Location: Children's Nutrition Research CenterTitle: GLP-2 delays the onset but does not prevent NEC in preterm piglets) Author
|Burrin, Douglas - Doug|
Submitted to: Pediatric Research
Publication Type: Abstract Only
Publication Acceptance Date: 3/1/2010
Publication Date: 5/1/2010
Citation: Burrin, D.G., Stoll, B., Olutoye, O., Benight, N. 2010. GLP-2 delays the onset but does not prevent NEC in preterm piglets [abstract]. Pediatric Research. Paper No. 1458.63. Interpretive Summary:
Technical Abstract: Necrotizing enterocolitis (NEC) remains the most serious gastrointestinal disease in preterm infants. Total parenteral nutrition (TPN) prior to enteral formula feeding increases the NEC incidence in preterm pigs (Bjornvad et al. Am J Physiol, 295:G1092). TPN reduces intestinal blood flow and leads to epithelial cell hypoxia and inflammation. Glucagon-like peptide 2 (GLP-2) is a trophic gut hormone that potently stimulates blood flow and induces anti-inflammatory actions in the intestine. We tested the hypothesis that GLP-2 treatment during TPN and enteral feeding periods would reduce the NEC incidence in preterm pigs. We studied 12-day preterm pigs (n=12/group) given either complete TPN or TPN+GLP-2 (100 ug/kg/d) given continuously, i.v. for 2-d after birth then fed formula enterally for 24-48 hrs. GLP-2 was continued i.v. during formula feeding. The GLP-2 treatment prolonged mean survival time (41 v. 29 hr) during the 48 hr after formula feeding. However, after 48 hr formula feeding, the NEC incidence (67% vs. 75%), clinical severity scores (12.7 vs. 15.5), and histological severity scores (1.7 vs. 2.0) were not different in GLP-2 and control pigs, respectively. GLP-2 increased mucosal weight and villus height in the proximal and distal small intestine, but reduced stomach weight compared to control pigs. We concluded that treatment with GLP-2 during a period of TPN induced trophic effects in the preterm intestine. However, GLP-2 only delayed the onset of NEC and did not have a preventive effect on this serious inflammatory disease in the preterm intestine.