg.d-1 and sows were

fed 2.5 kg.d-1 of a dry sow diet (13.5 MJ DE/kg, 16.0% total protein, 0.80% total lysine), once

daily in the morning. Following confirmation of pregnancy, gilts and sows were ranked by

weight within parity for each replicate week of the study, and allocated alternately to each

treatment group (n = 120 per treatment and parity in total). Control gilts and sows were not

injected, to enable comparison with performance under current commercial management. Gilts

and sows allocated to the pST-injection groups were injected i.m. daily with 1 mL sterile water

containing 2.5 or 4.0 mg pST respectively, which was calculated to provide a dose of ~15 g

pST.kg-1.d-1 in both parity groups, based on previous live weight data from the herd. Gilts and

sows were injected daily with pST from d 25 of pregnancy until d 50 (short-term pST) or d 100

of pregnancy (long-term pST). Dams entered the farrowing house between d 108 and 110 of

pregnancy (d 109 ± 1), and were fed 3 kg.d-1 of a lactation diet (14.9 MJ DE/kg, 19.2% total

protein, 0.89% total lysine) until farrowing, and were then fed 3 times per day to appetite with

this lactation diet until weaning. Gilts and sows farrowed naturally at term (referred to as

treatment pregnancy). Within 24 h of farrowing, a minimal cross-fostering approach was used to

equalize litter size to 10 piglets in gilt litters and 12 piglets in sow litters where possible. Sows

were weaned in the 4th week of lactation on a set day each week. Litters were weaned at 26.6 ±

0.1 d after birth, and all dams were mated by artificial insemination at the first post-weaning

estrus. Dam removals and reasons for removal were recorded throughout the treatment



6

pregnancy, lactation and up to the subsequent farrowing (subsequent pregnancy). Dams were fed

2.6 kg.d-1 of a commercial dry sow diet (12.9 MJ DE.kg-1, 14.5% total protein, 0.62% total

lysine) throughout the subsequent pregnancy and were transferred to the lactation diet upon entry

to the farrowing house as described above.



7

Maternal and Progeny Measures

Pregnant dams were weighed and backfat depth measured by ultrasound at the P2 site (65

mm from the midline over the final rib, using linear array 3.5 mHz live ultrasound; Noveko,

Canada), before the start of treatments at d 20 to 24 of pregnancy, at d 50 of pregnancy, on

transfer to the farrowing shed at d 104 to 111 of pregnancy, and at weaning. A subset (~60% of

dams in order to minimize disturbance of dams on day of birth) were weighed and backfat P2

recorded on the day of farrowing for each replicate week of the study. Numbers of live piglets,

still births, and mummified piglets were recorded within 24 h of birth. Total litter weight and

number were recorded on the day of delivery, after fostering, at d 14 of lactation, and at weaning.

Pre-weaning piglet losses, reasons for removal, and dates at removal were recorded throughout

lactation. Numbers of live piglets, still births, and mummified piglets were recorded within 24 h

of birth for the subsequent pregnancy.

Statistical Analyses

The effects of maternal parity, treatment, and their interaction on maternal and litter

outcomes were analysed using a 2-way ANOVA. Replicate week was also included as a factor in

full factorial statistical models in analyses of maternal weight, P2, and lactation performance,

which varied between replicate week. Replicate week did not affect litter size or size at birth and

was not included in these models. Specific contrasts were performed to test the a priori

hypotheses that short-term maternal pST treatment or long-term maternal pST treatment increase

litter weight and average piglet weight at birth, but do not impair subsequent maternal

reproductive performance. Chi-square analysis was used to test the effects of maternal parity and

treatment, and treatment within each parity, on dam removals. Pearson correlation tests were



8

used to investigate relationships between average litter birth size, survival, and pre-weaning

growth. All tests were carried out using SPSS v16.0 for Windows (SPSS Inc. USA) and data are

presented as mean ± SEM unless otherwise indicated.

RESULTS

Maternal Weight and Backfat Depth

Maternal weight at d 25 of pregnancy, before commencement of injections, was higher in

sows than gilts (P < 0.001, Gilts: 164.9 ± 0.8 kg; Sows: 238.9 ± 1.1 kg), tended to vary with

replicate week (P = 0.083) and did not differ between treatments (P = 0.998). Maternal pST

treatment increased maternal weight at the end of treatment, at d 50 in all pST-treated dams (P ≤

0.004; Figure 1) and at d 109 in dams treated with pST from d 25 to 100 (P ≤ 0.001), regardless

of parity. In those dams treated with pST from d 25 to d 50 of pregnancy, maternal weight

returned to similar levels as controls after the end of treatment and these animals were of similar

weight to controls at d 109 of pregnancy (P > 0.45; Figure 1). Daily maternal weight change

from d 50 of pregnancy to d 109 was higher in pigs treated with pST until d 100 of pregnancy

than in controls (P = 0.035), but was lower in pigs treated with pST until d 50 of pregnancy than

in controls (P = 0.020). Gilts grew faster during this period than sows (P ≤ 0.001), and the

difference in rate of weight gain between parities varied between replicate week of the study (P =

0.035). Maternal weight on the day after farrowing was increased in dams treated with pST from

d 25 to 100 of pregnancy (P = 0.01), but not in dams treated with pST from d 25 to 50 of

pregnancy (P > 0.7), compared to controls. Dams that were gilts during treatment were lighter on

the day after farrowing than sows (P ≤ 0.001) and the weight difference between parities varied



9

with replicate wk of the study (P = 0.016). Maternal weight at weaning did not differ between

treatment groups (P > 0.4, Figure 1). Weight at weaning was lower in dams that were gilts during

treatment (P ≤ 0.001), varied between replicate week of the study (P = 0.040), but effects of

parity and treatment did not differ with replicate week (P > 0.17 for each). Daily maternal weight

loss during lactation tended to be greater in dams treated with pST from d 25 to 50 of pregnancy

(P = 0.068; 477 ± 44 g.d-1), and was increased in dams treated with pST from d 25 to 100 of

pregnancy (P = 0.011; 643 ± 54 g.d-1), compared to controls (465 ± 59 g.d-1). Sows also lost

weight more rapidly than gilts during lactation (P ≤ 0.001; sows: 722 ± 46 g.d-1; gilts: 333 ± 34

g.d-1). Maternal weight loss during lactation varied between replicate week (P ≤ 0.001), but

effects of parity and treatment did not differ with replicate week (P > 0.16 for each).

