Review: Mammary development in swine: effects of

hormonal status, nutrition and management

C. Farmer
Agriculture and Agri-Food Canada, Dairy and Swine R & D Centre, 2000 College St., Sherbrooke, Québec,
Canada J1M 0C8 (e-mail: chantal.farmer@agr.gc.ca). Received 14 June 2012, accepted 10 September 2012.
Farmer, C. 2013. Review: Mammary development in swine: effects of hormonal status, nutrition and management. Can. J.
Anim. Sci. 93: 17. There are three phases of rapid mammary accretion in swine, namely, from 90 d of age until puberty,
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during the last third of gestation and throughout lactation. Nutrition, endocrine status and management of gilts or sows
during those periods can affect mammary development. More specifically, in growing gilts, feed restriction as of
90 d of age hinders mammary development and either supplying the phytoestrogen genistein or increasing circulating
concentrations of prolactin stimulates mammogenesis. In late gestation, inhibition of relaxin or prolactin drastically
diminishes mammary development and overly increasing dietary energy has a detrimental effect on mammogenesis. It also
appears that feeding of the gestating sow can affect the mammary development of her offspring once it reaches puberty.
Various management factors such as litter size, nursing intensity and use or non-use of a teat in the previous lactation will
affect the amount of mammary tissue present at the end of lactation. Mammary development is followed by the essential
process of involution whereby a rapid and drastic regression in parenchymal tissue takes place. It can occur either after
weaning or in early lactation when teats are not being regularly suckled. Despite our current knowledge, much remains to
be learned in order to develop the best management strategies for replacement gilts, and gestating and lactating sows that
will maximize their milk production.

Key words: Gestation, hormones, lactation, mammary development, nutrition, sow

Farmer, C. 2013. Revue : Développement mammaire chez le porc : effets du statut hormonal, de la nutrition et de la régie.
For personal use only.

Can. J. Anim. Sci. 93: 17. Il y a trois phases de développement mammaire rapide chez le porc, soit, de 90 jours d’âge à la
puberté, pendant le dernier tiers de la gestation et tout au long de la lactation. La nutrition, le statut endocrinien et la régie
des cochettes et des truies pendant ces périodes peuvent affecter leur développement mammaire. Plus spécifiquement, chez
les cochettes en croissance, une restriction alimentaire à partir du jour 90 est néfaste pour leur développement mammaire
alors qu’un supplément avec le phytoestrogène génistein ou une augmentation des concentrations circulantes de prolactine
stimule la mammogénèse. En fin de gestation, une inhibition de la relaxine ou de la prolactine diminue drastiquement le
développement mammaire et un apport trop élevé d’énergie dans la diète est nuisible pour la mammogénèse. Il semble aussi
que l’alimentation de la truie en gestation puisse affecter le développement mammaire de ses rejetons à la puberté. Plusieurs
facteurs de régie tels la taille de la portée, l’intensité de la tétée et l’utilisation ou non d’une tétine dans la lactation
précédente affectent la quantité de tissu mammaire présent en fin de lactation. Le développement mammaire est suivi du
processus essentiel d’involution constitué d’une régression rapide et drastique du tissu parenchymateux. Cette involution
peut avoir lieu soit après le sevrage ou en début de lactation si une tétine n’est pas utilisée régulièrement. Malgré nos
connaissances actuelles, il est évident qu’il reste beaucoup à apprendre afin de développer les meilleurs systèmes de régie
pour les cochettes de remplacement et les truies en gestation et lactation qui permettront de maximiser leur production
laitière.

