XII - 12th International Symposium - Digestive Physiology of Pigs
XII - 12th International Symposium - Digestive Physiology of Pigs
XII - 12th International Symposium - Digestive Physiology of Pigs
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<strong>Digestive</strong><br />
<strong>Physiology</strong><br />
<strong>of</strong> <strong>Pigs</strong><br />
3000 Invited review: Long-term effects <strong>of</strong> pre and<br />
early postnatal nutrition and environment on the gut.<br />
J. P. Lallès,* INRA, INRA, UR1341 ADNC, F-35590 Saint-<br />
Gilles, France.<br />
The Developmental Origins <strong>of</strong> Health and Disease<br />
(DOhAD) hypothesis formulated in the early eighties has<br />
stimulated research on long-term effects <strong>of</strong> early nutrition<br />
and environment over the last decades. Long-term is<br />
understood in this review as physiologically relevant<br />
periods such as after weaning, around sexual maturity and<br />
in adulthood, as opposed to early developmental periods.<br />
The small and large intestines as targets for long-term<br />
issues have received little attention until recent years while<br />
the stomach has been considered very rarely. Data have<br />
accumulated in laboratory animal models but they are still<br />
scarce in the swine species. Following the epidemics <strong>of</strong><br />
metabolic diseases and obesity in Westernised countries,<br />
experimental evidence has been published showing that<br />
nutritional factors, including energy, fat and fatty acids,<br />
protein and micronutrients do impact various facets<br />
<strong>of</strong> gut function. These include alterations in intestinal<br />
digestive, absorptive, secretory, barrier and defense<br />
systems, <strong>of</strong>ten in a way potentially detrimental to the host.<br />
Environmental factors with long-term influence include<br />
stress (e.g., maternal deprivation; neonatal gut irritation),<br />
chemical pollutants (e.g., bisphenol A) and gut microbiota<br />
disturbances (e.g., by antibiotics). Examples <strong>of</strong> such longterm<br />
effects on the gut will be provided in both laboratory<br />
animals and pigs, together with underlying physiological<br />
mechanisms whenever available. Experimental evidence<br />
for the involvement <strong>of</strong> underlying epigenetic modifications<br />
(e.g., genomic DNA methylation) in long-term studies has<br />
just started to emerge with regard to the gastrointestinal<br />
tract. Also, interactions between the microbiota and the<br />
host are being considered has potential players in the early<br />
programming <strong>of</strong> gut functions. Finally suggestions for future<br />
research, especially in the swine species will be provided to<br />
better understand, and then control, early programming as<br />
an attempt to optimize vital functions <strong>of</strong> the gastrointestinal<br />
tract throughout adult life.<br />
Key words: nutrition, gut, long term<br />
3001 Long-term impact <strong>of</strong> piglet weaning age on<br />
intestinal epithelial barrier function and stress responsiveness.<br />
A. J. Moeser,* E. L. Overman, S. M. D’Costa,<br />
and J. Xu, North Carolina State University, College <strong>of</strong> Veterinary<br />
Medicine, Raleigh, NC, USA.<br />
There is increasing evidence that the development and<br />
long-term function <strong>of</strong> the gastrointestinal system can be<br />
pr<strong>of</strong>oundly influenced by stressful experiences occurring<br />
in early life. Previous studies indicate that early weaning<br />
(weaning < 21 d <strong>of</strong> age) induces intestinal damage that<br />
is mediated by activation <strong>of</strong> intestinal stress signaling<br />
pathways (Moeser et al., 2006, 2007; Smith et al., 2010);<br />
however, the long-term effects <strong>of</strong> early weaning stress<br />
on intestinal function and stress responsiveness are<br />
unknown. In these studies, we investigated the impact <strong>of</strong><br />
early weaning on intestinal epithelial barrier function and<br />
