Figure 2
From: Inhibition of C1-Ten PTPase activity reduces insulin resistance through IRS-1 and AMPK pathways

DHTS improves diabetic phenotypes. (A) Effects of DHTS on Akt phosphorylation in the skeletal muscle of db/db mice. (Right) Relative Akt phosphorylation (S473) normalized to total Akt. Data are presented as the mean ± SEM (n = 8–9); *P < 0.05 and ***P < 0.001. (B) Oral glucose tolerance test (OGTT) and area under the curve (AUC) in vehicle- and DHTS-treated db/db mice. Data are presented as the mean ± SEM (n = 4); *P < 0.05. (C) Effects of DHTS on glucose uptake in myotubes. Dexamethasone-treated L6 myotubes were incubated with the indicated concentrations of DHTS for 1 h, and glucose uptake was measured. Data are presented as the mean ± SEM of six biological replicates, and similar results were obtained from three independent experiments; ***P < 0.001. (D) Effects of DHTS on muscle atrophy in db/db mice. Representative images of tibialis anterior (TA) muscle sections stained with antibody to laminin and Hoechst 33342. The images were taken at 25× magnification; scale bar = 20 μm. Mean cross-sectional area (CSA) of TA muscle fibers (bottom left). Frequency distribution of the CSA of fibers plotted as frequency histograms (bottom right). More than 1000 myofibers from two or three sections per mouse were measured. Data are presented as the mean ± SEM (n = 5); **P < 0.01. (E) DHTS-induced inhibition of Murf1 expression. After L6 myotubes were incubated with DMSO or 1 μM DHTS for 24 h, the cells were cotreated with dexamethasone for 24 h. Data are presented as the mean ± SEM (n = 4); *P < 0.05.