Fig. 6: Long-term rFGF4 treatment improves skeletal muscle glucose disposal in db/db and DIO mice.

a–d db/db mice were treated every other day for 37 days with rFGF4 (1.0 mg/kg body weight) or a buffer control; littermate db/m mice served as additional controls. a Phosphorylation levels of AMPKα, GS, and AKT and expression levels of GLUT4 as determined by western blotting (left panel) and quantitation using ImageJ software (right panel) (n = 4). b, c Representative periodic acid–Schiff staining (PAS; magenta denotes glycogen) (b) and glycogen content (c) of skeletal muscle in db/db mice (n = 6). d Real-time PCR analysis of expression of Pkm, Hk2, Shda, Pdha1, and Pdk4 mRNAs (n = 6). Scale bars, 100 μm. e–g DIO mice were treated every other day for 30 days with rFGF4 (1.0 mg/kg body weight) or a buffer control. e Phosphorylation levels of AMPKα, GS, and AKT and expression levels of GLUT4 were determined in skeletal muscle by western blotting (left panel) and quantified using ImageJ software (right panel) (n = 6). f Glycogen content of skeletal muscle in DIO mice (n = 5). g Real-time PCR analysis of expression of Pkm, Hk2, Shda, Pdha1, and Pdk4 mRNAs (n = 6). Data are presented as mean +/− SEM. Statistical comparisons in (a, c) are one-way ANOVA tests with Tukey’s multiple comparisons tests. Statistical comparisons in (d–g) are unpaired two-tailed tests. Source data are provided as a Source data file.