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 />
(1.4 g/kg BW) in trial 2. In each trial, 36 piglets were weaned<br />
on average at 22 d <strong>of</strong> age and 6.1 kg <strong>of</strong> BW, distributed<br />
among treatments (12 pigs/treatment) in individual pens,<br />
and fed ad libitum a prestarter diet. During the first 6 d after<br />
weaning, feed intake was recorded daily and all piglets<br />
were intragastrically infused once daily at 7 p.m. with 50<br />
mL <strong>of</strong> either water (control) or treatment solutions. On d<br />
5 plasma was obtained from 6 pigs/treatment at −15, 0,<br />
30, 60, and 120 min relative to infusions and on d 6 the<br />
remaining 6 pigs/treatment were weighed, sacrificed, and<br />
their intestines were collected for later analyses. Data<br />
were analyzed as a mixed-effect model with pig treated<br />
as random variable. Compared with control, CDC at 60<br />
mg/kg BW increased (P < 0.05) mean plasma GLP-2 by<br />
77%, small intestine length, intraepithelial lymphocytes and<br />
cleaved caspase in the ileum; tended to increase ileum<br />
weight and length (P < 0.08) and mean plasma GLP-1 (P<br />
< 0.13) without affecting (P > 0.8) intake and final BW. At<br />
120 mg/kg BW, CDC also increased (P < 0.05) GLP-1 and<br />
GLP-2, but reduced intake by about 50% and reduced BW<br />
as well as ileal crypt depth. Other treatments did not affect<br />
measured parameters, except that BSE tended to depress<br />
GLP-1 (27%) and GLP-2 (42%) compared with control. In<br />
conclusion, oral CDC treatment potently enhanced GLP-2<br />
secretion in weanling piglets, but the mitigation <strong>of</strong> weaninginduced<br />
intestinal atrophy was apparently counterbalanced<br />
by increased inflammation and reduced feed intake.<br />
Key words: bile acids, gut growth, pigs<br />
2033 Effect <strong>of</strong> feeding immunoglobulin (IgG) on gastrointestinal<br />
structure in newborn pigs. J. Wolinski* 1 ,<br />
M. Slupecka 1 , P. Ochniewicz 1 , O. Fedkiv 2 , O. Prykhodko 2 ,<br />
G. Ushakova 3 , G. Skibo 4 , T. Kovalenko 4 , I. Osadchenko 4 ,<br />
K. Goncharova 4 , K. Szwiec 2 , B. Weström 2 , and S. G. Pierzynowski<br />
2,5 , 1 The Kielanowski Institute <strong>of</strong> Animal <strong>Physiology</strong><br />
and Nutrition, Jablonna, Poland, 2 Dept <strong>of</strong> Biology,<br />
Lund University, Lund, Sweden, 3 Dept <strong>of</strong> Biochemistry and<br />
Biophysics, Dnepropetrovsk National University, Dnepropetrovsk,<br />
Ukraine, 4 Bogomoletz Institute <strong>of</strong> <strong>Physiology</strong>, Kiev,<br />
Ukraine, 5 Dept <strong>of</strong> Medical Biology, Institute <strong>of</strong> Rural Health,<br />
Lublin, Poland.<br />
Colostrum ingestion leads to increased gut growth and<br />
maturation and is an indispensable source <strong>of</strong> antibodies<br />
(IgG) protecting the newborn pig against infection. Here<br />
we studied the effect <strong>of</strong> feeding purified IgG on the GI tract<br />
structure. Newborn littermate pigs were either fed colostrum<br />
(Col), an elemental diet (ED) without or supplemented with<br />
purified serum IgG (ED+IgG) via a stomach tube, 10 mL/<br />
kg, during 24 h or then only ED up to 72 h where after they<br />
were sacrificed. For morphometric studies slides were<br />
prepared from the GI tract and stained with hematoxylin and<br />
eosin. Feeding the ED supplemented with IgG (ED+IgG)<br />
compared with not resulted in an increase <strong>of</strong> thickness <strong>of</strong><br />
stomach mucosa (from 404 to 443 μm; P < 0.0001) and<br />
muscularis (from 1053 to 1187 μm; P < 0.05) similar to the<br />
values observed in Col-fed piglets at 72h. The addition<br />
with IgG had no affect on the stomach mucosal thickness<br />
after 24h. The duodenal and jejunal morphology became<br />
affected due IgG supplementation (ED+IgG) compared<br />
