title: Intrauterine growth restriction delays feeding-induced gut adaptation in term newborn pigs.
abstract: BACKGROUND
  Neonates born after intrauterine growth restriction (IUGR) show higher mortality and morbidity and greater feeding problems postnatally.
  
  
  OBJECTIVE
  We tested the hypothesis that IUGR affects the intestinal structure, function, microbiology and proinflammatory cytokine expression during the immediate neonatal period.
  
  
  METHODS
  We firstly compared organ weights and intestinal digestive enzyme activities between control and IUGR newborn piglets delivered by cesarean section at full term or prematurely (91% gestation). Next, we compared intestinal structure, function and microbiota in spontaneously delivered control and IUGR term piglets during the period 0-5 days of age, when intestinal adaptation is normally very rapid.
  
  
  RESULTS
  At the time of birth, organ weights and intestinal enzyme activities were not notably affected by IUGR, neither for preterm nor term pigs, except that IUGR was associated with a relatively long and thin intestine. Between birth and 5 days of age, the normal developmental pattern in the ileum and colon appeared to be delayed in term IUGR piglets, as indicated by lower ileal density (weight per unit length) and villous area (-20 to -30%), higher expression of the peptide transporter PEPT1 (+150% on day 2) and enhanced bacterial adhesion and translocation during days 2-5 (all p < 0.05). Further, expression of the proinflammatory cytokine IL-6 was modified in the intestine of term IUGR piglets at birth without any change in IL-1β.
  
  
  CONCLUSIONS
  IUGR is associated with a longer and thinner intestine at birth, and during the immediate postnatal period, intestinal adaptation and bacterial colonization are altered in IUGR piglets born at full term.
authors.affiliation: INRA, UMR 1079, SENAH, Saint-Gilles, France.
authors.forename: Romain
authors.initials: R
authors.lastname: D'Inca
authors.forename: Christèle
authors.initials: C
authors.lastname: Gras-Le Guen
authors.forename: Lianqiang
authors.initials: L
authors.lastname: Che
authors.forename: Per T
authors.initials: PT
authors.lastname: Sangild
authors.forename: Isabelle
authors.initials: I
authors.lastname: Le Huërou-Luron
mesh_terms: D000222:Adaptation, Physiological; D000818:Animals; D000831:Animals, Newborn; D001724:Birth Weight; D015169:Colony Count, Microbial; D005260:Female; D005317:Fetal Growth Retardation / Q000378:metabolism* / Q000382:microbiology; D041981:Gastrointestinal Tract / Q000201:enzymology / Q000378:metabolism* / Q000382:microbiology; D006651:Histocytochemistry; D042845:Laccase / Q000378:metabolism; D010447:Peptide Hydrolases / Q000378:metabolism; D000074011:Peptide Transporter 1; D011247:Pregnancy; D012313:RNA / Q000737:chemistry / Q000235:genetics; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013393:Sucrase / Q000378:metabolism; D013552:Swine; D027981:Symporters / Q000235:genetics / Q000378:metabolism*; D000520:alpha-Glucosidases / Q000378:metabolism
chemical_list: D000074011:Peptide Transporter 1; D027981:Symporters; D012313:RNA; D042845:Laccase; D000520:alpha-Glucosidases; D013393:Sucrase; D010447:Peptide Hydrolases