Maturation of gastrointestinal (GI) function in neonates is stimulated by enteral nutrition, whereas parenteral nutrition induces GI atrophy and malfunction. We investigated whether preterm birth alters the GI responses to parenteral and enteral nutrition. Pigs were delivered either preterm (107 d gestation) or at term (115 d gestation) and fed total parenteral nutrition (TPN) or enteral sow's milk (ENT) for 6 d after birth. Immaturity of the preterm pigs was documented by reduced blood pH, oxygen saturation and neutrophil granulocyte function, impaired intestinal immunoglobulin G uptake from colostrum, and altered relative weights of visceral organs (small intestine, liver, spleen, pancreas, and adrenals). For both ages at delivery, increases occurred in pancreatic weight (30-75%) and amylase activity (0.5- to 13-fold) after birth, but much more in ENT than in TPN pigs (P < 0.05). Six days of TPN feeding was associated with reduced intestinal weight for both delivery groups (60% of values in ENT, P < 0.001), but only in term TPN pigs was the weight lower than at birth (-20%, P < 0.05). Likewise, it was only in term TPN pigs that intestinal maltase activity increased, compared with ENT, and the absorption of glucose and proline decreased. Only in preterm pigs did TPN feeding increase lactase activity (+50% compared with ENT, P < 0.05). For both delivery ages, the mRNA of lactase-phloridzin hydrolase and sodium-coupled glucose transporter 1 were increased in TPN, compared with ENT. In conclusion, the trophic effect of enteral vs. parenteral nutrition on the GI tract is also present after preterm birth, but the postnatal maturation of many GI functions is modified, compared with term birth. The effects of nutritional regimen on the maturation of the gut epithelium in neonates depend on gestational age at birth.
Uptake of colostrum just after birth is essential to stimulate intestinal growth and function, and in many species, including pigs, colostrum also provides immunological protection via the absorption of immunoglobulin G (IgG). In this study, intestinal growth, IgG absorptive capacity and enzyme activities were investigated in newborn pigs in response to different diets. Newborn piglets were bottle-fed porcine colostrum (PC), bovine colostrum (BC), porcine plasma (PP), porcine milk (PM), bovine colostrum containing porcine plasma (BCP) or a milk replacer (MR) every 3 h (15 mL/kg) for up to 2 d. Bovine serum albumin (BSA) was added to the diets as a macromolecule marker. The percentage of absorbed BSA just after birth was highest for piglets fed the PC diet (30-50%), lower for those fed the BC and BCP diets (23-30%) and lowest for the PP, PM and MR diet-fed piglets (7-20%, P < 0.05 relative to those fed colostrum). Porcine IgG was absorbed more efficiently than bovine IgG. Intestinal closure occurred earlier in MR and BCP piglets (within 12 h after birth) than in PC pigs. At 2 d of age, intestinal mucosal weight (+120% increase from birth) and villus morphology were similar in the PC, BCP and MR groups. All 3 groups also had increased aminopeptidase A activity compared with values at birth (+100% increase). Compared with PC pigs, the BCP group had higher sucrase and maltase activities (+50% and +200%, respectively) and lower aminopeptidase N activity (-50%, P < 0.05). Similarly, MR pigs showed elevated sucrase activity (+40%) and lowered maltase, lactase and aminopeptidase N activities (-20% to -50%, P < 0.05) compared with PC pigs. We conclude that porcine and bovine colostrum contain factors that stimulate the intestinal endocytotic and enzymatic capacity in newborn pigs. A milk replacer can produce normal gut growth, but may be inefficient in mediating normal macromolecule transport and disaccharidase activity. Bovine colostrum mixed with porcine plasma proteins may be a useful substitute for porcine colostrum in artificial rearing of newborn pigs.
We wished to determine whether exogenous glucagon-like peptide (GLP)-2 infusion stimulates intestinal growth in parenterally fed immature pigs. Piglets (106-108 days gestation) were given parenteral nutrient infusion (TPN), TPN + human GLP-2 (25 nmol. kg(-1). day(-1)), or sow's milk enterally (ENT) for 6 days. Intestinal protein synthesis was then measured in vivo after a bolus dose of [1-(13)C]phenylalanine, and degradation was calculated from the difference between protein accretion and synthesis. Crypt cell proliferation and apoptosis were measured in situ by 5-bromodeoxyuridine (BrdU) and terminal dUTP nick-end labeling (TUNEL), respectively. Intestinal protein and DNA accretion rates and villus heights were similar in GLP-2 and ENT pigs, and both were higher (P < 0.05) than in TPN pigs. GLP-2 decreased fractional protein degradation rate, whereas ENT increased fractional protein synthesis rate compared with TPN pigs. Percentage of TUNEL-positive cells in GLP-2 and ENT groups was 48 and 64% lower, respectively, than in TPN group (P < 0.05). However, ENT, but not GLP-2, increased percentage of BrdU-positive crypt cells above that in TPN piglets. We conclude that GLP-2 increases intestinal growth in premature, TPN-fed pigs by decreasing proteolysis and apoptosis, whereas enteral nutrition acts via increased protein synthesis and cell proliferation and decreased apoptosis.
Preterm birth and formula feeding predispose to small intestinal dysfunction, which may lead to necrotizing enterocolitis (NEC). In piglets, we tested whether the physiological and environmental transitions occurring at birth affect the response of the immature intestine to enteral feeding. Pig fetuses (106 days gestation, term = 115 days) were prepared with esophageal feeding tubes and fed either sow's colostrum (n = 8) or infant formula (n = 7) in utero. After 24 h of oral feeding, the pig fetuses were delivered by cesarean section and their gastrointestinal morphology and function were compared with those of preterm newborn (NB) littermates that were not fed (n = 8) or fed colostrum (n = 7) or formula (n = 13) for 24 h after birth. Before birth, both colostrum and formula feeding resulted in marked increases in intestinal mass, brush-border enzyme activities, and plasma glucagon-like peptide 2 concentrations, to levels similar to those in NB colostrum-fed piglets. In contrast, NB formula-fed piglets showed reduced intestinal growth, decreased brush-border enzyme activities, and intestinal lesions, reflecting NEC. NB formula-fed pigs also showed impaired enterocyte endocytotic function and decreased antioxidative capacity, whereas brush-border enzyme mRNA levels were unaltered, relative to NB colostrum-fed pigs. Our results indicate that the feeding-induced growth and enzyme maturation of the immature intestine are not birth dependent. However, with a suboptimal diet (milk formula), factors related to preterm birth (e.g., microbial colonization and metabolic and endocrine changes) make the immature intestine sensitive to atrophy and development of NEC.
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