Maternal P2 backfat depth (Figure 2, overall mean: 15.3 ± 0.1 mm) at d 25 of pregnancy,

efore commencement of injections, did not differ between parities (P > 0.8) nor treatment groups

(P > 0.9), but varied between replicate week (P ≤ 0.001), and effects of parity also varied

between replicate week (P = 0.001). Maternal P2 backfat depth at d 50 of pregnancy was also

unaffected by parity or treatment (P > 0.4 for each), varied with replicate week (P ≤ 0.001), and

effects of parity varied with replicate week (P ≤ 0.001). Dams treated with pST from d 25 to 100

of pregnancy gained P2 backfat depth more slowly between d 50 and 109 of pregnancy than

control dams (P = 0.015), while the rate of P2 backfat gain from d 25 to 109 was not different

from controls in dams whose pST treatment stopped at d 50 (P > 0.6). Consequently, maternal

P2 backfat depth before farrowing was higher in gilts than sows (P = 0.001), reduced in dams

treated with pST from d 25 to 100 of pregnancy (P = 0.001), but not in those treated from d 25 to

50 only (P = 0.165), and varied with replicate week (P ≤ 0.001). Rate of maternal P2 backfat loss

during lactation did not differ between treatments (P > 0.6) or parities (P > 0.2), but did vary



10

between replicate week (P ≤ 0.001). Consequently, maternal P2 backfat depth at weaning (Figure

2) was less in dams treated with pST from d 25 to 100 than controls (P = 0.034), but not reduced

in dams whose treatment finished at d 50 (P > 0.6).

Litter Outcomes for Treatment Pregnancy

Effects of maternal treatment on gestation length differed between parities (P = 0.033,

Table 1). In gilts, gestation length was unaffected by maternal treatment, but in sows, gestation

length was reduced following pST treatment from d 25 to 100 of pregnancy (P ≤ 0.001; Table 1).

Numbers of total and live born piglets (each P ≤ 0.001) and still born piglets (P = 0.010)

were higher in sows than in gilts (Table 1). Numbers of mummified piglets tended to be higher in

sow litters than in gilt litters (P = 0.062), and were higher in litters from dams treated with pST

from d 25 to 50 of pregnancy (P = 0.014) than controls, and not altered in litters from dams that

were treated with pST from d 25 to 100 of pregnancy (P = 0.146). Total piglet numbers were

lower in litters from dams treated with pST from d 25 to 100 than in controls (P = 0.038), and

were not reduced in litters from dams treated with pST from d 25 to 50 of pregnancy (P = 0.166).

Numbers of still born piglets tended to be increased in litters from dams treated with pST from d

25 to 50 compared to controls (P = 0.079) and were not altered in litters from dams treated with

pST from d 25 to 100 of pregnancy (P > 0.9). Consequently, the numbers of live born piglets in

each litter were reduced by ~0.6 piglets/litter following pST treatment either from d 25 to 50 of

pregnancy (P = 0.018) or from d 25 to 100 of pregnancy (P = 0.024), compared to control litters

(Table 1).

Average piglet birth weight (Table 1) was higher in sows than in gilts (P ≤ 0.001) and

was increased by maternal pST treatment to a greater extent in sows than gilts (treatment x



11

parity, P = 0.051). In gilts, maternal treatment affected average birth weight (P = 0.029), such

that average piglet birth weight was increased in litters from dams treated with pST from d 25 to

100 of pregnancy (P = 0.008), but not in litters from dams treated with pST from d 25 to 50 of

pregnancy (P = 0.114). Similarly in sows, maternal treatment affected average piglet birth weight

(P ≤ 0.001), with increased birth weight in progeny of dams treated with pST from d 25 to 100 of

pregnancy (P ≤ 0.001), but not in litters from sows treated with pST from d 25 to 50 (P = 0.147).

When corrected for litter size, average piglet birth weight was higher in sows than gilts (P ≤

0.001), and effects of maternal treatment differed between parities (treatment x parity, P = 0.01,

Table 1). Effects of treatment on progeny birth weight was therefore analysed separately for

sows and gilts, using the average litter sizes for each parity. In gilts, birth weight corrected for an

average gilt litter size of 12.02 piglets was altered by maternal treatment (P = 0.039), such that

average piglet birth weight was increased in litters from gilts treated with pST from d 25 to 100

of pregnancy (P = 0.014, 1.49 ± 0.02 kg) and tended to be increased in litters from gilts treated

with pST from d 25 to 50 of pregnancy (P = 0.071, 1.47 ± 0.02 kg), relative to control litters

(1.42 ± 0.02 kg). In sows, birth weight corrected for an average sow litter size of 13.03 piglets

was also altered by maternal treatment (P ≤ 0.001), such that average piglet birth weight was

increased in litters from sows treated with pST from d 25 to 100 of pregnancy (P ≤ 0.001, 1.72 ±

0.02 kg), but not increased in litters from sows treated with pST from d 25 to 50 of pregnancy (P

> 0.5, 1.59 ± 0.02 kg), relative to control litters (1.57 ± 0.02 kg).

Lactation Feed Intake, Litter Survival and Growth

Lactation duration was shorter in sows than in gilts (P ≤ 0.001; sows: 25.9 ± 0.1 d; gilts:

27.4 ± 0.1 d) due to differences in mating date between parities, and a common weaning date for



12

each replicate week. Gilts were ~ 1.8 d further advanced in gestation on entry to the farrowing

house than sows. Lactation lengths were similar between treatments in gilts (P > 0.27). Due to

the shorter gestation length in sows treated with pST from d 25 to 100, this group had longer

lactations than control sows (P ≤ 0.001), while lactation lengths of sows treated with pST from d

25 to 50 were not different from controls (P > 0.7). Litter size after fostering was higher in sows

than gilts (P ≤ 0.001) and did not differ between treatments (Table 2). Average litter size after

fostering in gilts was greater than the target of 10 piglets as insufficient dams were available to

reduce litter size to 10 in all gilt litters. Litter sizes remained higher in sows than gilts throughout

lactation, and the numbers of piglets that were removed or died between fostering on day 1 and

weaning did not differ between maternal treatments (P > 0.5, Table 2), while effects of parity

varied between replicate week (P = 0.041), and there was no effect of parity overall (P = 0.109).

Piglet losses (deaths and removals) during lactation were negatively correlated with average

piglet weight after fostering, overall (R = -0.277, P ≤ 0.001, n = 506), and within each parity (P

≤ 0.001 for each).

Sows ate more feed each day than gilts throughout lactation (P ≤ 0.001), feed intake

varied between replicate week (P ≤ 0.001), and effects of maternal treatments on feed intake

differed between parities (treatment x parity, P = 0.012; Table 2). Daily feed intakes during

lactation tended to differ between treatments in sows (P = 0.064) and differed between replicate

week (P ≤ 0.001), tending to be lower in sows that were treated with pST from d 25 to 50 of

pregnancy than in controls (P = 0.090), but not differing between sows treated with pST from d

25 to 100 and controls (P > 0.5). In gilts, daily feed intakes during lactation varied with

treatment (P ≤ 0.001), such that lactation feed intake was increased in gilts treated with pST from

d 25 to 100 of pregnancy (P = 0.001) or from d 25 to 50 of pregnancy (P = 0.021), relative to



13

control gilts (Table 2), and varied with replicate week (P ≤ 0.001). Total litter weight gain from

fostering to weaning (Table 2) was higher in sows than in gilts (P ≤ 0.001), varied between

replicate week (P ≤ 0.001), and effects of maternal treatment differed between parities (P =

0.022). Total litter weight gain did not differ between maternal treatments in gilts (P > 0.3), but

was affected by treatment in sows (P = 0.014). Effects of treatment on litter weight gain over

lactation reflected mostly differences between the 2 groups of pST-treated sows, as total litter

weight gain over lactation was lower in sows treated with pST from d 25 to 50 of pregnancy,

compared to litters of sows treated with pST from d 25 to 100 of pregnancy (P = 0.015). Relative

to control sows, total litter weight gain over lactation tended to be less in sows that were treated

with pST from d 25 to 50 (P = 0.085) and was not different in sows treated with pST from d 25

to 100 (P = 0.217; Table 2).

