Responses of Preterm Pigs Fed Bovine Colostrum and Formulas with either Lactose or Maltodextrin as the Sources of Carbohydrate

Abstract

Enteral nutrition is restricted for neonatal preterm infants because of the increased risk of necrotizing enterocolitis (NEC), particularly when breast milk is not available. However, prolonged reliance on parenteral nutrition is associated with other adverse outcomes. Despite interest in providing aggressive enteral nutritional support to realize the growth potential of the preterm infant, delayed advancement to full enteral nutrition support is common. This is especially true for the increasing numbers of infants that are now surviving birth at 28 weeks of gestation and earlier and are at greater risk of food intolerance and NEC. A consequence is extrauterine growth restriction remains prevalent among preterm infants, increasing the risk of intellectual and developmental disabilities. There is a need to improve enteral nutrition support for neonatal preterm infants when breast milk is not available. Because of the ethical constraints associated with using preterm infants as test subjects, we used preterm pigs relevant to 32 week preterm infants to evaluate survival, NEC incidence and severity, and growth to 6–7 days of feeding bovine colostrum (control) or one of two formulas with either lactose or maltodextrin as the source of carbohydrate (120 ml/kg‐d). At conclusion of the feeding regimen blood chemistries, intestinal dimensions and gross pathology, and weights of other organs were recorded, and rates of intestinal glucose uptake were measured as an indicator of small intestine digestive functions. Feeding the formula with maltodextrin resulted in a 50% incidence of NEC with 30% mortality. NEC was not detected among pigs fed colostrum or the lactose‐based milk replacer. Growth of pigs fed bovine colostrum was minimal or even negative (−0.70 ± 0.26) and was lower than growth of surviving pigs fed the formulas with maltodextrin or lactose (0.77 ± 0.27 and 0.93 ± 0.18). Significant treatment differences were detected for the majority of measured analytes. Notably were the higher sodium, chloride, blood urea nitrogen, and serum lipids of pigs fed colostrum compared with the pigs fed the two milk replacers. Pigs fed colostrum had heavier small intestines (g/kg; P<0.05), but not higher total small intestine capacities to transport glucose. Our findings indicate colostrum protects preterm pigs against NEC, but does not promote body weight gain or enhance intestinal absorption, and should not be used as a control for chronic feeding studies. Using maltodextrin, but not lactose in formula increases NEC risk. Preterm pigs are a relevant and translational large animal model for evaluating how carbohydrates and other nutrients influence NEC risk, growth, health, and development after preterm birth.