Long-chain (n-3) PUFA exert beneficial effects on inflammatory bowel diseases in animal models and clinical trials. In addition, pattern recognition receptors such as toll-like receptors (TLR) and nucleotide-binding oligomerization domain proteins (NOD) play a critical role in intestinal inflammation. We hypothesized that fish oil could alleviate Escherichia coli LPS-induced intestinal injury via modulation of TLR4 and NOD signaling pathways. Twenty-four weaned piglets were used in a 2 × 2 factorial design and the main factors included a dietary treatment (5% corn oil or 5% fish oil) and immunological challenge (LPS or saline). After feeding fish oil or corn oil diets for 21 d, pigs were injected with LPS or saline. At 4 h postinjection, blood samples were collected and pigs were killed. EPA, DHA, and total (n-3) PUFA were enriched in intestinal mucosa through fish supplementation. Fish oil improved intestinal morphology, indicated by greater villus height and villus height:crypt depth ratio, and intestinal barrier function, indicated by decreased plasma diamine oxidase (DAO) activity and increased mucosal DAO activity as well as enhanced protein expression of intestinal tight junction proteins including occludin and claudin-1. Moreover, fish oil decreased intestinal TNFα and PGE(2) concentrations and caspase-3 and heat shock protein 70 protein expression. Finally, fish oil downregulated the mRNA expression of intestinal TLR4 and its downstream signals myeloid differentiation factor 88, IL-1 receptor-associated kinase 1, TNFα receptor-associated factor 6, and NOD2, and its adaptor molecule, receptor-interacting serine/threonine-protein kinase 2. Fish oil decreased the protein expression of intestinal NFκB p65. These results indicate that fish oil supplementation is associated with inhibition of TLR4 and NOD2 signaling pathways and concomitant improvement of intestinal integrity under an inflammatory condition.

Dietary nutrients are essential for gastrointestinal (GI) growth and function, and nutritional support of GI growth and development is a significant component of infant care. For healthy full-term neonates, nutritional provisions of the mother's milk and/or formula will support normal maturation of structure and function of the GI tract in most infants. The composition of breast milk affects GI barrier function and development of a competent mucosal immune system. The functional nutrients and other bioactive components of milk support a microenvironment for gut protection and maturation. However, premature infants struggle with feeding tolerance impairing normal GI function, leading to intestinal dysfunction and even death. The high prevalence worldwide of enteric diseases and dysfunction in neonates has led to much interest in understanding the role of nutrients and food components in the establishment and maintenance of a functioning GI tract. Neonates who do not receive enteral feeding as either mother's milk or formula are supported by total parental nutrition (TPN). The lack of enteral nutrition can compound intestinal dysfunction, leading to high morbidity and mortality in intestinally compromised infants. Reciprocally, enteral stimulation of an immature GI tract can also compound intestinal dysfunction. Therefore, further understanding of nutrient interactions with the mucosa is necessary to define nutritional requirements of the developing GI tract to minimize intestinal complications and infant morbidity. Piglet models of intestinal development and function are similar to humans, and this review summarizes recent findings regarding nutrient requirements for growth and maintenance of intestinal health. In particular, this article reviews the role of specific amino acids (arginine, glutamine, glutamate, and threonine), fatty acids (long chain polyunsaturated, medium chain, and short chain), various prebiotic carbohydrates (short-chain fructo-oligosaccharide, fructo--oligosaccharide, lacto-N-neotetraose, human milk oligosaccharide, polydextrose, and galacto-oligosaccharide), and probiotics that have been examined in the suckling piglet model of intestinal health.

Supplementation of formula with 3'- or 6'-sialyllactose can enrich ganglioside SA in the brain and modulate gut-associated microbiota in neonatal pigs. We propose 2 potential routes by which sialyllactose may positively affect the neonate: serving as a source of SA for neurologic development and promoting beneficial microbiota.

The neonatal pig ranks among the most prominent research models for the study of pediatric nutrition and metabolism. Its precocial development at birth affords ready adaptation to artificial rearing systems, and research using this model spans a wide array of nutrients. Sophisticated in vitro and in vivo methodologies supporting both invasive, reduction-science research as well as whole-animal preclinical investigations have been developed. Potential applications may dually benefit both agricultural and medical sciences (e.g., "agrimedical research"). The broad scope of this review is to outline the fundamental elements of the piglet model and to highlight key aspects of relevance to various macronutrients, including lipids, carbohydrates, proteins/amino acids, and calcium/phosphorus. The review examines similarities between piglets and infants and also piglet idiosyncrasies, concluding that, overall, the piglet represents an adaptable and robust model for pediatric nutrition and metabolism research.

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