Mots clés: Gestation, développement mammaire, hormones, lactation, nutrition, truie

Milk is the main energy source for piglets and is therefore
essential for their growth and survival. Nevertheless,
sows cannot produce enough milk to sustain optimal
growth of their litters. This is true as of approximately
8 to 10 d of age and the situation worsens as lactation
progresses (Harrell et al. 1993). This problem was
exacerbated in recent years with the introduction of
hyperprolific sow lines. It is therefore imperative to
develop management strategies that will increase sow
milk yield. One crucial factor determining sow milking
potential is the number of mammary cells that are
present at the onset of lactation (Head and Williams
1991). Mammary development occurs at distinctive
periods and is regulated by numerous factors. The
present review summarizes our current knowledge on
the effects of nutrition, hormonal status and manage-
ment schemes on mammary development in swine.
ONTOGENY OF MAMMARY DEVELOPMENT
Mammary glands of newborn piglets consist mainly of
subcutaneous stromal tissue and have a poorly devel-
oped duct system (Hughes and Varley 1980). Accumula-
tion of mammary tissue and mammary DNA, which is
indicative of cell number, is slow until 90 d of age. The
rate of accretion of mammary tissue and DNA then
Abbreviations: GRF, growth hormone-releasing factor;
IGFBP-5, insulin-like growth factor binding protein-5