Average piglet weights after fostering (Figure 3) were increased in litters from dams

treated with pST from d 25 to 50 of pregnancy (P = 0.011), and in litters from dams treated with

pST from d 25 to 100 of pregnancy (P ≤ 0.001), were higher in litters from sows than in those

from gilts (P ≤ 0.001), and did not vary with replicate week of the study (P = 0.194). Average

piglet weights at d 14 of lactation (Figure 3) were increased following maternal pST treatment

from d 25 to 100 of pregnancy (P = 0.037), and were not increased following maternal pST

treatment from d 25 to 50 of pregnancy (P > 0.5), were higher in sow than gilt progeny (P ≤

0.001), and varied with replicate week of the study (P = 0.009). Average piglet weights at

weaning (Figure 3) were increased following maternal pST treatment from d 25 to 100 of

pregnancy (P = 0.017), but were not increased following maternal pST treatment from d 25 to 50

of pregnancy (P > 0.8). Average piglet weights at weaning were also higher in sow progeny than

gilt progeny (P ≤ 0.001), and varied between replicate week (P ≤ 0.001). Piglet growth rates



14

from fostering to d 14 of lactation and from d 14 of lactation to weaning (Table 2) were faster in

sow litters than in gilt litters (P ≤ 0.001 for each period), and were not affected by maternal

treatments (P > 0.4 for each period), and varied between replicate week of the study (P ≤ 0.05

for each period). Piglet growth rates over the whole lactation, from fostering to weaning, were

higher in sow than in gilt litters (P ≤ 0.001), varied between replicate week of the study (P ≤

0.001), and effects of maternal treatment differed between parities (P = 0.048). In gilt litters,

piglet lactation growth rates were not affected by maternal treatment (P > 0.4). In sow litters,

piglet lactation growth rates were reduced in litters from sows treated with pST from d 25 to 50

(P = 0.018), but not changed in litters from sows treated with pST from d 25 to 100 of pregnancy

(P > 0.3), compared to control litters (Table 2).

Maternal Removals during Treatment Pregnancy and Subsequent Lactation

The numbers of dams removed between the commencement of the study and entry to the

farrowing house (d 25 to 109), or from late pregnancy through lactation to weaning (d 109 of

pregnancy to weaning), were not different between parities, nor between maternal treatment

groups overall (Table 3). From commencement of treatments until entry to the farrowing house,

however, removal numbers of gilts differed between treatments (P = 0.024), such that 12% of

gilts treated with pST from d 25 to d 100 of pregnancy were removed before entry to the

farrowing house, compared to a 5% removal rate in controls (P = 0.062). While these removals

reflected a variety of causes (including 4 d 25 to 100 pST-treated gilts not transferred to the

farrowing house for unknown reasons), it is important to note that there were no differences in

rates of pregnancy loss between treatments, and similar numbers of gilts in each treatment were

culled for physical causes (2 control, 1 d 25 to 50 pST, 3 d 25 to 100 pST). Maternal parity and



15

treatments did not affect total dam removals during farrowing and lactation (Table 3). Rates of

farrowing difficulties and lactation failure also did not differ between groups, despite differences

in piglet size and lactational demand (Table 3).

Subsequent Maternal Reproductive Performance

A total of 500 dams remained on the trial at weaning from the lactation immediately

following the treatment pregnancy (242 gilts and 258 sows). Removals of dams between

weaning and the subsequent mating were higher in sows than gilts (P ≤ 0.001), were not affected

by maternal treatment in gilts (P=0.99) and varied with maternal treatment in sows (P = 0.037;

Table 4). In sows, removals before the subsequent mating were highest in sows treated with pST

from d 25 to 100 of the preceding pregnancy (Table 4). The majority of the 18 sows culled

before mating in this group were removed either due to foot and leg problems (9 of 18) or due to

poor body condition at weaning (6 of 18). Sows that were removed from the herd before re-

mating (33 of 258 weaned) were thinner (P = 0.001) at d 25 of pregnancy before commencing

treatment, were thinner (P = 0.003) and tended to be lighter (P = 0.068) on the day after

farrowing, lost more weight (P = 0.003) and backfat depth (P = 0.023) during lactation, weaned

heavier litters (P = 0.024) with a greater litter weight gain during lactation (P = 0.008), and ate

less during lactation (P = 0.005) compared to the sows that remained in the herd and were

remated following the treatment pregnancy and lactation.

A total of 456 dams were mated at the first post-weaning estrus. Weaning-remating

interval did not differ between sows and gilts from the treatment pregnancy (P = 0.135), nor

between maternal treatment groups in the treatment pregnancy (P = 0.535). The proportion of

dams that farrowed following this subsequent mating, tended to be higher in gilts than sows (P =



16

0.069, gilts: 80.7%, sows: 73.6%), largely due to parity differences in conception rates (Table 4).

Treatment in the previous pregnancy did not affect subsequent litter size (P > 0.16 for all

measures). The numbers of total born (12.0 ± 0.2), live born (11.0 ± 0.2) and mummified (0.20 ±

0.03) piglets were similar in dams that were gilts or sows during the previous (treatment)

pregnancy (P > 0.1 for each). Parity did affect the numbers of stillborn piglets, which were

greater in the higher parity sows (gilts at previous pregnancy: 0.8 ± 0.1, sows at previous

pregnancy: 1.2 ± 0.1, P = 0.024).

DISCUSSION

Sustained maternal pST treatment, from d 25 to 100 of pregnancy, increased average

progeny birth weight in both parities, with the magnitude of the response around 2-fold greater in

sow litters (+180 g, 11.6%) than in gilt litters (+80 g, 5.6%). Thus, maternal factors associated

with adolescent and primiparous (gilt) pregnancies may limit the responses that underlie pST-

induced increases in fetal growth. Our results are consistent with maternal somatotropin acting as

a “driver” of fetal growth, including previous reports of decreased maternal somatotropin in

human pregnancies with poor fetal growth (Mirlesse et al., 1993; Chowden et al., 1996).

Potential mechanisms for effects of pST on fetal growth include mobilization of maternal

nutrient reserves for fetal growth, which could be limited in gilts who are themselves growing. In

early, mid, or late gestation, maternal treatment with pST at doses at least 2-fold higher than

those used in the present study increased or tended to increase maternal plasma glucose and

insulin concentrations (Kveragas et al., 1986; Schneider et al., 2002; Gatford et al., 2003).

