Chronic zinc deficiency alters gut microbiota structure and function in vivo (Gallus gallus)

Abstract Number Theme Presentation Type Cover Approved
0211 Dietary assessment: methods and results Poster Not Approved


Abstract Content


Zinc (Zn)-deficiency is a highly prevalent micronutrient insufficiency primarily caused by a lack of adequate dietary-Zn and/or poorly bioavailable dietary-Zn. Although the gut is a vital organ for Zn-utilization, and therapeutic Zn-administration positively influences gut health, the significance of the gut microbial ecology to the host during Zn-deficiency is unclear. OBJECTIVES: Characterization of distinct bacterial-shifts induced by chronic dietary-Zn-depletion.


Cecal-samples from Zn-replete (42µg/g-dietary-Zn) and Zn-deficient (2.5µg/g-dietary-Zn) treatment-groups (Gallus-gallus, n=14, 4-weeks) were harvested for bacterial DNA-extraction and sequenced using bar-coding of the 16S-rRNA gene V4-hypervariable-region. Microbiota diversity was assessed through measures of ß-diversity (weighted-UniFrac-distances), a-diversity (Chao1-index), and overall species-richness.


Zn-depletion induces significant taxonomic shifts and decreases overall species-richness and diversity, establishing a microbial profile resembling that of various other pathological states. Metagenomic-analysis showed that predicted KEGG-pathways responsible for macro-and micro-nutrient uptake are significantly depleted in Zn-deficiency, and, along with decreases in beneficial short-chain-fatty-acids, such depletions induce notable functional and metabolic alterations which may further preclude an optimal host Zn-status. We identified four bacterial species; Enterococcus-sp., Ruminococcus-lactaris, Clostridium-lactatifermentans, and Clostridium-clostridioforme positively correlated with Zn-adequacy, and two bacterial species; Clostridium-indolis and Unclassified-S24-7-positively correlated with Zn-insufficiency as candidate microbes which may play a significant role in the utilization of dietary-Zn during a prolonged deficiency.


We characterized a unique cecal-microbiota during Zn-deficiency, and provide evidence for these perturbations as influencers of the Zn-deficient phenotype. With additional research, such microbial alterations could be used to designate a Zn-deficiency profile, which could be used as an additional physiological-biomarker to assess deficiency stage/risk.

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