Can. J. Anim. Sci. (2013) 93: 17 doi:10.4141/CJAS2012-066 1

 2 CANADIAN JOURNAL OF ANIMAL SCIENCE
increases four- to sixfold (Sorensen et al. 2002) so that
by the time the gilt is mated, mammary glands are still
very small but contain an extensive duct system with
various budlike outgrowths (Turner 1952). The onset of
puberty has a stimulatory effect on mammogenesis as it
was reported that parenchymal tissue mass increases by
51% and extraparenchymal tissue mass decreases by
16% in gilts that have reached puberty compared with
gilts of a similar age that have not started cycling
(Farmer et al. 2004).
In pregnant gilts, quantitative development of the
mammary glands is slow in the first two-thirds of
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gestation, while almost all accumulation of mammary
tissue and DNA takes place in the last third (Hacker and
Hill 1972; Kensinger et al. 1982; Sorensen et al. 2002).
Ji et al. (2006) also reported a significant increase in
weight of mammary glands between days 45 and 112 of
gestation, with accelerated mammary accretion occur-
ring after day 75. During this period of rapid mammary
development, mammary glands undergo major histo-
logical changes as the adipose and stromal tissues are
replaced by lobuloalveolar tissue to become the milk
secretory apparatus (Hacker and Hill 1972; Kensinger
et al. 1982; Ji et al. 2006). Ji et al. (2006) reported a shift
in mammary gland composition going from a high lipid
content to a high protein content during the last third of
For personal use only.
gestation. Both histological changes and differences in
DNA concentrations in mammary tissues from gilts
indicate increased tissue differentiation between days
75 and 90 of gestation, with maximum cell concentra-
tions present by day 90. Then, between days 90 and
105, abundant secretion accumulates in the mammary
alveoli, indicating the onset of the lactogenic process
(Kensinger et al. 1982). Interestingly, location of the
gland on the udder affects its development during
gestation. The wet weight of middle glands (3rd, 4th
and 5th pairs) is greater than that of posterior glands
(6th, 7th and 8th pairs) on both day 102 and day 112 of
gestation (Ji et al. 2006).
Mammary gland development does not stop at the end
of gestation but it continues during lactation. Average
mammary weight of the suckled glands increases linearly
from 381 g on day 5 of lactation up to 593 g on day 21
(57% increase). The increase in mammary volume during
lactation is the consequence of both cellular hyperplasia
and hypertrophy (Kim et al. 1999a). Mammary growth
in lactation is related to the position of the gland on the
udder, being greater for the five more anterior teat pairs
than for more posterior teat pairs (Kim et al. 2000),
and there are indications that it may be related to the
intensity of the post-ejection massage (Thodberg and
Sorensen 2006). Mammary development is also affected
by parity because mammary gland wet weight increased
by 70, 20 and 30% between day 113 of gestation and day
26 of lactation, for sows of parity 1, 2 and 3, respectively
(Beyer et al. 1994).
Interestingly, there is a correlation between the size of
a mammary gland (either in terms of weight or DNA)
and its milk yield, as estimated by the growth of the
piglet suckling that teat (Nielsen et al. 2001). Further-
more, mammary parenchymal tissue of sows that
produce more milk (i.e., 5.25 vs. 4.46 kg average piglet
weight gain from days 2 to 21 of lactation) contains
more DNA and more RNA per teat at the end of
lactation than that of sows with a lower milk yield
(Farmer et al. 2010b). These findings substantiate the
importance of understanding the various factors that
can have an impact on mammary development so that
we can then try to stimulate it. The following two
sections cover studies where the effects of hormonal
status and nutrition on mammary development were
investigated in swine. Table 1 provides a summary of the
various treatments used and their effects on mammary
parenchymal mass and parenchymal DNA.
HORMONAL EFFECTS ON MAMMARY
DEVELOPMENT
Estrogens play an essential role for mammary develop-
ment in swine, as evidenced by the impact of the onset
of puberty on mammogenesis (Farmer et al. 2004;
Sorensen et al. 2006). Kensinger et al. (1986) also
demonstrated that the drastic increase in metabolic
activity of the mammary gland occurring in late gesta-
tion is associated with the increase in estrogens of fetal
origin; indeed, mammary DNA was related to cir-
culating concentrations of estrogen in sows on day
110 of gestation. An earlier study showed that zearale-
none, a mycotoxin with estrogen-like activities, does
affect mammary development. An increase in mam-
mary glandular elements due to ductal hyperplasia was
observed in sows receiving zearalenone (Chang et al.
1979). Recently, an attempt was made to specifically
stimulate mammary development in gilts by providing
a source of estrogens. When 2.3 g d1 of the phytoestro-
gen genistein was added to the diet of growing gilts from
90 to 183 d of age, there was an increase in mammary
parenchymal DNA, indicative of hyperplasia, at the end
of the treatment period (Table 1, Farmer et al. 2010a).
A project is currently being carried out at the Sher-
brooke Dairy and Swine R & D Centre (Canada) to
determine the impact of providing a similar dose of
genistein to gilts in the last third of pregnancy on their
mammary development.
Relaxin is a polypeptide hormone produced by the
corpora lutea of pregnant sows. Using a classical
replacement therapy study with ovariectomized preg-
nant gilts, Hurley et al. (1991, Table 1) clearly demon-
strated that relaxin plays a major role in promoting
mammary parenchymal growth in the last third of
pregnancy. However, the potential effects of exogenous
relaxin on mammogenesis of intact gestating gilts are
not known. Exogenous growth hormone was shown to
increase milk yield in sows (Harkins et al. 1989) and the
potential stimulatory effect of its releasing factor (GRF)
on mammary development of lactating sows was
studied. Yet, results were not probing because three
 FARMER * REVIEW: MAMMARY DEVELOPMENT IN SWINE 3

Table 1. Effects of nutritional, hormonal and management treatments on mammary parenchymal mass [or surface area for Hurley et al. (1991)] and
parenchymal DNA concentration in various published studies in swine. The treatment was preceded by S when done in sows and by G when done in gilts

Effects on:

Parenchymal Parenchymal
Treatmentz massy DNAy Reference

Hormonal treatment
G: genistein from dx 90 to 183 12.2%O 44.4%O Farmer et al. (2010a)
G: inhibit relaxin d 80110 gestation 47.0%n no data Hurley et al. (1991)
G: GRF d 100 gestation to 29 lactation 28.5%n 26.2%O Farmer et al. (1997)
G: inhibit prolactin d 70110 gestation 42.5%n 15.2%n Farmer et al. (2000)
G: inhibit prolactin d 90110 gestation 46.0%n 3.6%n Farmer and Petitclerc (2003)
G: prolactin for 29 d (75 kg onward) 116.4%O 160.9%O Farmer and Palin (2005)
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S: prolactin d 223 lactation 0.6%O 1.8%n Farmer et al. (1999)

