Premature delivery reduces intestinal cytoskeleton, metabolism, and stress response proteins in newborn formula-fed pigs.
OBJECTIVE
Preterm infants often show intolerance to the first enteral feeds, and the structural and functional basis of this intolerance remains unclear. We hypothesized that preterm and term neonates show similar gut trophic responses to feeding but different expression of intestinal functional proteins, thus helping to explain why preterm neonates are more susceptible to feeding-induced disorders such as necrotizing enterocolitis (NEC).


METHODS
Incidence of feeding-induced NEC, intestinal mass, and brush border enzyme activities, and the intestinal proteome in preterm cesarean-delivered pigs were compared with the corresponding values in pigs delivered spontaneously at term.


RESULTS
For both preterm and term pigs, mucosal mass and maltase activity increased (50%-100%), whereas lactase decreased (-50%), relative to values at birth. Only preterm pigs were highly NEC sensitive (30% vs 0% in term pigs, P < 0.05). By gel-based proteomics, 36 identified proteins differed in expression, with most proteins showing downregulation in preterm pigs, including proteins related to intestinal structure and actin filaments, stress response, protein processing, and nutrient metabolism.


CONCLUSIONS
Despite that enteral feeding induces rapid gut tropic response in both term and preterm neonates, the expression level of cellular proteins related to mucosal integrity, metabolism, and stress response differed markedly (including complement 3, prohibitin, ornithine carbamoyltransferase, and arginosuccinate synthetase). These proteins may play a role in the development of functional gut disorders and NEC in preterm neonates.
School of Biological Sciences, University of Hong Kong, Hong Kong SAR, China.
Pingping
P
Jiang
Jennifer Man-Fan
JM
Wan
Malene S
MS
Cilieborg
Wai-Hung
WH
Sit
Per Torp
PT
Sangild
D000818:Animals; D000831:Animals, Newborn; D002585:Cesarean Section; D003433:Crosses, Genetic; D003598:Cytoskeletal Proteins / Q000096:biosynthesis / Q000737:chemistry / Q000378:metabolism*; D003718:Denmark; D004195:Disease Models, Animal; D004198:Disease Susceptibility / Q000209:etiology / Q000378:metabolism / Q000473:pathology; D020345:Enterocolitis, Necrotizing / Q000209:etiology / Q000378:metabolism / Q000473:pathology; D005260:Female; D005526:Food, Formulated; D018507:Gene Expression Regulation, Developmental; D006360:Heat-Shock Proteins / Q000096:biosynthesis* / Q000737:chemistry / Q000378:metabolism; D007413:Intestinal Mucosa / Q000201:enzymology / Q000378:metabolism* / Q000473:pathology; D007421:Intestine, Small / Q000201:enzymology / Q000378:metabolism* / Q000473:pathology; D008297:Male; D009929:Organ Size; D011247:Pregnancy; D047928:Premature Birth / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D034421:Sus scrofa
D003598:Cytoskeletal Proteins; D006360:Heat-Shock Proteins