The key findings of this study (Figure 10) are: (1) the mRNA, protein, and TMAO-producing function of FMO3 are potently stimulated by TCDD exposure in mice; (2) both male and female Fmo3−/− mice exhibit glucose intolerance when exposed to TCDD, despite normal fasting metabolic hormone levels; (3) TCDD exposure reorganizes the gut microbiome, and TCDD-driven microbiome reorganization is dramatically altered in Fmo3−/− mice; and (4) TCDD-driven expression of AhR target (i.e., Cyp1a1), heme metabolism, pro-inflammatory, and pro-fibrotic genes is dysregulated in Fmo3−/− mice. This evidence concerns the gene AHR and Glucose intolerance.