RESUMO
Although diet composition has been implicated as a major factor in the etiology of various gastrointestinal diseases, conclusive evidence remains elusive. This is particularly true in diseases such as necrotizing enterocolitis where breast milk as opposed to commercial formula appears to confer a protective effect to the immature gut. Yet the mechanism by which this occurs continues to remain speculative. In the present study we hypothesize that the basic chemical composition of diet fundamentally selects for specific intestinal microbiota which may help explain disparate disease outcome and therapeutic direction. Complimentary animal and human studies were conducted on young piglets (21 d.)(n = 8)(IACUC protocols 08070 and 08015) and premature infants (adjusted gestational age 34-36 weeks) (n = 11)(IRB Protocol 15895A). In each study, cecal or stool contents from two groups (Breast milk-fed (BF) vs. Formulafed (FF)) were analyzed by gas chromatography/masss pectrometry (GC/MS) and comprehensive metabolic profiles generated and compared. Concurrently, bacterial community structure was assayed and respective representative microbiota of the groups determined by 16SrRNA gene amplicon pyrosequencing. Statistical modeling and analysis was done using SIMCA-P+ and R software. GC/MS metabolomics identified clear differences between BF and FF groups in the intestinal environment of piglets and humans. Sugars, amino-sugars, fatty acids, especially unsaturated fatty acids, and sterols were identified as being among the most important metabolites for distinguishing between BF and FF groups. Joint analysis (AU)
Aunque se ha implicado a la composición de la dieta como un factor principal en la etiología de varias enfermedades gastrointestinales, la evidencia concluyente sigue siendo esquiva. Esto es particularmente cierto en enfermedades como la enterocolitis necrosante en la que la leche materna, en contraposición de las fórmulas comerciales, parece conferir un efecto protector para el intestino inmaduro o el ecosistema intestinal juvenil del intestino inmaduro, si bien el mecanismo por el que esto ocurre sigue siendo una especulación. La hipótesis de nuestro estudio es que la composición química básica de la dieta selecciona fundamentalmente microbióticos intestinales específicos que pueden explicar los resultados dispares de la enfermedad y tener implicaciones terapéuticas. Se realizaron estudios adicionales en animales y humanos en lechones (21 d.) (n = 8) (protocolos IACUC08070 y 08015) y lactantes prematuros (edad gestacional ajustada de 34-36 semanas) (n = 11) (Protocolo IRB15895A). En cada estudio, se analizaron los contenidos cecales y fecales de ambos grupos (alimentación materna(AM) y alimentación con fórmula (AF)) mediante cromatografía de gases/espectrometría de masas (CG/EM) y se generaron y compararon perfiles metabólicos completos. De forma concurrente, se probó la estructura de la comunidad bacteriana y se determinaron los representantes (AU)