Increased maternal plasma glucose drives increased fetal growth, as seen in infants of mothers



17

with diabetes during pregnancy (Cardell, 1953). In castrate male pigs, daily somatotropin

injections reduced whole-body insulin sensitivity within a day of the initial injection (Kerber et

al., 1998). Whether elevated somatotropin decreases insulin sensitivity similarly in pregnant

sows and gilts, and hence increases glucose transport across the placenta and fetal growth, has

not been evaluated. An increased plasma insulin:glucose ratio as well as increased plasma insulin

and glucose concentrations occurred in gilts treated with pST doses 2 and 4 times higher than

those of the present study (Gatford et al., 2003), providing indirect evidence of insulin resistance

in pST-treated gilts. We have also reported increased fetal plasma glucose at d 50 in fetuses

from gilts treated from d 25 to 50 with pST doses similar to the present study, although pST did

not affect maternal plasma insulin or glucose concentrations in that small study (Gatford et al.,

2000). Increased allantoic and amniotic glucose concentrations have been reported at d 28 in

gilts treated with pST from d 10 to 27 of pregnancy, also consistent with increased glucose

transport to the fetus (Rehfeldt et al., 2001). Placental growth and function may also be increased

directly or indirectly by maternal pST, given that the porcine placenta expresses receptors for

pST as well as for IGF-I (Chastant et al., 1994; Sterle et al., 1998). Furthermore, circulating

levels of IGF-I increase in pST-treated pigs, with increased expression of IGF-I in maternal liver

at the end of pST treatment, no immediate change in IGF-I expression in reproductive tissues,

but increased placental IGF-I expression at d 62 of gestation in gilts treated with pST from d 10

to 27 of pregnancy (Sterle et al., 1995; Sterle et al., 1998; Freese et al., 2005). Maternal pST

administration increased placental growth in gilts at d 44 of gestation in one study (Sterle et al.,

1995), although not in gilts or sows at d 50 of gestation in a more recent study (Gatford et al.,

2009). We hypothesize that pST increases placental growth to a greater extent in the second half

of gestation, and that the smaller uterine size of gilts may limit their capacity for pST-induced



18

increases in placental growth and hence capacity to increase placental exchange area for nutrient

transfer. Effects of pST on placental function have not been directly measured in pigs, although

fetal plasma glucose was increased after 25 d of maternal pST treatment in gilts, indicative of

increased placental function (Gatford et al., 2000). Maternal somatotropin treatment increases

placental nutrient transfer in sheep (Harding et al., 1997), and increased function as well as size

may contribute to pST-induced increases in fetal growth. Similarly, maternal IGF-I treatment

increases placental nutrient transport to the fetus during treatment in early-mid pregnancy as well

as at term (Sferruzzi-Perri et al., 2006; Sferruzzi-Perri et al., 2007), which may indicate that pST

improves placental function at least partially via increasing maternal circulating IGF-I

concentrations.

In the present study, birth weight was only increased following the long-term maternal

treatment with pST, although we know that 25 d of maternal pST treatment increases fetal

growth at the end of treatment at d 50 in both parities (Gatford et al., 2009). This lack of increase

in sow and gilt progeny birth weights when pST treatment is discontinued at d 50 of pregnancy is

consistent with our previous study in gilts (Gatford et al., 2004), and indicates that effects of

pST, for example on placental development, do not persist sufficiently to maintain heavier

fetuses once the elevated pST is withdrawn. In sows, but not gilts, sustained maternal pST

treatment also decreased gestation length, possibly due to greater stimulus of maternal

endometrial stretch receptors by large piglets combined with the larger litter sizes of sows than

gilts. Similarly, in low risk human pregnancies, gestation length is longer in small than large

fetuses (Johnsen et al., 2008). This earlier farrowing increased lactation length in these sows, as

all pigs are weaned on a single day under commercial management in this piggery, which uses an

“all-in, all-out” system to minimize disease transmission. Sows treated with pST from d 25 to



19

100 of pregnancy were able to maintain similar growth rates in suckling progeny throughout this

longer lactation and with heavier litters, compared to control dams.

Maternal pST treatment in early-mid pregnancy decreased litter size, whether or not

treatment was continued to d 100 of pregnancy. Numbers of mummified piglets were increased

(0.16 piglets/litter) following pST treatment between d 25 and 50 of pregnancy, thus withdrawal

of treatment may induce fetal loss in late pregnancy. This effect did not account for the total

decrease in live-born piglets, however, and given that still birth numbers did not increase, any

loss of fetuses in pST-treated dams must have been early in the treatment period, with

subsequent resorption of these conceptuses. This result contrasts with previous studies

suggesting that maternal pST increases embryo survival in early-mid gestation in the pig (Kelley

et al., 1995). Treatment with pST at doses ~2-fold of those of the present study from d 30 to 43

of pregnancy progressively decreased maternal plasma progesterone during treatment (Yuan et

al., 1996), and this might contribute to embryo losses in early pregnancy if it also occurs at these

lower pST doses. Pregnancy failures (numbers either NIP at pregnancy check, abortions, or

returning to estrus) were not increased in pST-treated gilts or sows, however, indicating that any

effects on fetal survival do not act on the litter as a whole.

Differences in piglet weights between groups increased during lactation, so that progeny

from dams treated with pST from d 25 to 100 of pregnancy were an average of ~110 g heavier at

birth and ~300 g heavier at weaning than progeny of control dams. Piglet growth rates during

lactation did not differ between maternal treatments and the overall increase in treatment effect

on piglet weight at weaning compared to birth could be explained by the shorter gestation

lengths in sows given long-term pST treatment which, combined with weaning on a single day,

increased lactation lengths by nearly a day in this group, so that piglets in this group were older



20

and heavier at weaning. Effects of maternal pST treatment on weight at weaning appear to

primarily reflect the increased birth weight of these piglets, with little direct effect on maternal

drivers of lactation.

Maternal treatment with pST for 25 or 75 days of pregnancy did not affect rates of

pregnancy loss or cull rates of dams during farrowing or lactation, despite heavier piglets and

increased demand for milk. Nevertheless, long-term pST treatment increased the numbers of

sows culled after weaning of the litter from the treatment pregnancy, mostly due to foot and leg

problems or poor condition. Interestingly, long-term maternal pST in gilts did not increase post-

weaning cull rates, although maternal pST increased dam weight at farrowing and decreased dam

P2 backfat at weaning similarly in sows and gilts. Given that pST increases bone growth and

density, particularly in adolescents (Mukherjee et al., 2004), we hypothesize that treating gilts

with pST during a period of rapid bone growth may have increased bone density and strength,

preventing foot and leg problems induced by increased maternal weight. Treatment with pST

stimulates bone resorption and bone formation, and,, in adult humans, results in a biphasic effect

on bone mass, with an initial decrease in bone mass due to increased bone resorption followed by

increasing density as bone formation increases (Ohlsson et al., 1998). Thus, it is possible that in

the adult pig, bone density may have been adversely affected by treatment with pST for 75 d and

contributed to increased cull rates in sows. Maternal lactation food intake was increased by

sustained gestation pST treatment in gilts, and not altered in sows, which might explain why gilts

in this treatment did not have increased cull rates for poor condition at weaning. This may mean,

however, that sustained pST treatment at ~15 g.kg-1.d-1 does not adversely affect gut health.

