Excess Dietary Zinc Intake in Neonatal Mice Causes Oxidative Stress and Alters Intestinal Host–Microbe Interactions

摘要: Scope Greater than 68% of young infants are exposed to dietary zinc (Zn) levels that higher the Tolerable Upper Intake Limit. However, consequences excess Zn during early life on intestinal function and host-microbe interactions unknown. Methods results Neonatal mice gavaged with 100 µg d-1 from postnatal day (PN) 2 through PN10 indices compared unsupplemented mice. Excess causes oxidative stress, increases goblet cell number mucus production, associated increased permeability systemic inflammation. Over 900 genes differentially expressed; 413 display a fold-change >1.60. The Gene Ontology Biological processes most significantly affected include biological adhesion, immune system, metabolic processes, response stimulus. Key highly upregulated ALDH2, MT1, TMEM6, CDK20, COX62b, while CALU, ST3GAL4, CRTC2, SLC28A2, COMMA1 downregulated. These changes microbiome enriched in pathogenic taxa including Pseudomonadales Campylobacter, greater expression bacterial stress genes. Conclusion may have unforeseen influences epithelial signaling pathways, barrier function, luminal ecology intestine long-term health.