maltodextrin has been researched along with Enterocolitis--Necrotizing* in 3 studies
3 other study(ies) available for maltodextrin and Enterocolitis--Necrotizing
Article | Year |
---|---|
Maltodextrin-induced intestinal injury in a neonatal mouse model.
Prematurity and enteral feedings are major risk factors for intestinal injury leading to necrotizing enterocolitis (NEC). An immature digestive system can lead to maldigestion of macronutrients and increased vulnerability to intestinal injury. The aim of this study was to test in neonatal mice the effect of maltodextrin, a complex carbohydrate, on the risk of intestinal injury. The goal was to develop a robust and highly reproducible murine model of intestinal injury that allows insight into the pathogenesis and therapeutic interventions of nutrient-driven intestinal injury. Five- to 6-day-old C57BL/6 mice were assigned to the following groups: dam fed (D); D+hypoxia+ Topics: Animals; Animals, Newborn; Cytokines; Disease Models, Animal; Enterocolitis, Necrotizing; Goblet Cells; Hypoxia; Inflammation Mediators; Intestinal Mucosa; Intestine, Small; Klebsiella pneumoniae; Mice, Inbred C57BL; Microvilli; Mucin-2; Permeability; Polysaccharides; Tight Junction Proteins | 2020 |
The Risk of Necrotizing Enterocolitis Differs Among Preterm Pigs Fed Formulas With Either Lactose or Maltodextrin.
When breast milk is unavailable for preterm infants, formulas are needed that won't increase the risk of necrotizing enterocolitis (NEC). Adding novel ingredients to formula to reduce NEC has not been effective clinically. Instead, we tested the prediction that NEC can be reduced by removing the maltodextrin now included in preterm formulas.. The preterm pig model of spontaneous NEC was used to evaluate growth, health, and intestinal responses to 6 to 7 days of feeding formulas that were identical except for the source of carbohydrate; either 100% lactose or maltodextrin; colostrum was used as the control.. Formula with maltodextrin resulted in a 50% incidence of NEC with 30% mortality. The lactose formula and colostrum resulted in a 0% incidence of NEC. Growth was highest for pigs fed the formula with lactose, intermediate with maltodextrin, and minimal when bovine colostrum was fed (P < 0.05). Although the small intestine was larger when colostrum was fed (P < 0.05), because rates of glucose uptake were lower (P < 0.05), total small intestine capacities to transport glucose were similar for healthy pigs in all 3 groups.. If lactose-based formulas reduce NEC clinically, the transition of preterm infants to enteral feeding can be accelerated, improving growth and development, and shortening reliance on parenteral nutrition. Although colostrum protects against NEC, chronic feeding does not promote body weight gain after preterm birth. The preterm pig can be used for preclinical studies that evaluate the mechanisms by which carbohydrates and other ingredients influence growth, development, health, and risk of NEC. Topics: Animals; Animals, Newborn; Colostrum; Enterocolitis, Necrotizing; Female; Humans; Incidence; Infant Formula; Infant, Newborn; Infant, Premature; Infant, Premature, Diseases; Lactose; Male; Polysaccharides; Risk Factors; Swine; Treatment Outcome | 2018 |
Carbohydrate maldigestion induces necrotizing enterocolitis in preterm pigs.
Necrotizing enterocolitis (NEC) remains the most severe gastrointestinal disorder in preterm infants. It is associated with the initiation of enteral nutrition and may be related to immature carbohydrate digestive capacity. We tested the hypothesis that a formula containing maltodextrin vs. a formula containing lactose as the principal source of carbohydrate would predispose preterm pigs to a higher NEC incidence. Cesarean-derived preterm pigs were given total parenteral nutrition for 48 h followed by total enteral nutrition with a lactose-based (n = 11) or maltodextrin-based (n = 11) formula for 36 h. A higher incidence (91% vs. 27%) and severity (score of 3.3 vs. 1.8) of NEC were observed in the maltodextrin than in the lactose group. This higher incidence of NEC in the maltodextrin group was associated with significantly lower activities of lactase, maltase, and aminopeptidase; reduced villus height; transiently reduced in vivo aldohexose uptake; and reduced ex vivo aldohexose uptake capacity in the middle region of the small intestine. Bacterial diversity was low for both diets, but alterations in bacterial composition and luminal concentrations of short-chain fatty acids were observed in the maltodextrin group. In a second study, we quantified net portal absorption of aldohexoses (glucose and galactose) during acute jejunal infusion of a maltodextrin- or a lactose-based formula (n = 8) into preterm pigs. We found lower net portal aldohexose absorption (4% vs. 42%) and greater intestinal recovery of undigested carbohydrate (68% vs. 27%) in pigs acutely perfused with the maltodextrin-based formula than those perfused with the lactose-based formula. The higher digestibility of the lactose than the maltodextrin in the formulas can be attributed to a 5- to 20-fold higher hydrolytic activity of tissue-specific lactase than maltases. We conclude that carbohydrate maldigestion is sufficient to increase the incidence and severity of NEC in preterm pigs. Topics: alpha-Glucosidases; Aminopeptidases; Animal Nutritional Physiological Phenomena; Animals; Animals, Newborn; Cesarean Section; Digestion; Disease Models, Animal; Enteral Nutrition; Enterocolitis, Necrotizing; Galactose; Glucose; Humans; Hydrolysis; Infant Formula; Infant, Newborn; Intestinal Absorption; Intestines; Lactase; Lactose; Parenteral Nutrition; Polysaccharides; Premature Birth; Severity of Illness Index; Swine; Time Factors | 2009 |