Nutritional treatment
G: 34% feed restriction dx 2890 6.4%n 4.9%O Sorensen et al. (2006)
G: 26% feed restriction dx 90170 34.2%n 21.9%n Sorensen et al. (2006)
G: 20% feed restriction dx 90202 26.3%n 0% Farmer et al. (2004)
G: 14.4 vs 18.7% CP dx 90202 9.4%O 0% Farmer et al. (2004)
G: restricted growth from 912 and 1520 wkx: effect gestation 43.0%n 5.7%O Lyvers-Peffer and Rozeboom (2001)
G: 10% flaxseed dx 88212 11.4%O 15.8%n Farmer et al. (2007)
G: 10% flaxseed d 63 gestation to end lactation: effect on 30.9%O 11.6%O Farmer and Palin (2008)
offspring dx 220
G: feed restriction then over-feeding in prepuberty: effect dx 235 19.4%n 6.7%n Farmer et al. (2012a)
G: feed restriction then over-feeding in prepuberty: effect 2.4%O 4.3%n Farmer et al. (2012b)
gestation
G: 82% increase in dietary energy d 75105 gestation 21.4%n 1.0%n Weldon et al. (1991)
G: 53% increase in dietary protein d 75105 gestation 9.5%n 1.0%n Weldon et al. (1991)
G: 16 vs. 4 g d1 of lysine intake d 25105 gestation 6.0%n 2.5%n Kusina et al. (1999)
For personal use only.

Management strategy
S: increasing litter size from 6 to 12 65%O 67%O Kim et al. (1999b)
S: non-suckling of teat in lactation 1: effect on d 17 of lactation 2 13.2%n 4.5%n Farmer et al. (2012c)

z
Effects on glands collected on the last day of treatment unless mentioned otherwise.
y
A decrease or increase in values does not indicate statistical significance.
x
Days or weeks of age.

