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. Author manuscript; available in PMC: 2020 Sep 4.
Published in final edited form as: Nature. 2020 Mar 4;579(7798):279–283. doi: 10.1038/s41586-020-2074-6

Extended Data Figure 2.

Extended Data Figure 2.

Glucagon-stimulated glucose production requires activation of the PLC and PKA pathways, converging to activate InsP3 signaling. In vitro glucose production and VPC flux in isolated hepatocytes with and without ET-18-OCH3 (n=3), U-73122 (n=3, with the exception of KO-glucagon-U-73122, in which n=2), H-89 (n=6), vasopressin (n=3), 2-APB (n=3), caffeine (n=3), KN-93 (n=6), and thapsigargin (n=3). In all panels, *P<0.05, **P<0.01, ***P<0.001 vs. WT-glucagon-drug; §P<0.05, §§P<0.01, §§§P<0.001 vs. WT +glucagon -drug by the 2-tailed unpaired Student’s t-test. If no statistical comparison is denoted, the groups were not significantly different. The mean±S.E.M. is shown.