intestinal responsiveness to subsequent production stress.<br />
<strong>XII</strong> INTERNATIONAL SYMPOSIUM ON<br />
DIGESTIVE PHYSIOLOGY OF PIGS<br />
116<br />
Session V<br />
Yorkshire-Hampshire-Large White-cross piglets were<br />
weaned either at 18 d <strong>of</strong> age (early weaned) or 28 d <strong>of</strong><br />
age (late weaned) and housed under normal production<br />
conditions. At 12 weeks post-weaning, a subset <strong>of</strong> pigs<br />
(n = 6) within each weaning age group were subjected<br />
to 3 h <strong>of</strong> mixing/commingling stress. Following the stress<br />
period, colon was harvested for assessment <strong>of</strong> intestinal<br />
epithelial barrier function by measuring transepithelial<br />
electrical resistance (TER) and mucosal-to-serosal flux <strong>of</strong><br />
FITC dextran (4 kDa) in colonic tissues mounted on Ussing<br />
chambers. In addition, histological analysis <strong>of</strong> intestinal<br />
tissues were performed. Under baseline conditions (no<br />
mixing stress) colon from early weaned pigs exhibited<br />
impaired intestinal barrier function demonstrated by lower<br />
TER and greater FD4 flux rates compared with colon from<br />
late weaned pigs (P < 0.05). Histological analysis revealed<br />
increased inflammatory cells (mast cells, neutrophils, and<br />
lymphocytes) in early weaned colonic tissues compared<br />
with late weaned pigs. Compared with unstressed controls,<br />
mixing stress in early weaned pigs caused reductions in<br />
colonic TER (P < 0.05) and elevations in FD4 flux rates (P<br />
< 0.01) whereas no changes were observed in late-weaned<br />
pigs subjected to the same stress. These data indicate<br />
that early life stress, such as early weaning, can have a<br />
long-lasting impact on intestinal barrier function and stressresponsiveness<br />
in the pig.<br />
Key words: intestinal barrier function, stress, early life<br />
3002 Butyrate supplementation to gestating sows and<br />
piglets induces muscle and adipose tissue oxidative<br />
genes and improves growth performance. H. Lu and K.<br />
Ajuwon,* Purdue University, West Lafayette, IN, USA.<br />
The immediate post-weaning period <strong>of</strong>ten leads to postweaning<br />
growth check in growing pigs due to changes<br />
in the diet, mixture <strong>of</strong> pigs from different litters, stress <strong>of</strong><br />
moving and greater exposure to pathogen load. To alleviate<br />
this early growth and disease challenge, antibiotics have<br />
been used for decades to improve piglet survivability<br />
and performance. Antibiotics are now highly discouraged<br />
in pig diets due to increased risk <strong>of</strong> developing highly<br />
resistant pathogenic strains from continuous antibiotic use.<br />
We tested the effect <strong>of</strong> prenatal and postnatal butyrate<br />
supplementation on growth performance <strong>of</strong> piglets. In the<br />
first study, piglets were supplemented with 0.3% butyrate<br />
in a liquid feeding system from 4 d after birth to weaning<br />
(d21). Butyrate led to increased average daily gain <strong>of</strong> the<br />
supplemented piglets by 13% compared with saline treated<br />
control pigs. Gene expression analysis reveals significant<br />
induction <strong>of</strong> PGC-1α in muscle, adipose tissue and ileum.<br />
PPARα was also significantly induced in the subcutaneous<br />
adipose tissue and muscle (longissimus dorsi) <strong>of</strong> butyrate<br />
supplemented piglets. In vitro, butyrate increased (P<br />
< 0.05) fatty acid oxidation in primary adipocytes and<br />
suppressed basal lipolysis by 62% compared with untreated<br />
cells. Butyrate significantly suppressed lipogenesis<br />
( 14 C-glucose incorporation into lipids) in adipocytes. This<br />
was accompanied by an approximately 30% reduction in<br />
the mRNA expression <strong>of</strong> fatty acid synthase (P < 0.05)<br />
in butyrate treated cells vs. controls. Additionally, piglets<br />
born to sows that were supplemented with 0.3% butyrate