title: Modulation of the gut microbiota with antibiotic treatment suppresses whole body urea production in neonatal pigs.
abstract: We examined whether changes in the gut microbiota induced by clinically relevant interventions would impact the bioavailability of dietary amino acids in neonates. We tested the hypothesis that modulation of the gut microbiota in neonatal pigs receiving no treatment (control), intravenously administered antibiotics, or probiotics affects whole body nitrogen and amino acid turnover. We quantified whole body urea kinetics, threonine fluxes, and threonine disposal into protein, oxidation, and tissue protein synthesis with stable isotope techniques. Compared with controls, antibiotics reduced the number and diversity of bacterial species in the distal small intestine (SI) and colon. Antibiotics decreased plasma urea concentrations via decreased urea synthesis. Antibiotics elevated threonine plasma concentrations and turnover, as well as whole body protein synthesis and proteolysis. Antibiotics decreased protein synthesis rate in the proximal SI and liver but did not affect the distal SI, colon, or muscle. Probiotics induced a bifidogenic microbiota and decreased plasma urea concentrations but did not affect whole body threonine or protein metabolism. Probiotics decreased protein synthesis in the proximal SI but not in other tissues. In conclusion, modulation of the gut microbiota by antibiotics and probiotics reduced hepatic ureagenesis and intestinal protein synthesis, but neither altered whole body net threonine balance. These findings suggest that changes in amino acid and nitrogen metabolism resulting from antibiotic- or probiotic-induced shifts in the microbiota are localized to the gut and liver and have limited impact on whole body growth and anabolism in neonatal piglets.
authors.affiliation: Pediatrics, Neonatology, Erasmus Medical College, Sophia Children's Hospital, Rotterdam, The Netherlands.
authors.forename: Patrycja
authors.initials: P
authors.lastname: Puiman
authors.forename: Barbara
authors.initials: B
authors.lastname: Stoll
authors.forename: Lars
authors.initials: L
authors.lastname: Mølbak
authors.forename: Adrianus
authors.initials: A
authors.lastname: de Bruijn
authors.forename: Henk
authors.initials: H
authors.lastname: Schierbeek
authors.forename: Mette
authors.initials: M
authors.lastname: Boye
authors.forename: Günther
authors.initials: G
authors.lastname: Boehm
authors.forename: Ingrid
authors.initials: I
authors.lastname: Renes
authors.forename: Johannes
authors.initials: J
authors.lastname: van Goudoever
authors.forename: Douglas
authors.initials: D
authors.lastname: Burrin
mesh_terms: D000596:Amino Acids / Q000097:blood / Q000378:metabolism; D000818:Animals; D000831:Animals, Newborn / Q000378:metabolism*; D000900:Anti-Bacterial Agents / Q000494:pharmacology*; D001644:Bifidobacterium / Q000502:physiology; D015153:Blotting, Western; D001835:Body Weight / Q000502:physiology; D041981:Gastrointestinal Tract / Q000187:drug effects* / Q000382:microbiology*; D007150:Immunohistochemistry; D007700:Kinetics; D054892:Metagenome / Q000187:drug effects*; D055262:Mucin-2 / Q000096:biosynthesis / Q000302:isolation & purification; D009077:Mucins / Q000096:biosynthesis; D009584:Nitrogen / Q000378:metabolism; D009929:Organ Size / Q000502:physiology; D010084:Oxidation-Reduction; D016133:Polymerase Chain Reaction; D012150:Polymorphism, Restriction Fragment Length; D019936:Probiotics; D014176:Protein Biosynthesis / Q000502:physiology; D013552:Swine; D013912:Threonine / Q000494:pharmacology; D014508:Urea / Q000097:blood / Q000378:metabolism*
chemical_list: D000596:Amino Acids; D000900:Anti-Bacterial Agents; D055262:Mucin-2; D009077:Mucins; D013912:Threonine; D014508:Urea; D009584:Nitrogen