Indeed, the doses at which gastric ulceration is reported to occur in lactating sows are 2 or 4

times the dose of the present study (Smith et al., 1991). Sows that were culled post-weaning had



21

lower fat reserves before mating, weaned heavier litters and ate less during lactation. This

indicates that culling may remove highly productive sows from the herd, and retention of sows in

poor condition to regain condition before mating should be considered. Maintaining high

lactation feed intake or adopting a management system such as skip-a-heat mating (Clowes et al.,

1994) to allow the sow to regain body condition may be necessary to avoid possible adverse

effects of maternal pST on sow retention. In those dams that were mated after weaning, neither

parity nor pST treatment affected weaning-remating interval, conception rates or subsequent

litter size, confirming that these treatments did not adversely affect subsequent reproduction in a

pregnancy without further administration of pST.

Our results show that long-term maternal pST treatment during pregnancy increased birth

weight in gilts and sows, with the responses ~2-fold greater in the latter. Similar to previous

studies in gilts, pST treatment in early-mid pregnancy only did not increase progeny size at birth.

Strategies to increase lactation feed intake and/or managing the sow differently after weaning

may improve progeny growth in lactation and prevent adverse effects on post-weaning cull rates

in sows. We are now investigating whether long-term pST treatment can also increase post-

weaning progeny growth and performance to a greater extent in sows than gilts.

IMPLICATIONS

In the present study, long-term maternal somatotropin treatment increased progeny birth and

weaning weights to a greater extent in sows than in gilts. These benefits of maternal

somatotropin treatment from d 25 to 100 of gestation were partially offset by a 0.6 piglet

reduction in numbers of live born piglets and 12% increase in sow, but not gilt, cull rates after



22

weaning. Strategies to increase maternal bone strength and reduce maternal weight loss during

lactation are needed to avoid increased cull rates of multiparous sows treated with somatotropin

during the previous pregnancy. The average increases of 7.3% in birth weight (corrected for litter

size) and 4.2% in weaning weight in dams treated with somatotropin for 75 d from early to late

pregnancy are likely to improve subsequent growth rates and performance of progeny. These are

currently being evaluated.

LITERATURE CITED

Campbell, R. G., and A. C. Dunkin. 1982. The effect of birth weight on the estimated milk

intake, growth and body composition of sow-reared piglets. Anim. Prod. 35: 193-197.

Cardell, B. S. 1953. The infants of diabetic mothers: a morphological study. J. Obstet. Gynaecol.

Brit Empire 60: 834-853.

Chastant, S., P. Monget, and M. Terqui. 1994. Localization and quantification of insulin-like

growth factor-I (IGF-I) and IGF-II/mannose-6-phosphate (IGF-II/M6P) receptors in pig

embryos during early pregnancy. Biol. Reprod. 51: 588-596.

Chowden, J. A., D. Evain-Brion, J. Pozo, E. Alsat, L. M. Garcia-Segura, and J. Argente. 1996.

Decreased expression of placental growth hormone in intrauterine growth retardation.

Pediatr. Res. 39: 736-739.

Clowes, E. J., F. X. Aherne, and G. R. Foxcroft. 1994. Effect of delayed breeding on the

endocrinology and fecundity of sows. J. Anim. Sci. 72: 283-291.

Dwyer, C. M., J. M. Fletcher, and N. C. Stickland. 1993. Muscle cellularity and postnatal growth

in the pig. J. Anim. Sci. 71: 3339-3343.



23

Fahmy, M. H., and C. Bernard. 1971. Causes of mortality in Yorkshire pigs from birth to 20

weeks of age. Can. J. Anim. Sci. 51: 351-359.

Freese, L. G., C. Rehfeldt, R. Fuerbass, G. Kuhn, C. S. Okamura, K. Ender, A. L. Grant, and D.

E. Gerrard. 2005. Exogenous somatotropin alters IGF axis in porcine endometrium and

placenta. Domest. Anim. Endocrinol. 29: 457-475.

Gatford, K. L., J. M. Boyce, K. Blackmore, R. J. Smits, R. G. Campbell, and P. C. Owens. 2004.

Long-term, but not short-term, treatment with somatotropin during pregnancy in underfed

pigs increases the body size of progeny at birth. J. Anim. Sci. 82: 93-101.

Gatford, K. L., M. J. De Blasio, C. T. Roberts, M. B. Nottle, K. L. Kind, W. H. Wettere, R. J.

Smits, and J. A. Owens. 2009. Responses to maternal growth hormone or ractopamine

during early-mid pregnancy are similar in primiparous and multiparous pregnant pigs. J.

Endocrinol. 203: 143-154.

Gatford, K. L., J. E. Ekert, K. Blackmore, M. J. De Blasio, J. M. Boyce, J. A. Owens, R. G.

Campbell, and P. C. Owens. 2003. Variable maternal nutrition and growth hormone

treatment in the second quarter of pregnancy in pigs alter semitendinosus muscle in

adolescent progeny. Br. J. Nutr. 90: 283-293.

Gatford, K. L., J. A. Owens, R. G. Campbell, J. M. Boyce, P. A. Grant, M. J. De Blasio, and P.

C. Owens. 2000. Treatment of underfed pigs with GH throughout the second quarter of

pregnancy increases fetal growth. J. Endocrinol. 166: 227-234.

Gondret, F., L. Lefaucheur, I. Louveau, B. Lebret, X. Pichodo, and Y. Le Cozler. 2005.

Influence of piglet birth weight on postnatal growth performance, tissue lipogenic

capacity and muscle histological traits at market weight. Livestock Prod. Sci. 93: 137-

146.



24

Harding, J. E., P. C. Evans, and P. D. Gluckman. 1997. Maternal growth hormone treatment

increases placental diffusion capacity but not fetal or placental growth in sheep.

Endocrinology 138: 5352-5358.

Johnsen, S. L., T. Wilsgaard, S. Rasmussen, M. A. Hanson, K. M. Godfrey, and T. Kiserud.

2008. Fetal size in the second trimester is associated with the duration of pregnancy,

small fetuses having longer pregnancies. BMC Pregnancy and Childbirth 8: 25

doi:10.1186/1471-2393-1188-1125.

Kelley, R. L., S. B. Jungst, T. E. Spencer, W. F. Owsley, C. H. Rahe, and D. R. Mulvaney. 1995.

Maternal treatment with growth hormone alters embryonic development and early

postnatal growth of pigs. Domest. Anim. Endocrinol. 12: 83-94.

Kerber, J. A., D. Wray-Cahen, R. D. Boyd, and D. E. Bauman. 1998. Decreased Glucose

Response to Insulin is Maximal Within 24 Hours of Somatotropin Injection in Growing

Pigs. Domest. Anim. Endocrinol. 15: 267-270.

King, R. H., B. P. Mullan, F. R. Dunshea, and H. Dove. 1997. The influence of piglet body

weight on milk production of sows. Livestock Prod. Sci. 47: 169-174.

