Fig. 4

Low testosterone-induced suppression of hepatic insulin signaling played a certain role in the development of insulin resistance in castrated db/db mice. a Representative immunoblots (top) and the ratio (bottom) of hepatic phosphorylated Akt (p-Akt) versus total Akt in sham operated, sham operated + testosterone (T) supplemented, castrated, or castrated + T supplemented mice (7 weeks of age) treated from 4 to 7 weeks of age (n = 10–13/group). b The ratio of muscular p-Akt versus total Akt, as assessed by immunoblotting, in the mice (7 weeks of age) in each group (n = 8–11/group). c Hepatic mRNA levels of G6pc, Pck1, and Gck as determined by quantitative real-time PCR (qRT-PCR) at 7 weeks of age (16 h-fasted) (n = 10–13/group). d A photograph of a mouse receiving the continuous anastrozole infusion from an osmotic pump (arrowhead). In addition, a T pellet was implanted under the cervical skin (arrow). e IpGTT analysis in 7-week-old db/db mice fed NCD in each group (n = 8–10/group) as indicated. The area under the curve (AUC glucose) is shown in the right panel. Glucose homeostasis was exacerbated by castration and ameliorated upon T supplementation. f IpITT analysis in 7-week-old mice in each group (n = 8–9/group) as indicated. The blood glucose levels 120 min after insulin loading were significantly higher in castrated than in sham operated mice, and were significantly lower in the T replacement after castration group than in the castrated group. Results are expressed as means ± s.e.m. *P < 0.05, **P < 0.01 between the indicated groups. ^†P < 0.01 versus sham operated or sham operated + T and A supplemented mice. ^‡P < 0.05 versus sham operated mice at each time, 2-way ANOVA. ^§P < 0.01, ^#P < 0.01 versus castrated + T and A supplemented, sham operated + T and A supplemented, or sham operated mice, respectively, at each time, 2-way ANOVA