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Published on: June 24, 2020
Preterm birth makes the immature intestine sensitive to feeding-induced intestinal atrophy
Charlotte Reinhard Bjornvad1, Mette Schmidt, Yvette Miata Petersen
1Department of Human Nutrition, Royal Veterinary and Agricultural University, Rolighedsvej 30, DK-1958 Frederiksberg C., Denmark.
Insights
Preterm birth and formula feeding can harm the immature gut, increasing necrotizing enterocolitis (NEC) risk. However, intestinal development is not birth-dependent, but preterm birth factors with suboptimal diets increase NEC vulnerability.
Area of Science:
- Neonatal physiology
- Gastroenterology
- Developmental biology
Background:
- Preterm birth and formula feeding are risk factors for small intestinal dysfunction and necrotizing enterocolitis (NEC).
- The impact of birth-related physiological and environmental changes on the immature intestine's response to feeding is not fully understood.
Purpose of the Study:
- To investigate how physiological and environmental transitions at birth influence the immature intestine's response to enteral feeding in piglets.
- To compare the effects of in-utero feeding versus postnatal feeding with either sow's colostrum or infant formula.
Main Methods:
- Pig fetuses were fed sow's colostrum or infant formula in utero via esophageal tubes.
- Postnatally, fetuses were delivered and their gastrointestinal morphology and function compared with preterm newborn littermates fed colostrum or formula.
- Measurements included intestinal mass, brush-border enzyme activities, plasma glucagon-like peptide 2, enterocyte function, and antioxidative capacity.
Main Results:
- In-utero feeding with either colostrum or formula increased intestinal mass and enzyme activity to levels similar to colostrum-fed newborns.
- Postnatal formula feeding in preterm piglets led to reduced intestinal growth, decreased enzyme activity, intestinal lesions (NEC), impaired enterocyte function, and reduced antioxidative capacity.
- Brush-border enzyme mRNA levels were not significantly different between formula-fed and colostrum-fed preterm piglets.
Conclusions:
- Feeding-induced growth and enzyme maturation of the immature intestine are not dependent on the timing of birth.
- Suboptimal diets (infant formula) combined with factors of preterm birth (microbial, metabolic, endocrine changes) sensitize the immature intestine to atrophy and NEC development.
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.
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