Diet creates metabolic niches in the "immature gut" that shape microbial communities.

摘要: 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 diseases such necrotizing enterocolitis where breast milk opposed to commercial formula appears confer “protective effect” “immature gut.” Yet mechanism by which this occurs continues remain speculative. In present study we hypothesize that basic chemical fundamentally selects for specific intestinal microbiota may help explain disparate disease outcome and therapeutic direction. Complimentary animal human studies were conducted on young piglets (21 d.)(n = 8) (IACUC protocols 08070 08015) premature infants (adjusted gestational age 34-36 weeks) (n 11) (IRB Protocol 15895A). each study, cecal or stool contents from two groups (Breast milk-fed (BF) vs. Formulafed (FF)) analyzed gas chromatography/mass spectrometry (GC/MS) comprehensive metabolic profiles generated compared. Concurrently, bacterial community structure was assayed respective representative determined 16S rRNA gene amplicon pyrosequencing. Statistical modeling analysis done using SIMCA-P+ R software. GC/MS metabolomics identified clear differences between BF FF environment humans. Sugars, amino-sugars, fatty acids, especially unsaturated sterols being among most important metabolites distinguishing groups. Joint pinpointed sets (p < 0.05) associated with dominant taxa. The