daily injections (12 mg each) of GRF in late gestation
and throughout lactation decreased mammary parench-
ymal mass and increased parenchymal DNA on day 30
of lactation, so that total parenchymal DNA was
unaltered (Table 1, Farmer et al. 1997).
Prolactin is the hormone which has received most
attention in terms of its effects on mammary develop-
ment in swine. As early as 1945, there were indications
that feeding ergot to late-pregnant sows had a detri-
mental effect on mammary development. Almost no
mammary development was present in any of the treated
sows whereas all control sows had normal mammary
development (Nordskog and Clark 1945). A negative
impact of ergots on mammary development when fed
8 d before farrowing was also reported more recently
(Kopinski et al. 2007). This is most interesting due to the
finding that endotoxins have an inhibitory effect on
prolactin secretion, thereby showing a relation between
suppression of prolactin and insufficient milk yield in
sows (Smith and Wagner 1984). The first demonstration
of the essential role of prolactin for mammary develop-
ment in pregnant gilts was made over 10 yr ago via
inhibition of prolactin, using the dopamine agonist
bromocriptine (Table 1, Farmer et al. 2000). It was
subsequently shown that the specific time-window
where prolactin exerts most of its stimulatory effect on
the mammary gland is from 90 to 110 d of gestation
(Table 1, Farmer and Petitclerc 2003). Prolactin also
affects mammogenesis in growing gilts. The first indica-
tion of this came from a trial where prolactin was
provided to gilts in an attempt to affect their growth
performance (McLaughlin et al. 1997). These authors
reported apparent mammary development with injec-
tions of 2 mg d1 of recombinant porcine prolactin for
28 d, starting at 75 kg body weight. Mammary glands of
treated gilts were characterized by distended alveolar
and ductal lumina as well as the presence of secretory
material. Yet, no measures of mammary composition
were made. In a later experiment, injections of 4 mg d1
of recombinant porcine prolactin to gilts for 29 d, as of
75 kg body weight, led to a 116% increase in mammary
parenchymal tissue mass and a 160.9% increase in
parenchymal DNA (Table 1, Farmer and Palin 2005).
However, mammary secretions were also present, which
raises the question as to whether such a dose of prolactin
would have positive or negative effects on future milk
yield. When given during lactation, recombinant porcine
prolactin had no significant effects on either milk yield
 4 CANADIAN JOURNAL OF ANIMAL SCIENCE
or mammary composition. This absence of effect was
thought to be due to the fact that mammary receptors
for prolactin were already saturated in control animals,
thereby preventing the exogenous prolactin from having
any biological action (Table 1, Farmer et al. 1999).
Much remains to be known about the potential of
increasing circulating concentrations of prolactin on
mammary development and subsequent milk yield.
However, due to unavailability of porcine prolactin in
large enough quantities for in vivo studies, such experi-
ments were not carried out. The plant extract silymarin
(from milk thistle) could be a potential tool to increase
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prolactin concentrations in swine, as suggested by its
hyperprolactinemic property in rats (Capasso et al.
2009) and its hypergalactenemic action in women (Di
Pierro et al. 2008) and cows (Tedesco et al. 2004). Yet, a
recent study showed that prolactin concentrations were
not increased in multiparous post-weaned sows (Loisel
et al. 2013), but this was likely due to the dose or to
reproductive experience of the animals, and an experi-
ment is currently undergoing in our laboratory to test its
potential stimulatory effects on prolactin concentrations
and mammogenesis in late-gestating gilts using a greater
dose.
NUTRITION EFFECTS ON MAMMARY
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DEVELOPMENT
Nutrition in the growing, gestation or lactation periods
can affect mammary development in swine. A 34% feed
restriction of growing gilts from 28 d (weaning) to 90 d
of age had no significant impact on mammogenesis,
whereas a 20% (Table 1, Farmer et al. 2004) or a 26%
(Table 1, Sorensen et al. 2006) feed restriction from
90 d of age until puberty drastically reduced mammary
parenchymal mass. Interestingly, the effect of feed
restriction on mammogenesis is only seen as of 90 d of
age, being the first period of rapid mammary develop-
ment in growing gilts. It therefore appears that high
feeding levels from 90 d of age to puberty have a stimu-
latory effect on mammary development in gilts. On the
other hand, reducing dietary crude protein from 18.7
to 14.4% in that same period does not affect mammo-
genesis (Table 1, Farmer et al. 2004). Furthermore,
dietary supplementation with 10% flaxseed from 88 d
until 212 d of age did not lead to significant changes in
mammary development of gilts (Table 1, Farmer et al.
