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1 Division of Animal Nutrition, The Royal Veterinary and Agricultural University, Frederiksberg, Denmark
2 Division of Reproduction, The Royal Veterinary and Agricultural University, Frederiksberg, Denmark
3 Danish Institute of Agricultural Sciences, Tjele, Denmark
4 Division of Anatomy, The Royal Veterinary and Agricultural University, Frederiksberg, Denmark
* To whom correspondence should be addressed. E-mail: psa{at}kvl.dk.
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 affects the response of the immature intestine to enteral feeding. Pig fetuses (106 d gestation, term=115 d) were prepared with oesophageal 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 (F) were delivered by caesarean section and their gastrointestinal morphology and function was compared with that of preterm newborn (NB) littermates, 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 (GLP-2) concentrations, to levels similar to those in NB colostrum fed piglets. In contrast, NB formula fed pigs showed reduced intestinal growth, decreased brush-border enzyme activities and intestinal lesions, reflecting necrotising enterocolitis (NEC). NB formula fed pigs also showed impaired enterocyte endocytotic function and decreased antioxidative capacity, while 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 is not birth-dependent. However, when feeding a suboptimal diet (milk formula), factors related to preterm birth (e.g. microbial colonization, metabolic and endocrine changes), make the immature intestine sensitive to atrophy and development of NEC.
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