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. Author manuscript; available in PMC: 2019 Jan 11.
Published in final edited form as: Cell. 2018 Jan 4;172(1-2):234–248.e17. doi: 10.1016/j.cell.2017.12.001

Figure 1. A decreased rate of hepatic glycogenolysis is the primary determinant of the switch from glucose to fat oxidation during starvation.

Figure 1

(A) Plasma glucose. (B) Hepatic glucose production from net hepatic glycogenolysis, gluconeogenesis from oxaloacetate (i.e. VPC), and gluconeogenesis from glycerol. *P<0.05 vs. 8 hr fasted rats and §§§§P<0.0001 vs. 16 hr fasted rats, in both cases comparing gluconeogenesis from oxaloacetate. (C) Percent glucose oxidation in the TCA cycle [pyruvate dehydrogenase flux (VPDH)/citrate synthase flux (VCS)]. *P<0.05, **P<0.01, ***P<0.001, ****P<0.0001 vs. fed rats; ####P<0.0001 vs. 6 hr fasted rats, §P<0.05, §§P<0.01 vs. 16 hr fasted rats. (D)–(E) Plasma leptin and corticosterone. (F) Endogenous glucose production before and 2 hrs after treatment with a glycogen phosphorylase inhibitor. (G)–(H) Plasma leptin and corticosterone in glycogen phosphorylase inhibitor-treated rats. In panels (F)–(H), data from the same rats before and after treatment with the inhibitor were compared by the paired Student’s t-test; in all other panels, ANOVA with Bonferroni’s multiple comparisons test was used. Data are the mean±S.E.M. of n=6–8 per group. See also Fig. S1 and S2.