|Burrin, Douglas - Doug|
|GHONEIM, NADA - Children'S Nutrition Research Center (CNRC)|
|STOLL, BARBARA - Children'S Nutrition Research Center (CNRC)|
|THYMANN, THOMAS - University Of Copenhagen|
|SANGILD, PER - University Of Copenhagen|
Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: 11/15/2012
Publication Date: 12/2/2012
Citation: Burrin, D.G., Ghoneim, N., Stoll, B., Thymann, T., Sangild, P.T. 2012. Preterm piglets are a clinically relevant model of pediatric GI disease [abstract]. Conference of Research Workers in Animal Diseases, Session: Immunology 120, December 2-4, 2012, Chicago, Illinois. Available: http://www.abstractsonline.com/plan/start.aspx?mkey=%7BCDAC4DF3%2DE5E6%2D427E%2DA230%2D2F588B938865%7D.
Technical Abstract: The goal of our research is to establish how nutritional support, enteral versus parenteral, affects gut function and susceptibility to disease in early development. We and others have used the neonatal pig to establish unique models of clinically relevant problems in pediatric gastroenterology, especially necrotizing enterocolitis (NEC). We are using the premature pig model to establish the critical elements of pathogenesis and strategies for prevention of NEC. Among the established neonatal animal models of NEC, piglets and rodents have dominated the field. Advantages for rodents include the low cost, rapid postnatal development, and capacity for genetic modification, but their size and differences in gastrointestinal tract (GIT) development from humans makes nutritional studies more difficult. Piglets, however, have more anatomic, physiologic, and immunologic similarities to humans, and their size allows for ease of surgical procedures, blood sampling, and dietary manipulation. The similarities in GIT function and development of preterm pigs to those of preterm human neonates is also critical in studying diseases of prematurity such as NEC. Our previous studies using piglets established that prematurity and microbial colonization are necessary elements in the pathogenesis of NEC. More recently we have shown that total parenteral nutrition (TPN) support prior to introduction of formula feeding increases the incidence of NEC. We also demonstrated that malabsorption of carbohydrates, namely maltodextrins, in infant formula can trigger bacterial overgrowth and promote the onset of NEC. Current studies are aimed at establishing the optimal lipid and carbohydrate composition of infant formula that minimizes or prevents NEC. The presentation will review recent findings and highlight the significance of the neonatal pig as a model for human infant NEC.