title: Preterm birth makes the immature intestine sensitive to feeding-induced intestinal atrophy.
abstract: Preterm birth and formula feeding predispose to small intestinal dysfunction, which may lead to necrotizing enterocolitis (NEC). In piglets, we tested whether the physiological and environmental transitions occurring at birth affect the response of the immature intestine to enteral feeding. Pig fetuses (106 days gestation, term = 115 days) were prepared with esophageal feeding tubes and fed either sow's colostrum (n = 8) or infant formula (n = 7) in utero. After 24 h of oral feeding, the pig fetuses were delivered by cesarean section and their gastrointestinal morphology and function were compared with those of preterm newborn (NB) littermates that were not fed (n = 8) or fed colostrum (n = 7) or formula (n = 13) for 24 h after birth. Before birth, both colostrum and formula feeding resulted in marked increases in intestinal mass, brush-border enzyme activities, and plasma glucagon-like peptide 2 concentrations, to levels similar to those in NB colostrum-fed piglets. In contrast, NB formula-fed piglets showed reduced intestinal growth, decreased brush-border enzyme activities, and intestinal lesions, reflecting NEC. NB formula-fed pigs also showed impaired enterocyte endocytotic function and decreased antioxidative capacity, whereas brush-border enzyme mRNA levels were unaltered, relative to NB colostrum-fed pigs. Our results indicate that the feeding-induced growth and enzyme maturation of the immature intestine are not birth dependent. However, with a suboptimal diet (milk formula), factors related to preterm birth (e.g., microbial colonization and metabolic and endocrine changes) make the immature intestine sensitive to atrophy and development of NEC.
authors.affiliation: Department of Human Nutrition, Royal Veterinary and Agricultural University, Rolighedsvej 30, DK-1958 Frederiksberg C., Denmark.
authors.forename: Charlotte Reinhard
authors.initials: CR
authors.lastname: Bjornvad
authors.forename: Mette
authors.initials: M
authors.lastname: Schmidt
authors.forename: Yvette Miata
authors.initials: YM
authors.lastname: Petersen
authors.forename: Søren Krogh
authors.initials: SK
authors.lastname: Jensen
authors.forename: Hanne
authors.initials: H
authors.lastname: Offenberg
authors.forename: Jan
authors.initials: J
authors.lastname: Elnif
authors.forename: Per Torp
authors.initials: PT
authors.lastname: Sangild
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D001284:Atrophy; D053767:Glucagon-Like Peptide 2; D004763:Glucagon-Like Peptides; D041943:Infant Formula / Q000008:administration & dosage*; D007421:Intestine, Small / Q000196:embryology / Q000254:growth & development / Q000378:metabolism* / Q000473:pathology*; D009929:Organ Size / Q000187:drug effects; D010455:Peptides / Q000378:metabolism*; D047928:Premature Birth / Q000150:complications / Q000378:metabolism* / Q000473:pathology*; D013552:Swine; D014810:Vitamin E / Q000378:metabolism*
chemical_list: D053767:Glucagon-Like Peptide 2; D010455:Peptides; D014810:Vitamin E; D004763:Glucagon-Like Peptides