Mode of delivery affects diet‐induced small intestine atrophy and dysfunction in preterm pigs

Abstract

In preterm neonates, total parenteral nutrition (TPN) followed by formula feeding can cause small intestinal (SI) mucosal atrophy and dysfunction, potentially leading to necrotizing enterocolitis (NEC). It is unknown if this susceptibility is affected by mode of delivery at birth. In contrast to cesarean delivery, vaginally delivered neonates are exposed to elevated levels of glucocorticoids, putative stimulators of SI development, and a more stable maternally influenced microbiota. A preterm pig model was used to determine if vaginal delivery could prevent TPN and formula induced SI atrophy and dysfunction. Preterm pigs (93% gestation) were delivered vaginally (VD) or via cesarean section (CS), maintained on TPN for 36 hours, then fed sow's colostrum (COL) or infant milk formula (FORM) for 48 hours. NEC lesions were increased in FORM groups, and minimal in COL groups. Relative to VD-FORM, distal SI villus heights increased 14% in CS-FORM and VD-COL and increased 43% (P<0.05) in CS-COL. Relative dry weights of the SI mucosal layer were lower (10–14%, P<0.01) in VD-FORM pigs compared to other treatment groups. Compared to VD-FORM, aminopeptidases A and N activities were increased in VD-COL and CS-FORM (20-25%) and increased in CS-COL (37%, P<0.05). Lactase and maltase activities were lowest in VD-FORM, higher in CS-FORM (22–27%), and highest in both COL groups (45–50%, P<0.01). TPN and formula induced SI atrophy and dysfunction was most pronounced in vaginally delivered pigs compared to cesarean delivered pigs. The premature SI may be more susceptible and respond inappropriately to the endocrine changes and microbial colonization patterns of vaginal delivery.