Altering the intestinal microbiota during a critical developmental window has lasting metabolic consequences.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 25126780.
- Also identified by DOI 10.1016/j.cell.2014.05.052 and PMC identifier 4134513.
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Abstract
Acquisition of the intestinal microbiota begins at birth, and a stable microbial community develops from a succession of key organisms. Disruption of the microbiota during maturation by low-dose antibiotic exposure can alter host metabolism and adiposity. We now show that low-dose penicillin (LDP), delivered from birth, induces metabolic alterations and affects ileal expression of genes involved in immunity. LDP that is limited to early life transiently perturbs the microbiota, which is sufficient to induce sustained effects on body composition, indicating that microbiota interactions in infancy may be critical determinants of long-term host metabolic effects. In addition, LDP enhances the effect of high-fat diet induced obesity. The growth promotion phenotype is transferrable to germ-free hosts by LDP-selected microbiota, showing that the altered microbiota, not antibiotics per se, play a causal role. These studies characterize important variables in early-life microbe-host metabolic interaction and identify several taxa consistently linked with metabolic alterations. PAPERCLIP:
Medical subject headings
- Anti-Bacterial Agents
- Disease Models, Animal
- Intestines
- Microbiota
- Obesity
- Penicillins