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This Article Full Text Full Text (PDF) All Versions of this Article: 295/5/G1092    most recent 00414.2007v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Bjornvad, C. R. Articles by Sangild, P. T. PubMed PubMed Citation Articles by Bjornvad, C. R. Articles by Sangild, P. T.

INFLAMMATION/IMMUNITY/MEDIATORS

Enteral feeding induces diet-dependent mucosal dysfunction, bacterial proliferation, and necrotizing enterocolitis in preterm pigs on parenteral nutrition

Departments of ¹Human Nutrition, ²Large Animals and ³Anatomy and Cell Biology, Faculty of Life Sciences, University of Copenhagen, Frederiksberg, Denmark; ⁴Department of Animal Health, Welfare and Nutrition, Faculty of Agricultural Sciences, University of Aarhus, Tjele, Denmark; ⁵Department of Surgery, Maastricht University, Maastricht, The Netherlands; ⁶National Veterinary Institute, Technical University of Denmark, Copenhagen, Denmark; and ⁷U. S. Department of Agriculture/ Agricultural Research Service Children's Nutrition Research Center, Houston, Texas

Submitted 14 September 2007 ; accepted in final form 19 September 2008

Preterm neonates have an immature gut and metabolism and may benefit from total parenteral nutrition (TPN) before enteral food is introduced. Conversely, delayed enteral feeding may inhibit gut maturation and sensitize to necrotizing enterocolitis (NEC). Intestinal mass and NEC lesions were first recorded in preterm pigs fed enterally (porcine colostrum, bovine colostrum, or formula for 20–40 h), with or without a preceding 2- to 3-day TPN period (n = 435). Mucosal mass increased during TPN and further after enteral feeding to reach an intestinal mass similar to that in enterally fed pigs without TPN (+60–80% relative to birth). NEC developed only after enteral feeding but more often after a preceding TPN period for both sow's colostrum (26 vs. 5%) and formula (62 vs. 39%, both P < 0.001, n = 43–170). Further studies in 3-day-old TPN pigs fed enterally showed that formula feeding decreased villus height and nutrient digestive capacity and increased luminal lactic acid and NEC lesions, compared with colostrum (bovine or porcine, P < 0.05). Mucosal microbial diversity increased with enteral feeding, and Clostridium perfringens density was related to NEC severity. Formula feeding decreased plasma arginine, citrulline, ornithine, and tissue antioxidants, whereas tissue nitric oxide synthetase and gut permeability increased, relative to colostrum (all P < 0.05). In conclusion, enteral feeding is associated with gut dysfunction, microbial imbalance, and NEC in preterm pigs, especially in pigs fed formula after TPN. Conversely, colostrum milk diets improve gut maturation and NEC resistance in preterm pigs subjected to a few days of TPN after birth.

neonate; colostrum; formula; intestine; bacterial colonization