Kveragas, C. L., R. W. Seerley, R. J. Martin, and W. L. Vandergrift. 1986. Influence of

exogenous growth hormone and gestational diet on sow blood and milk characteristics

and on baby pig blood, body composition and performance. J. Anim. Sci. 63: 1877-1887.

Mirlesse, V., F. Frankenne, E. Alsat, M. Poncelet, G. Hennen, and D. Evain-Brion. 1993.

Placental growth hormone levels in normal pregnancy and in pregnancies with

intrauterine growth retardation. Pediatr. Res. 34: 439-442.

Mukherjee, A., R. D. Murray, and S. M. Shalet. 2004. Impact of growth hormone status on body

composition and the skeleton. Horm. Res. 62 Suppl. 3: 35-41.



25

National Health and Medical Research Council of Australia. 2004. Australian code of practice

for the care and use of animals for scientific purposes, 7th edition. 7 ed. Australian

Government Publishing Service, Canberra.

Ohlsson, C., B.-A. Bengtsson, O. G. P. Isaksson, T. T. Andreassen, and M. C. Slootweg. 1998.

Growth Hormone and Bone. Endocr. Rev. 19: 55-79.

Rehfeldt, C., and G. Kuhn. 2006. Consequences of birth weight for postnatal growth

performance and carcass quality in pigs as related to myogenesis. J. Anim. Sci. 84 (E

suppl.): E113-E123.

Rehfeldt, C., G. Kuhn, G. Nürnberg, E. Kanitz, F. Schneider, M. Beyer, K. Nürnberg, and K.

Ender. 2001. Effects of exogenous somatotropin during early gestation on maternal

performance, fetal growth, and compositional traits in pigs. J. Anim. Sci. 79: 1789-1799.

Roehe, R., and E. Kalm. 2000. Estimation of genetic and environmental risk factors associated

with pre-weaning mortality in piglets using generalized linear mixed models. Anim. Sci.

70: 227-240.

Schneider, F., E. Kanitz, D. E. Gerrard, G. Kuhn, K. P. Brüssow, K. Nürnberg, I. Fiedler, G.

Nürnberg, K. Ender, and C. Rehfeldt. 2002. Administration of recombinant porcine

somatotropin (rpST) changes hormone and metabolic status during early pregnancy.

Domest. Anim. Endocrinol. 23: 455-474.

Sferruzzi-Perri, A. N., J. A. Owens, K. G. Pringle, J. S. Robinson, and C. T. Roberts. 2006.

Maternal Insulin-Like Growth Factors-I and -II Act via Different Pathways to Promote

Fetal Growth. Endocrinology 147: 3344-3355.



26

Sferruzzi-Perri, A. N., J. A. Owens, P. Standen, R. L. Taylor, G. K. Heinemann, J. S. Robinson,

and C. T. Roberts. 2007. Early treatment of the pregnant guinea pig with IGFs promotes

placental transport and nutrient partitioning near term. Am. J. Physiol. 292: E668-E676.

Smith, V. G., A. D. Leman, W. J. Seaman, and F. VanRavenswaay. 1991. Pig weaning weight

and changes in hematology and blood chemistry of sows injected with recombinant

porcine somatotropin during lactation. J. Anim. Sci. 69: 3501-3510.

Sterle, J. A., C. K. Boyd, J. T. Peacock, A. T. Koenigsfeld, W. B. Lamberson, D. E. Gerrard, and

M. C. Lucy. 1998. Insulin-like growth factor (IGF)-I, IGF-II, IGF-binding protein-2 and

pregnancy-associated glycoprotein mRNA in pigs with somatotropin-enhanced fetal

growth. J. Endocrinol. 159: 441-450.

Sterle, J. A., T. C. Cantley, W. B. Lamberson, M. C. Lucy, D. E. Gerrard, R. L. Matteri, and B.

N. Day. 1995. Effects of recombinant porcine growth hormone on placental size, fetal

growth, and IGF-I and IGF-II concentrations in pigs. J. Anim. Sci. 73: 2980-2985.

van der Lende, T., and D. de Jager. 1991. Death risk and preweaning growth of piglets in relation

to the within-litter weight distribution at birth. Livestock Production Science 28: 73-84.

Wigmore, P. M. C., and N. C. Stickland. 1983. Muscle development in large and small pig

fetuses. J. Anat. 137: 235-245.

Yuan, W., J. A. Sterle, T. C. Cantley, W. R. Lamberson, B. N. Day, and M. C. Lucy. 1996.

Responses of porcine corpora lutea to somatotropin administration during pregnancy. J.

Anim. Sci. 74: 873-878.



27

Table 1 – Effects of maternal treatment and parity on treatment pregnancy outcomes1

Outcome Gilts Sows Significance

Control Short-term

pST

Long-term

pST

Control Short-term

pST

Long-term

pST

Treatment Parity Treatment

*parity

Gestation length, d 116.4 ± 0.1 116.4 ± 0.1 116.1 ± 0.1 116.3 ± 0.1 116.4 ± 0.1 115.5 ± 0.1 ≤0.001 0.016 0.0332

Litter size at birth

No of litters 114 116 107 114 109 113

Total piglets 12.1 ± 0.2 12.1 ± 0.2 11.7 ± 0.3 13.5 ± 0.3 12.7 ± 0.3 12.8 ± 0.3 0.107 ≤0.001 0.433

Live born piglets 11.5 ± 0.2 11.3 ± 0.3 11.0 ± 0.3 12.7 ± 0.3 11.6 ± 0.3 12.0 ± 0.3 0.028 ≤0.001 0.247

Still born piglets 0.7 ± 0.1 0.9 ± 0.2 0.7 ± 0.1 1.0 ± 0.1 1.2 ± 0.2 0.9 ± 0.1 0.136 0.010 0.826

Mummies 0.11 ± 0.03 0.32 ± 0.09 0.28 ± 0.06 0.29 ± 0.05 0.41 ± 0.08 0.32 ± 0.07 0.048 0.062 0.589

Progeny size at birth

Average birth weight, kg 1.42 ± 0.02 1.47 ± 0.02 1.50 ± 0.03 1.55 ± 0.02 1.60 ± 0.02 1.73 ± 0.02 ≤0.001 ≤0.001 0.0513

Average birth weight, kg 4 1.40 ± 0.02 1.45 ± 0.02 1.47 ± 0.02 1.59 ± 0.02 1.61 ± 0.02 1.75 ± 0.02 ≤0.001 ≤0.001 0.0105