2007).
Nutrition of growing gilts can also affect their mam-
mary development at the end of gestation. Lyvers-Peffer
and Rozeboom (2001) studied the effects of a growth-
altering feeding regimen before puberty on mammary
development at the end of gestation. They used dietary
fiber to achieve alternating phases of moderate and
maximum growth during distinct pre-pubertal periods
and found that gilts fed moderately from 9 to 12 and 15
to 20 wk of age had less mammary parenchyma on day
110 of gestation (Table 1). In a later experiment using a
similar approach, specific periods of diet deprivation
followed by over-allowance in growing gilts did not have
any beneficial effect on mammary development after
puberty; in fact, this feeding regime led to a decrease in
parenchymal tissue (Table 1, Farmer et al. 2012a). This
same treatment also did not affect parenchymal mass at
the end of gestation (Table 1) but there was a tendency for
percent protein to be reduced in mammary parenchyma
from treated gilts (Farmer et al. 2012b).
Nutrition during pregnancy definitely affects mam-
mary development at the end of gestation. An early
study where body composition of sows was altered by
manipulating protein and energy intakes during gesta-
tion demonstrated that fat (36 mm backfat) and leaner
gilts (24 mm backfat) had similar mammary weights but
there was a drastic reduction (approximately threefold)
in mammary DNA concentration in fat gilts on day
112 of gestation compared with leaner gilts (Head and
Williams 1991). Yet, these body conditions are not
representative of what is currently seen commercially
and it is not known if such a difference in mammary
DNA would be seen between lean gilts and leaner
gilts (approximately 12 mm backfat). Weldon et al.
(1991) showed that increasing dietary energy (5.76 vs.
10.5 Mcal ME d1) as of day 75 of gestation decreased
mammary parenchymal weight and parenchymal DNA
on day 105 of gestation (Table 1). On the other hand,
increasing protein intake (330 vs. 216 g CP d1) had no
effects on mammogenesis (Table 1, Weldon et al. 1991).
This finding was later corroborated by Kusina et al.
(1999), who showed that varying lysine intakes of 4, 8 or
16 g d1 from days 25 to 105 of gestation did not
alter mammary development at the end of gestation
(Table 1).
A recent report indicated that nutrition of sows in
gestation and lactation can affect mammary develop-
ment of their offspring. Indeed, dietary supplementation
with 10% flaxseed from day 63 of gestation until the
end of lactation increased mammary parenchymal mass
of the offspring at puberty (Table 1, Farmer and Palin
2008). This is a first demonstration of such an in
utero effect in swine, and it opens new avenues in
terms of development of feeding strategies to enhance
mammogenesis.
Nutrition during the last phase of rapid mammary
accretion, namely lactation, also affects mammary
development. Kim et al. (1999b) fed lactating sows
four diets that were a combination of different protein
(32 or 65 g lysine d 1) and energy (12 or 17.5 Mcal ME
d 1) levels. Wet and dry weights of suckled mammary
glands were positively affected by both energy and
protein intakes.
MAMMARY INVOLUTION
When piglets are weaned, mammary glands undergo a
process of involution with a very rapid regression
occurring during the first 7 d after weaning (Ford et al.
2003). Changes in mammary tissue are quite dramatic,
with wet weight and DNA contents of parenchymal
 FARMER * REVIEW: MAMMARY DEVELOPMENT IN SWINE 5
tissue decreasing by more than two-thirds and close to
two-thirds, respectively, in this critical period. Signifi-
cant changes are seen as early as in the first 2 d post-
weaning. There is an increase in parenchymal fat and
a corresponding decrease in parenchymal protein in
the initial 2 to 3 d after weaning, which could reflect a
transitory accumulation of milk lipid in mammary
epithelial cells (Ford et al. 2003). Mammary glands
that were not suckled during lactation did not show
further loss of parenchymal tissue after weaning (Ford
et al. 2003), corroborating earlier findings of Kim et al.
(2001) whereby unsuckled mammary glands in early
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lactation regress at a rate similar to that seen post-
weaning. Namely, there was a 2/3 decrease in mammary
tissue weight within 7 to 10 d of non-use in early lactation
followed by a much slower regression rate thereafter.
Interestingly, mammary gland regression on day 21 of
lactation was not affected by litter size (varying from 6 to
12 pigs) but was affected by nutrition. On day 5 of
lactation, the weight of unsuckled glands was 91%
greater when sows were fed a high-energy high-protein
diet (17.5 Mcal ME d1, 65 g lysine d1) compared
with sows fed a low-energy low-protein diet (12 Mcal
ME d1, 32 g lysine d1, Kim et al. 2001). However,
the impact of the extent and rapidity of regression of
unsuckled mammary glands on their future development
For personal use only.
