Fig. 3.

FGF19 inhibits GSK3 signaling to increase liver glycogen in mice. (A) Mice fasted overnight were treated i.v. with vehicle or 1 mg/kg FGF19 and killed 10 min later. Proteins from liver homogenates were separated by SDS-PAGE and identified by Western blotting with the indicated antibodies. Results represent triplicate experiments. (B) The ability of glycogen synthase in the homogenates of the same livers to incorporate radiolabeled uridine 5′-diphosphate–glucose into glycogen in the absence and presence of glucose-6-phosphate was measured, and the ratio was shown as glycogen synthase activity (n = 3). (C) Mice fed ad libitum were injected subcutaneously with vehicle or 1 mg/kg FGF19 at 6 p.m. and the next morning at 8 a.m. Then, 6 hours after the last injection, the animals were killed, and liver weight and glycogen content were determined (n = 6). (D) Liver glycogen content was determined in wild-type and Fgf15^−/− mice fed ad libitum (n = 5). (E) Oral glucose tolerance test in wild-type and Fgf15^−/− mice (n = 6). Values are means ± SEM. Asterisks (*) refer to differences between wild-type and Fgf15^−/− groups; number signs (#) refer to differences between Fgf15^−/− and Fgf15^−/− plus FGF19 groups. Statistics by two-tailed t test. *P < 0.05, **P < 0.005, #P < 0.05, ##P < 0.005.