with ED group. Interestingly, at 24h IgG addition had<br />
<strong>XII</strong> INTERNATIONAL SYMPOSIUM ON<br />
DIGESTIVE PHYSIOLOGY OF PIGS<br />
107<br />
Session IV<br />
increased (P < 0.0001) the values <strong>of</strong> measured parameters<br />
in duodenum (mucosa thickness from 274 to 380 μm, villi<br />
length from 200 to 288 μm, crypt depth from 87 to 96 μm)<br />
into those observed in col-fed piglets. Similar results were<br />
also obtained in the jejunum with IgG treatment. However,<br />
the effects <strong>of</strong> IgG treatment became more incoherent in<br />
the distal direction along small intestine. In conclusion,<br />
our results show that feeding an ED supplemented with<br />
IgG improved the morphology <strong>of</strong> the GI tract toward that<br />
<strong>of</strong> colostrum-fed piglets and indicates a beneficial per se<br />
effect <strong>of</strong> IgG on the GI tract in neonatal pigs.<br />
Key words: immunoglobulin G, colostrum, gut morphology<br />
2034 Chenodeoxycholic acid improves intestinal permeability<br />
in piglets. Y. van der Meer 1 , W. J. J. Gerrits* 1 ,<br />
M. van den Bosch 2 , J. J. Holst 3 , W. Kulik 4 , and T. A. T. G.<br />
van Kempen 5 , 1 Animal Nutrition Group, Wageningen University,<br />
Wageningen, The Netherlands, 2 Provimi Holding<br />
B.V., Velddriel, The Netherlands, 3 Department <strong>of</strong> Biomedical<br />
Sciences, University <strong>of</strong> Copenhagen, Copenhagen,<br />
Denmark, 4 Academic Medical Center, University <strong>of</strong> Amsterdam,<br />
Amsterdam, The Netherlands, 5 North Carolina State<br />
University, Raleigh, North Carolina, USA.<br />
Piglets are highly susceptible to gut health-related<br />
problems. Intravenously administered chenodeoxycholic<br />
acid (CDCA) affects gut health mediated through GLP-2.<br />
To test if CDCA is a suitable feed additive for improving<br />
gut health, a trial was performed with newly weaned (21 d)<br />
piglets <strong>of</strong>fered a diet with or without 60 mg CDCA/kg feed<br />
(n = 24/trt). Upon weaning piglets were fasted for 16 h and<br />
then intragastrically dosed with 20 g test feed in 40 g water.<br />
Subsequently, a jugular blood sample was taken on either<br />
45, 90, 135, or 180 min for analysis <strong>of</strong> GLP-2, PYY, and<br />
glucose. Afterward, piglets were fed ad libitum. On d 3.5,<br />
7.5, and 10.5 post weaning, 8 piglets per treatment were<br />
sacrificed for determination <strong>of</strong> in vivo intestinal permeability<br />
using lactulose and Co-EDTA. Both markers were<br />
administrated intragastrically and after 2h, a blood sample<br />
was obtained through venipuncture. Immediately thereafter,<br />
intestines were harvested, and ex vivo permeability was<br />
measured using the everted gut sac technique with 4 kDa<br />
FITC-dextran as marker at 25, 50, and 75% <strong>of</strong> the length <strong>of</strong><br />
the small intestines. Average daily feed intake, daily gain,<br />
gain:feed, blood glucose, plasma GLP-2, and PYY were<br />
not affected by dietary CDCA (P > 0.10). Serum Co-EDTA<br />
and lactulose concentrations at d 10.5 tended to be lower in<br />
CDCA pigs compared with the control pigs (P = 0.054, P =<br />
0.089). The everted gut sac technique data did not show any<br />
treatment effects on permeability (P > 0.10), possibly due<br />
to reaction <strong>of</strong> the FITC-marker with light despite covering<br />
with aluminum foil. In conclusion, CDCA tended to improve<br />
intestinal permeability at 10.5 d post weaning when fed to<br />
newly weaned piglets, implying that CDCA deserves further<br />
study as a means for improving intestinal health.<br />
Key words: chenodeoxycholic acid, gut health, piglet<br />
2035 evaluation <strong>of</strong> immunoglobulin absorption from<br />
colostrum supplements gavaged to newborn piglets.<br />
J. Campbell* 1 , S. Jacobi 2 , Y. Liu 2 , K. Hard Robertson 3 , J.