1 Landrace x Large White gilts and sows (parities 2 and 3 at mating) were uninjected (controls), or injected daily with pST (gilts: 2.5 mg.d-1, sows: 4.0 mg.d-1, each ~15 g pST.kg-1.d-1) from d 25 to 50 of pregnancy (short-term pST) or from d 25 to 100 of pregnancy (long-term pST). Litter size and piglet weights were recorded within 24 h of birth. 2 Gestation length was unaffected by maternal treatment in gilts (P = 0.260), and varied between treatments in sows (P ≤ 0.001). In sows, gestation length was reduced following pST treatment from d 25 to 100 (P ≤ 0.001), but not following pST treatment from d 25 to 50 (P = 1.0), compared to controls. 3 Average birth weight was altered by maternal treatment in gilts (P = 0.029) and in sows (P ≤ 0.001). Maternal pST treatment from d 25 to 100 of pregnancy increased average birth weight relative to control litters, in gilts (P = 0.008) and in sows (P ≤ 0.001), and maternal pST treatment from d 25 to 50 of pregnancy did not increase average birth weight in either parity (P > 0.1 for each). 4 Corrected to an average total litter size of 12.53 piglets overall and within each parity (gilts: 12.02 piglets born, sows: 13.03 piglets born) for analyses of the treatment *parity interaction. 5 Average birth weight, corrected for litter size, was altered by maternal treatment in gilts (P = 0.039) and in sows (P ≤ 0.001). Maternal pST treatment from d 25 to 100 of pregnancy increased corrected average birth weight relative to control litters, in gilts (P = 0.014) and in sows (P ≤ 0.001), and maternal pST treatment from d 25 to 50 of pregnancy tended to increase corrected average birth weight relative to control litters in gilts (P = 0.071), but not in sows (P = 0.501).

by guest on May 18, 2011

jas.fass.orgD

ownloaded from


28

Table 2 – Effects of maternal treatment and parity on lactation outcomes6

Outcome Gilts Sows Significance Control Short-term

pST Long-term

pST Control Short-term

pST Long-term

pST Treatment Parity Treatment

*parity Litter size After fostering 10.4 ± 0.1 10.4 ± 0.1 10.4 ± 0.1 11.9 ± 0.2 12.0 ± 0.2 12.0 ± 0.1 0.734 ≤0.001 0.846 Day 14 of lactation 8.2 ± 0.2 8.3 ± 0.2 8.3 ± 0.4 10.0 ± 0.2 9.9 ± 0.2 10.2 ± 0.2 0.508 ≤0.001 0.711 Weaning 7.4 ± 0.2 7.7 ± 0.2 7.5 ± 0.2 9.3 ± 0.2 9.3 ± 0.2 9.8 ± 0.2 0.418 ≤0.001 0.162 Lactation piglet losses 3.0 ± 0.2 2.8 ± 0.2 2.9 ± 0.2 2.7 ± 0.2 2.7 ± 0.2 2.3 ± 0.2 0.524 0.109 0.302 Maternal feed intake Fostering – weaning, kg.d-

1 6.34 ± 0.08 6.57 ± 0.11 6.79 ± 0.08 7.51 ± 0.11 7.33 ± 0.12 7.57 ± 0.09 0.001 ≤0.001 0.0127

Total litter lactation weight gain Fostering – weaning, kg 34.5 ± 1.8 37.9 ± 2.0 36.1 ± 1.7 51.2 ± 1.6 47.5 ± 1.8 54.4 ± 1.7 0.265 ≤0.001 0.0228 Piglet growth rates Fostering - day 14, g.d-1 154 ± 6 165 ± 7 161 ± 7 214 ± 5 202 ± 5 211 ± 6 0.818 ≤0.001 0.085 Day 14 – weaning, g.d-1 235 ± 7 240 ± 6 245 ± 9 267 ± 6 249 ± 8 259 ± 7 0.480 0.001 0.199 Overall, g.d-1 196 ± 4 202 ± 5 202 ± 5 238 ± 4 224 ± 5 233 ± 5 0.488 ≤0.001 0.0489

6 Landrace x Large White gilts and sows (parities 2 and 3 at mating) were uninjected (controls), or injected daily with pST (gilts: 2.5 mg.d-1, sows: 4.0 mg.d-1, each ~15 g pST.kg-1.d-1) from d 25 to 50 of pregnancy (short-term pST) or from d 25 to 100 of pregnancy (long-term pST). Fostering was performed on the day of birth to achieve litter sizes at the start of lactation of 10 piglets (where possible) on first-lactation sows, and 12 piglets on older lactating sows. Lactating pigs were fed three times daily to appetite and feed offered was recorded daily. Litter size and piglet weights were recorded after completion of fostering, on the day of birth, and on d 14 of lactation and prior to weaning. 7 Daily feed intakes during lactation were affected by treatment in gilts (P ≤ 0.001), with a similar trend in sows (P = 0.064). In gilts, lactation feed intake was increased in dams treated with pST from d 25 to 100 of pregnancy (P ≤ 0.001), and in dams treated with pST from d 25 to 50 of pregnancy (P = 0.021), relative to control gilts. In sows, lactation feed intake was not different in dams treated with pST from d 25 to 100 of pregnancy (P > 0.5), and tended to be decreased in dams treated with pST from d 25 to 50 of pregnancy (P = 0.090), relative to control sows. 8 Litter weight gain throughout lactation was not affected by maternal treatments in gilts (P = 0.338), but was affected by maternal treatment in sows (P = 0.014). Litter weight gain throughout lactation was not different in sows treated with pST from d 25 to 100 of pregnancy (P = 0.217), but tended to be decreased in sows treated with pST from d 25 to 100 of pregnancy (P = 0.085), relative to litters of control sows. 9 Average piglet growth rate from fostering to weaning was not affected by maternal treatments in gilts (P = 0.436), but tended to be affected by maternal treatment in sows (P = 0.060). Average piglet growth rate from fostering to weaning was not different in sows treated with pST from d 25 to 100 of pregnancy (P = 0.309), but was decreased in sows treated with pST from d 25 to 100 of pregnancy (P = 0.018), relative to litters of control sows.


jas.fass.orgD

ownloaded from


29

Table 3 – Maternal removals from trial during treatment pregnancy and lactation10

Outcome Gilts Sows Significance (2) Control Short-

term pST Long-

term pST Control Short-

term pST Long-

term pST Treatment Parity

Dam numbers remaining on-trial at: Start of trial (d 25 of pregnancy) 120 120 120 120 120 120 Entry to farrowing house (d 109 of pregnancy)

114 116 106 116 112 115

Weaning (d 27 of lactation) 83 84 75 89 85 84 Dam removals from trial between: d 25 – 109 of pregnancy Pregnancy loss Total

1 6

2 4

2 14

4 4

3 8

4 5

0.938

0.17711

0.129 0.260

d 109 of pregnancy - weaning Farrowing-related Lactation failure Other Total (replicates 1 to 10) Dams in replicates 11 & 1212

2 3 6 11 20

0 4 8 12 20

1 2 8 11 20

2 0 5 7 20

1 2 6 9 18

1 2 8 11 20

0.364 0.578

0.418

0.704 0.162

0.178

10 Landrace x Large White gilts and sows (parities 2 and 3 at mating) were uninjected (controls), or injected daily with pST (gilts: 2.5 mg.d-1, sows: 4.0 mg.d-1, each ~15 g pST.kg-1.d-1) from d 25 to 50 of pregnancy (short-term pST) or from d 25 to 100 of pregnancy (long-term pST). Fostering was performed on the day of birth to achieve litter sizes at the start of lactation of 10 piglets (where possible) on first-lactation sows, and 12 piglets on older lactating sows. Dam removals and removal reasons were recorded throughout the trial, from allocation at d 25 of pregnancy until weaning of the litter following the treatment pregnancy. 11 In sows, dam removals during pregnancy did not differ between treatments (P = 0.448). In gilts, removal rates did differ between treatments (P = 0.024), such that 12% of gilts treated with pST from d 25 to 100 of pregnancy were removed prior to entry to the farrowing house, compared to a 5% removal rate in controls (P = 0.062). 12 Dams in replicates 11 and 12 of the study were not followed through lactation, as a subset of their progeny were removed at birth for muscle fibre analysis.


