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were also observed on early piglet growth (Oliviero
et al.
, 2009), colostrum intake of low
birth weight piglets, and litter performance (Loisel
et al.
, 2013). This is covered in more
details in Chapter 5 of this topic (Meunier-Salaün and Bolhuis, 2015).
15.3.2
Intra-uterine growth retardation and gut maturation
Over the last decade, average litter size of sows was increased by genetic selection. This
was associated with a reduction in the mean piglet birth weight and, concomitantly, with
an increased within-litter variation in birth weight leading to a rise in the proportion of
small piglets (less than 1 kg birth weight) in large litters (Le Dividich, 1999; Milligan
et al.
,
2002; Quiniou
et al.
, 2002). Pigs with IUGR exhibited consistently lower postnatal growth
rates and lower lean carcass percentages than normal or heavy birth weight littermates at
slaughter (Bee, 2004; Gondret
et al.
, 2006; Morise
et al.
, 2008; Poore
et al.
, 2004; Rehfeldt
et al.
, 2006).
Piglets with IUGR usually consume less colostrum than normal birth weight piglets.
The lower ability of newborn piglets with IUGR to reach mammary glands for the first
suckling reflects their lower vitality at birth (Quesnel
et al.
, 2012). However, growth
failure of piglets with IUGR is also related to the reduced intestinal size, i.e. reduced
weight (proportionate to body weight), length, wall thickness, villous height and crypt
depth, and to the lower intestinal trophic responses to enteral food introduction during
the early postnatal period (D'Inca
et al.
, 2010, 2011). In the first week after birth, piglets
with IUGR have a thinner intestine and at least a 40% lower surface area for exchange,
as estimated by the combined reduction of ileal weight/length ratio and villous sizes.
Increased cell death may account for the reduced mucosal density and villi size in the
intestines of IUGR piglets. Although the activity of intestinal enzymes is not markedly
affected by IUGR, a decreased PepT 1 expression in the distal intestine is seen and
indicates a delayed intestinal development. The developmental profile of epithelial barrier
functions in IUGR piglets was also altered by preventing the jejunal decrease and the ileal
increase in permeability to macromolecules, that occur in normal birth weight piglets
during the suckling period (Boudry
et al.
, 2011). This point appears crucial because of
the main role of the intestine in processing dietary molecules into available nutrients
for the organism, and in regulating the flux of antigenic materials that participate in the
maturation of GALT. Furthermore, the surface of follicles in jejunal PP is reduced in 2
day-old piglets with IUGR compared with normal birth weight piglets of the same age (S.
Ferret-Bernard, personal communication). The expression of several proteins involved in
the response to stress is also up-regulated in IUGR piglets (Wang
et al.
, 2008).
Binding property of intestinal mucosa to luminal bacteria seems to be affected in IUGR
piglets. Indeed, it was demonstrated that there is an increase in the adhesion of luminal
bacteria in 2 day-old IUGR piglets (D'Inca
et al.
, 2010). Therefore, in response to this
early challenge, the intestine from IUGR piglets sets up defence mechanisms to maintain
the intestinal barrier protection by enhancing mucin synthesis and IgA secretion (D'Inca
et al.
, 2010, 2011). Changes in properties of microbiota have also been reported. In
weaned pigs with IUGR, striking differences are seen in the fermentative activity of the
caecum, with greater acetate and propionate concentrations compared with normal birth
