Aldohexose malabsorption in preterm pigs is directly related to the severity of necrotizing enterocolitis.

Necrotizing enterocolitis (NEC) causes morbidity and mortality among preterm infants and is associated with nutrient malabsorption. Therefore, a preterm pig model that spontaneously develops NEC was used to investigate the relationship between severity of NEC lesions and galactose absorption in vivo and carrier-mediated glucose absorption by intact mid small intestine. Preterm pigs collected by caesarian section at 92% of gestation received parenteral nutrition with and without minimal enteral nutrition for 48 h before conversion to enteral nutrition with colostrum or an enteral formula. Pigs were killed when symptoms of NEC were observed or after 36-40 h of enteral nutrition. NEC lesions decreased in vivo absorption of galactose and mannitol by more than 50% and abolished carrier-mediated glucose uptake by tissues with lesions. Moreover, when NEC lesions were restricted to the colon, small intestinal tissues that seemed clinically healthy had decreased in vitro glucose absorption due to reduced uptake via the sodium-dependent glucose transporter with little or no involvement of the apical facilitative glucose carrier. The present findings reveal a direct relationship between the severity of NEC lesions and the magnitude of sugar malabsorption that is detectable before clinical symptoms are evident.