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Formula induces intestinal apoptosis in preterm pigs within a few hours of feeding
Marijke Oste1, Els Van Haver, Thomas Thymann
1Laboratory of Veterinary Anatomy and Embryology, Department of Veterinary Medicine, University of Antwerp, Belgium.
Insights
Early enteral nutrition, especially formula, can rapidly alter gut structure in preterm neonates, potentially increasing the risk of necrotizing enterocolitis (NEC). This highlights the critical role of nutrition in developing gastrointestinal health.
Area of Science:
- Neonatal physiology
- Gastroenterology
- Developmental biology
Background:
- Postnatal intestinal development is sensitive to nutrition.
- Preterm neonates are at high risk for gastrointestinal disorders like necrotizing enterocolitis (NEC).
- Early feeding responses are crucial for preventing NEC in vulnerable infants.
Purpose of the Study:
- To investigate early morphological responses to enteral nutrition in preterm piglets.
- To assess the impact of short-term enteral feeding on intestinal development.
- To correlate feeding strategies with NEC development markers.
Main Methods:
- Preterm piglets received parenteral nutrition (PN) followed by short enteral nutrition (EN) periods with colostrum or formula.
- Stereological measurements assessed mucosal surface density, cell proliferation, and apoptosis.
- Villus length, crypt depth, and NEC lesion scores were analyzed.
Main Results:
- Parenteral nutrition alone caused minimal mucosal atrophy but altered crypt depth and cell turnover.
- Eight hours of colostrum feeding rapidly increased mucosal volume.
- Formula feeding increased proliferating and apoptotic cells, correlating with higher NEC scores.
Conclusions:
- Short-term formula feeding induces rapid enterocyte turnover and mucosal changes.
- These rapid structural alterations may predispose preterm neonates to NEC.
- Early nutritional interventions require careful consideration in preterm infant feeding.
Background:
Nutrition regimens influence postnatal small intestinal development, which shows prominent changes after 6 hours of suckling. Such influences are particularly important in preterm neonates as inappropriate feeding responses may predispose to gastrointestinal disorders such as necrotizing enterocolitis (NEC). The authors investigated the early morphological responses to enteral feeding, prior to the time period when a large proportion of preterm pigs normally develop clinical NEC symptoms.
Methods:
Preterm piglets (106-107 days of gestation) were fed parenteral nutrition (PN) for 2 days with or without a subsequent 8-hour or 17-hour period of enteral nutrition (EN) with sow's colostrum or formula. Another group of piglets was delivered at 108-109 days of gestation and used for comparison to PN pigs before enteral feeding. Stereological measurements of the mucosal surface density and the volume densities of the tunica mucosa, tunica muscularis, proliferative, and apoptotic cells were made and related to microscopical NEC-lesion score. In addition, villus length and crypt depth were measured.
Results:
PN-fed piglets showed minimal PN-induced mucosal atrophy, although their crypts were deeper, together with lower cell proliferation and higher apoptotic indices, than newborn (NB) unfed piglets. After PN, enteral feeding with colostrum, for just 8 hours, induced a rapid increase in the mucosal volume density while formula feeding was associated with an elevated number of both proliferating and apoptotic cells and a higher NEC lesion score than PN- or colostrum-fed pigs.
Conclusion:
Enteral feeding of formula, for only a few hours, induces rapid enterocyte turnover and mucosal structural changes that may predispose to later development of NEC.
