Our results demonstrate that in nonfasted mice Tas1r3 deficiency markedly worsens glucose tolerance, regardless of whether the route of glucose administration is intragastric or intraperitoneal (Figs 2 and 3), indicating possible involvement of T1R3-mediated glucose sensing in intestinal enteroendocrine, pancreatic, and/or brain mechanisms controlling glucose metabolism. This evidence concerns the gene TAS1R3 and glucose measurement.