and milk yield is not known and definitely warrants
further research.
In a study where teats were blinded for either 24 or
72 h post-farrowing to prevent suckling by piglets, it was
demonstrated that regression of unsuckled mammary
glands during early lactation is reversible (gland rescue)
during the first 24 h but becomes irreversible within 3 d
(Theil et al. 2005). Yet, milk production from those
rescued glands that were unsuckled during 24 h remains
lower throughout lactation. Alterations in mammary
transcription of the a-lactalbumin, prolactin receptor
and IGFBP-5 genes were seen due to milk stasis (Theil
et al. 2005). It was concluded that regularly suckled
glands have greater cell proliferation, greater transcrip-
tion of a-lactalbumin and prolactin receptor genes, and
less IGFBP-5 transcription compared with rescued
(blinded for 24 h) or regressing (blinded for 3 d) glands.
In a later trial, Theil et al. (2006) showed the importance
of suckling intensity for mammary development and
regression. They compared no suckling, transient suck-
ling (until 12 to 14 h postpartum) or regular suckling of
mammary glands and reported that regularly suckled
glands maintained lactation whereas transiently suckled
and non-suckled glands regressed during lactation. In
fact, suckling during the first 12 to 14 h postpartum was
not sufficient to initiate and maintain lactation until
24 to 36 h postpartum but could induce mammary cell
proliferation for at least 6 d postpartum. Alterations in
gene transcription were also present between functional
and non-functional glands and indicated that a high
prolactin receptor transcription and a low IGFBP-5
transcription seem important for maintaining mammary
glands functional during lactation. Yet, the potential
effects of such alterations on mammary development
and milk yield during the next lactation are not known.
Ford et al. (2003) noted that mammary glands that were
suckled during lactation were larger than non-suckled
glands at the end of the involution process, suggesting a
possible beneficial effect on redevelopment during the
next gestation.
MANAGEMENT STRATEGIES AND MAMMARY
DEVELOPMENT
Fraser et al. (1992) were the first to suggest an effect of
teat use or non-use in one parity on its productivity in
the subsequent lactation. Yet, in their study there was a
confounding effect of treatment with teat location and it
is only recently that a clear demonstration was made
that non-suckling of a teat in first parity impairs its
development in second parity. In a study where either
the same teats or different teats were blinded during the
1st and 2nd lactation, teats which were not suckled in
1st parity had less parenchymal tissue and less parench-
ymal DNA at the end of the 2nd lactation than teats
which were previously suckled (Table 1, Farmer et al.
2012c). Furthermore, abundance of mRNA for the
prolactin receptor gene was reduced in teats which
were previously unsuckled and growth rate of the
piglets suckling them in 2nd lactation was also lower
(Farmer et al. 2012c).
Another management scheme that can affect mam-
mary development is litter size. Kim et al. (1999c)
reported that sows with a larger litter size (12 pigs) have
greater total mammary mass than sows with a smaller
litter size (6 pigs); however, the weight of individual
glands is lower. Changing the litter size from 6 to 12 pigs
led to a 65% increase in total mammary wet weight and a
67% increase in mammary DNA (Table 1). Percentages
of dry fat-free tissue, protein and DNA on day 21 of
lactation were quadratically affected by litter size.
CONCLUSION
In conclusion, mammary development can be altered by
many factors including nutrition and endocrine status of
the gilt or sow, but much still remains to be learned in
order to develop optimal management strategies for
replacement gilts, gestating gilts and lactating sows that
will maximize their milk production. It is clear that
feed restriction as of 90 d of age in growing gilts hinders
mammary development and there are also indications
that supplying the phytoestrogen genistein or increasing
concentrations of prolactin in growing gilts stimulate
mammogenesis. Nutrition during gestation can affect
mammary development; however, the ideal feeding
regimes for pregnant gilts or sows have not yet been
developed. Management schemes altering the number of
glands suckled as well as the duration of suckling of
these glands during lactation also have an impact on the
amount of mammary parenchymal tissue present at the
end of lactation.
 6 CANADIAN JOURNAL OF ANIMAL SCIENCE
ACKNOWLEDGMENTS
The author wishes to thank the numerous collaborators
she had over the years in performing research on
mammary development in swine.
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pregnant and lactating sows. Arch. Anim. Nutr. 46: 736.
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Lembo, F. and Borrelli, F. 2009. Silymarin BIO-C† , an extract
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