Importantly, our findings revealed that IAA treatment did not impair glucose tolerance nor insulin sensitivity in normal mice (Fig. S4J), suggesting that the metabolic dysfunctions induced by alterations in the composition of the gut microbiome are primarily mediated by the tryptamine/TAAR1 signaling axis but not the IAA/AhR signaling axis in the context of T2D. This evidence concerns the gene AHR and type 2 diabetes mellitus.