Chronic Zinc Deficiency Alters Chick Gut Microbiota Composition and Function

Abstract

Zinc (Zn) deficiency is a prevalent micronutrient insufficiency. Although the gut is a vital organ for Zn utilization, and Zn deficiency is associated with impaired intestinal permeability and a global decrease in gastrointestinal health, alterations in the gut microbial ecology of the host under conditions of Zn deficiency have yet to be studied. Using the broiler chicken (Gallus gallus) model, the aim of this study was to characterize distinct cecal microbiota shifts induced by chronic dietary Zn depletion. We demonstrate that Zn deficiency induces significant taxonomic alterations and decreases overall species richness and diversity, establishing a microbial profile resembling that of various other pathological states. Through metagenomic analysis, we show that predicted Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways responsible for macro- and micronutrient uptake are significantly depleted under Zn deficiency; along with concomitant decreases in beneficial short chain fatty acids, such depletions may further preclude optimal host Zn availability. We also identify several candidate microbes that may play a significant role in modulating the bioavailability and utilization of dietary Zn during prolonged deficiency. Our results are the first to characterize a unique and dysbiotic cecal microbiota during Zn deficiency, and provide evidence for such microbial perturbations as potential effectors of the Zn deficient phenotype.

A Pleiotropic Missense Variant in SLC39A8 Is Associated With Crohn’s Disease and Human Gut Microbiome Composition

“…51 Animal studies have indicated that zinc deficiency alters microbial function and composition. 52 Moreover, some ion channels, such as KCNN4, which share membrane transporter properties and roles with solute transporters, are activated by intracellular calcium and regulate Paneth cell secretion 53 with an impact on immune cell and epithelial cell function. 54 Therefore, we speculate that by disturbing the transmembrane domain of SLC39A8, Ala391Thr may alter zinc metabolism in functionally relevant cells, which might in turn affect innate and adaptive immunity, as well as the gut microbiota.…”

Protein- and zinc-deficient diets modulate the murine microbiome and metabolic phenotype

“…Alternatively, zinc-associated bacterial alterations may occur at a lower taxonomic level than were measured here. In chickens, chronic zinc deficiency promoted a significant increase in Proteobacteria, which is a phylum that represented a major proportion of the fecal microbiota of dZD mice (23, 24). However, this phylum constituted a major proportion of the well-nourished profile of 46-d-old mice, increasing notably from 36 d old, and may, therefore, be part of the microbial aging process.…”

The Combined Application of the Caco-2 Cell Bioassay Coupled with In Vivo (Gallus gallus) Feeding Trial Represents an Effective Approach to Predicting Fe Bioavailability in Humans

“…The Gallus gallus model was shown to exhibit the appropriate responses to Fe deficiency and that it can serve as a model for human Fe bioavailability. More specifically, it is a fast growing animal that is sensitive to dietary mineral deficiencies [60] and is very receptive to dietary manipulations [15,16,17,55,60,61,67,68,69,70,71]. There is also >85% homology between gene sequences of human and chicken intestinal divalent metal transporter 1 (DMT1, the major intestinal Fe transporter), duodenal cytochrome B (DcytB, Fe reductase), ZnT1 (a major intestinal Zn exporter) and Ferroportin (the major intestinal enterocyte Fe exporter), which are key proteins that are essential for Fe and Zn metabolism [72].…”