Improving Nutrition for Newborn Piglets

A summary of recent research into intestinal health and understanding lipid metabolism with a focus on newborn piglets by Dr Jack Odle of North Carolina State University. He has observed that a protein source can reduce rotaviral diarrhoea and how a long-chain fatty acid can help repair damaged intestine.
calendar icon 19 January 2009
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Dr Jack Odle

Dietary Modulation of Intestinal Health

Early postnatal morbidity and mortality are significant challenges to the swine industry. While piglets are exposed to many stressors soon after birth, gastrointestinal maladies are among the most severe. The neonatal intestine is instantly forced from being essentially inactive prior to birth to being the major “supply organ” responsible for providing nutrients to the piglet, which is born with very limited reserves.

In addition to the required dramatic increase in function, the intestine must also serve as the first line of defense against both viral and bacterial pathogens that are ubiquitous in the postnatal environment. Due to these roles, the overall health and vitality of the neonatal pig hinges on the intestine’s development and function.

Dr Odle’s recent research has focused on understanding the role of various nutritional, hormonal and pharmacological agents in mediating the growth, development and function of the piglet intestine.

One recent area of focus for Dr Odle’s group has been examining ways to improve intestinal repair in response to injury utilizing a rotoviral challenge model. In one such study, they examined the impact of dietary inclusion of plasma protein to determine if it could reduce rotavirus-induced intestinal damage in neonatal piglets or improve the recovery of the damaged intestinal tract (Corl et al., 2007).

In this study, piglets from 10 sows were collected at birth and housed individually in an artificial rearing system. Piglets (n = 64) received a liquid colostrum diet for the first 24 hours and were then blocked by litter and randomly assigned to one of four treatments in a 2×2 factorial design (n = 16 pigs per treatment).

Pigs were assigned to different rooms according to future rotavirus infection (noninfected versus rotavirus-infected) and to one of two experimental diets. One diet contained 15 per cent animal plasma proteins, while the other was soy-protein-based and did not contain any animal products except lactose. The diets were formulated to provide similar nutriture. After 4 days of receiving the experimental diets, piglets housed in one room were infected with rotavirus isolated from a commercial swine farm.

The data collected on the piglets indicated that dietary inclusion of plasma proteins reduced rotaviral diarrhoea and maintained animal growth despite infection.

Figure 1. Growth performance of piglets fed either soy protein or plasma protein based diets with or without a rotaviral challenge
(From Corl et al., 2007)

Figure 2. Dietary inclusion of plasma proteins prevented rotaviral diarrhoea in neonatal pigs
(From Corl et al., 2007)

In addition to working with the rotaviral challenge model, his group has also been examining the role of dietary long-chain polyunsaturated fatty acids (LCPUFA) in intestinal repair. Prostaglandins derived from arachadonic acid, a LCPUFA, have been shown to stimulate intestinal repair in response to injury (Blikslager et al., 1997).

In a study utilizing 96 neonatal pigs, Dr Odle’s group determined that they could enrich the intestinal cells with arachadonic acid by feeding it at supraphysiological levels. Sow-reared control piglets were compared with piglets fed five levels of arachadonic acid (ranging from 0 to 5 per cent of the diet) and a diet containing 5 per cent ecopentanoic acid to determine if intestinal cells could be dietarily enriched with arachadonic acid, which may improve the intestine’s ability to repair itself in response to injury (Hess et al., 2008).

A clear dose-dependent increase in intestinal cell concentrations of arachadonic acid was seen after just 8 days of the piglets receiving the experimental diets, and no further increase was seen in the highest arachadonic-acid-fed group after 16 days. No detrimental effects of dietary arachadonic acid on growth were detected.

Now that Dr Odle’s group has identified the dietary level and feeding duration needed to produce the maximal enrichment of intestinal cells with arachadonic acid, they can pursue further studies to determine if this enrichment can enhance piglet health.

Figure 3. Arachadonic acid concentration in the jejunum and ileum of pigs after feeding arachadonic acid for 4, 8 and 16 days
(From Hess et al., 2008)

Lipid Metabolism

In addition to examining the impact of LCPUFA on intestinal health, Dr Odle’s group has investigated the role of another LCPUFA, conjugated linoleic acid (CLA), on lipid metabolism in the neonatal pig.

Dietary supplementation of CLA has been previously shown to decrease fat deposition in growing pigs (Ostrowska et al., 1999) as well as to improve the carcass characteristics of finishing pigs (Gatlin et al., 2002).

In a recently published study, Dr Odle’s team examined the impact of dietary supplementation with CLA on neonatal piglets fed either high-fat or low-fat diets. Their objective was to examine the role of CLA in regulating body composition and lipid metabolism. A total of 24 neonatal pigs were studied in a 2×2 factorial experiment to examine high (25 per cent) or low (3 per cent) dietary fat with or without CLA supplementation (1 per cent).

CLA did not affect daily body weight gain, formula intake, or feed conversion in this study. Significant reductions in body fat accretion were detected with CLA. Interestingly, no interaction of CLA with dietary fat content could be discerned.

This demonstrates CLA’s ability to alter both fatty acid synthesis as well as direct fat deposition in neonatal pigs. Significant reductions in the expression of two key lipid metabolism enzymes, acetyl coA carboxylase (ACC-a) and lipoprotein lipase (LPL), occurred with dietary CLA. These changes in gene expression further support that CLA reduces both fatty acid synthesis and direct fat deposition in neonatal pigs because ACC-a is a key enzyme needed for fatty acid synthesis and LPL is needed for the uptake of fatty acids from circulation.

Figure 4. Tables from Corl et al., 2008.

In both of these research areas, Dr Odle is producing information that will help lead to transformational changes in the efficiency of swine production. While he also pursues research that is directed towards human medicine using the young pig as a model, he has been a tireless advocate for agricultural research throughout his distinguished career.


Blikslager, A.T., M.C. Roberts, J.M. Rhoads and R.A. Argenzio. 1997. Prostaglandins I2 and E2 have a synergistic role in rescuing epithelial barrier function in porcine ileum. J Clin Invest. 100:1928-1933.
Corl, B.A., S.A. Mathews Oliver, X. Lin, W.T. Oliver, Y. Ma, R.J. Harrell and J. Odle. 2008. Conjugated linoleic acid reduces body fat accretion and lipogenic gene expression in neonatal pigs fed low- or high-fat formulas. J. Nutr. 138: 449-454.
Gatlin, L.A., M.T. See, D.K. Larick, X. Lin and J. Odle. 2002. Conjugated linoleic acid in combination with supplemental dietary fat alters pork fat quality. J Nutr. 132:3105-3112.
Hess, H.A., B.A. Corl, X. Lin, S.K. Jacobi, R.J. Harrell, A.T. Blikslager, and J. Odle. 2008. Enrichment of intestinal mucosal phospholipids with arachidonic and eicosapentaenoic acids fed to suckling piglets is dose and time dependent. J. Nutr. 138: 2164-2171.
Ostrowska, E., M. Muralitharan , R.F. Cross, D.E. Bauman and F.R. Dunshea. 1999. Dietary conjugated linoleic acids increase lean tissue and decrease fat deposition in growing pigs. J Nutr. 129:2037-2042

Dr Odle is a William Neal Reynolds Professor and the senior member of the Swine Nutrition Group in the Animal Science Department at North Carolina State.

January 2009

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