OBJECTIVE: Elucidating why intrauterine growth restriction (IUGR) predisposes to some intestinal pathologies would help in their prevention. Intestinal microbiota could be involved in this predisposition; its initial setup is likely to be altered by IUGR because IUGR delays perinatal intestinal development and strongly interacts with intestinal physiology. Furthermore, because initial colonization determines adult intestinal microbiota, an IUGR-induced defect in initial microbiota would have long-term consequences. Thus, to characterize the effect of IUGR on intestinal microbiota, we compared the composition and activity of cecocolonic microbiota from birth to adulthood in rats with and without IUGR. MATERIALS AND METHODS: IUGR was induced by gestational isocaloric protein restriction. Pups were fed by unrestricted lactating mothers. At different ages (days 5, 12, 16, 22, 40, and 100), cecocolonic contents from rats with IUGR and controls were analyzed for concentrations of bacterial end products and numbers of main bacterial groups, and submitted to in vitro fermentation tests. RESULTS: IUGR affected gut colonization: bacterial density was increased at day 5 and decreased at day 12. In adulthood, rats with IUGR still differed from controls, harboring fewer Bifidobacterium sp at day 40 and more bacteria related to Roseburia intestinalis at day 100. In vivo, propionate concentration was decreased by IUGR before weaning, whereas the concentrations of other short-chain fatty acids were decreased at day 40, although the in vitro metabolic capability was unaffected overall. CONCLUSIONS: We showed that IUGR induced, per se, some neonatal and long-lasting alterations of the intestinal microbiota. The physiological consequences of these changes and their relation to the predisposing effect of IUGR to gut pathologies must now be explored.
OBJECTIVE: Elucidating why intrauterine growth restriction (IUGR) predisposes to some intestinal pathologies would help in their prevention. Intestinal microbiota could be involved in this predisposition; its initial setup is likely to be altered by IUGR because IUGR delays perinatal intestinal development and strongly interacts with intestinal physiology. Furthermore, because initial colonization determines adult intestinal microbiota, an IUGR-induced defect in initial microbiota would have long-term consequences. Thus, to characterize the effect of IUGR on intestinal microbiota, we compared the composition and activity of cecocolonic microbiota from birth to adulthood in rats with and without IUGR. MATERIALS AND METHODS: IUGR was induced by gestational isocaloric protein restriction. Pups were fed by unrestricted lactating mothers. At different ages (days 5, 12, 16, 22, 40, and 100), cecocolonic contents from rats with IUGR and controls were analyzed for concentrations of bacterial end products and numbers of main bacterial groups, and submitted to in vitro fermentation tests. RESULTS: IUGR affected gut colonization: bacterial density was increased at day 5 and decreased at day 12. In adulthood, rats with IUGR still differed from controls, harboring fewer Bifidobacterium sp at day 40 and more bacteria related to Roseburia intestinalis at day 100. In vivo, propionate concentration was decreased by IUGR before weaning, whereas the concentrations of other short-chain fatty acids were decreased at day 40, although the in vitro metabolic capability was unaffected overall. CONCLUSIONS: We showed that IUGR induced, per se, some neonatal and long-lasting alterations of the intestinal microbiota. The physiological consequences of these changes and their relation to the predisposing effect of IUGR to gut pathologies must now be explored.
Authors: Andrea G Braundmeier; Katherine M Lenz; Kristin S Inman; Nicholas Chia; Patricio Jeraldo; Marina R S Walther-António; Margret E Berg Miller; Fang Yang; Douglas J Creedon; Heidi Nelson; Bryan A White Journal: Front Physiol Date: 2015-04-01 Impact factor: 4.566