jas.fass.orgD

ownloaded from


30

Table 4 – Subsequent reproductive performance13

Outcome Gilts Sows Significance (2) Control Short-

term pST Long-

term pST Control Short-

term pST Long-

term pST Treatment

Parity Treatment within parity groups

Mating rates after treatment lactation No weaned and on-trial at end of treatment lactation

83 84 75 89 85 84

Removed before mating, % of nos weaned14

3 (3.6%) 3 (3.6%) 3 (4.0%) 9 (10.1%) 8 (9.4%) 18 (21.4%)

0.059 ≤0.001 Gilts (P = 0.988)

Sows (P = 0.037)

Mated, % of nos weaned 80 (96.4%)

81 (96.4%)

72 (96.0%)

80 (89.9%)

77 (90.6%)

66 (78.6%)

Weaning-remating interval, d 15 6.69 ± 0.67

6.70 ± 0.61

8.33 ± 1.03

8.83 ± 0.99

6.55 ± 0.93

8.30 ± 1.03

0.135 0.535 Gilts (P = 0.631)

Sows (P = 0.407)

Farrowing rates in dams mated after treatment lactation Farrowed, % of no mated 16 68

(85.0%) 60

(74.1%) 60

(83.3%) 58

(72.5%) 60

(77.9%) 46

(69.7%) 0.831 0.069 Gilts

(P = 0.169) Sows

(P = 0.521) Reasons for farrowing failure Failure to conceive Pregnancy loss ≥ 40 d after mating Other removals

9 0 3

14 3 4

9 2 1

18 1 3

8 5 4

15 2 3

13 Landrace x Large White gilts and sows (parities 2 and 3 at mating) were uninjected (controls), or injected daily with pST (gilts: 2.5 mg.d-1, sows: 4.0 mg.d-1, each ~15 g pST.kg-1.d-1) from d 25 to 50 of pregnancy (short-term pST) or from d 25 to 100 of pregnancy (long-term pST). Fostering was performed on the day of birth to achieve litter sizes at the start of lactation of 10 piglets (where possible) on first-lactation sows, and 12 piglets on older lactating sows. Weaning date, date and reason for all pre-mating removals, numbers mated at the first post-weaning estrus, and mating date were recorded for all dams weaned at the end of lactation following the treatment pregnancy. Pregnancy outcomes were recorded for all dams mated at the first post-weaning estrus. 14 2 analysis of treatment and parity effects and maternal treatment within parity group. 15 Kruskal-Wallis test was used for non-parametric data comparisons for analysis of treatment and parity effects and maternal treatment within parity group. 16 2 analysis of treatment and parity effects and maternal treatment within parity group.


jas.fass.orgD

ownloaded from


31

Figure 1. Long-term (75 d), but not short-term (25 d), maternal pST injections increase maternal

weight at farrowing and maternal weight loss during lactation17

Figure 2. Long-term maternal pST treatment decreases maternal P2 fat depth at farrowing and

weaning.18

Figure 3. Long-term maternal pST treatment and greater maternal parity increase litter average

piglet weights after fostering, at day 14 of lactation and at weaning19

17 Landrace x Large White gilts and sows (parities 2 and 3 at mating) were uninjected (controls), or injected daily with pST (gilts: 2.5 mg.d-1, sows: 4.0 mg.d-1, each ~15 g pST.kg-1.d-1) from d 25 to 50 of pregnancy (short-term pST) or from d 25 to 100 of pregnancy (long-term pST). Fostering was performed on the day of birth to achieve litter sizes at the start of lactation of 10 piglets (where possible) on first-lactation sows, and 12 piglets on older lactating sows. Dams were weighed and P2 backfat depth measured by ultrasound on d 25 of pregnancy (prior to first injections), and d 50 and d 109 of pregnancy. Weight and P2 backfat depth were measured in ~60% of dams on the day of farrowing and in all dams at weaning. 18 Landrace x Large White gilts and sows (parities 2 and 3 at mating) were uninjected (controls), or injected daily with pST (gilts: 2.5 mg.d-1, sows: 4.0 mg.d-1, each ~15 g pST.kg-1.d-1) from d 25 to 50 of pregnancy (short-term pST) or from d 25 to 100 of pregnancy (long-term pST). Fostering was performed on the day of birth to achieve litter sizes at the start of lactation of 10 piglets (where possible) on first-lactation sows, and 12 piglets on older lactating sows. Dams were weighed and P2 backfat depth measured by ultrasound on d 25 of pregnancy (prior to first injections), and d 50 and d 109 of pregnancy. Weight and P2 backfat depth were measured in ~60% of dams on the day of farrowing and in all dams at weaning. 19 Landrace x Large White gilts and sows (parities 2 and 3 at mating) were uninjected (controls), or injected daily with pST (gilts: 2.5 mg.d-1, sows: 4.0 mg.d-1, each ~15 g pST.kg-1.d-1) from d 25 to 50 of pregnancy (short-term pST) or from d 25 to 100 of pregnancy (long-term pST). Fostering was performed on the day of birth to achieve litter sizes at the start of lactation of 10 piglets (where possible) on first-lactation sows, and 12 piglets on older lactating sows. Lactating pigs were fed three times daily to appetite and feed offered was recorded daily. Litter size and piglet weights were recorded after completion of fostering, on the day of birth, and on d 14 of lactation and prior to weaning.



32

E-2009-2265.R2 Figure 1

Gilts

Days from mating

0 25 50 75 100 125

Liv

e w

eig

ht,

kg

160

180

200

220

240

Far

row

ing

Wea

ning

Sows

Days from mating

0 25 50 75 100 125 150220

240

260

280

300

Far

row

ing

Wea

ning

Control

pST, d 25-50pST, d 25-100



33

E-2009-2265.R2 Figure 2

Gilts

Days from mating

0 25 50 75 100 125

P2

back

fat,

mm

13

14

15

16

17

18

Far

row

ing

Wea

ning

Sows

Days from mating

0 25 50 75 100 125 15013

14

15

16

17

18

Far

row

ing

Wea

ning

Control

pST, d 25-50pST, d 25-100



34

E-2009-2265.R3 Figure 3

Post-fostering

Gilts Sows

Averagepiglet

weight,kg

0.0

0.5

1.0

1.5

2.0Lactation d 14

Gilts Sows0

1

2

3

4

5Weaning

Gilts Sows0

1

2

3

4

5

6

7

8

9

ControlpST, d 25-50pST, d 25-100



Maternal responses to daily maternal porcine somatotropin injections during early-mid pregnancy or...

Documents

Transcript of Maternal responses to daily maternal porcine somatotropin injections during early-mid pregnancy or...