Durairaj, K.; Gajendhran, B.; Manivel, G.; Gnanam, H.; Swaminathan, K.; Gilles, M.; Velmurugan, G.

In recent years, the synergistic role of endocrine-disrupting chemicals (EDCs) and gut microbiota in the development of diabetes has been increasingly documented in rodent models. However, most studies have focused on one or two EDCs with varying doses and exposure durations, limiting the identification of a shared microbial signature associated with EDC-induced glucose dysregulation. This meta-analysis aimed to identify a common gut microbiome pattern across rodent studies involving diverse EDC exposures linked to glucose dyshomeostasis. A systematic search yielded 3,748 studies, of which ten met the inclusion criteria, comprising sequence data from 189 samples. These studies evaluated gut microbiota alterations in diabetes induced by various EDCs, including pesticides, food additives, and heavy metals, across different exposure conditions. Meta-analysis revealed a consistent reduction in microbial diversity and an increased Firmicutes/Bacteroidetes ratio following EDC exposure. At the phylum level, Firmicutes, Proteobacteria, Desulfobacterota, and Patescibacteria were significantly enriched. Although beneficial genera such as Lactobacillus, Bifidobacterium, and Akkermansia showed a decreasing trend, these changes were not statistically significant. In contrast, xenobiotic-associated genera including Desulfovibrio, Pseudomonas, Parasutterella, and Candidatus Saccharimonas were significantly increased. Notably, sulfate-reducing bacteria were the only inflammation-associated group consistently elevated. These microbial alterations were distinct from those observed in high-fat diet-induced diabetic models. This study identifies a distinct gut microbiome signature associated with EDC exposure in rodent models of glucose imbalance. These findings suggest unique microbiome-mediated pathways in EDC-induced diabetes and highlight potential microbial targets for early intervention in environmentally driven metabolic disorders.