Recently, a closely relatedmolecule, imidazole propionate, was found to be elevated in circulationin individuals with T2D, and to impair glucosetolerance and insulin signaling in the liver. Increased levels of this molecule were attributed to altered microbialmetabolism of histidine., While imidazole propionateitself was not detected in our data sets, this study provides thefirst indication that altered histidine metabolism, the top pathwayidentified in our metabolomic analysis, may be impacting β cellfunction directly rather than just through systemic effects or effectson the liver. This evidence concerns the gene INS and type 2 diabetes mellitus.