FIGURE 4.

DDN displays hypoglycemic function in diabetic mouse models. A, DDN activates insulin signaling in db/db mice. Three-month-old mice were starved for 12 h and then orally administrated with vehicle (0.5% methylcellulose) or DDN (5 mg/kg). Cell lysates were prepared from liver and muscle tissues, which were collected at 1 and 2 h after drug administration and analyzed by immunoprecipitation and immunoblotting. B, DDN activates insulin signaling in ob/ob mice. Three-month-old mice were starved for 12 h and then orally administrated with vehicle (0.5% methylcellulose) or DDN (5 mg/kg). Cell lysates were prepared from liver and muscle tissues, which were collected at 1 and 2 h after drug administration and analyzed by immunoprecipitation and immunoblotting. C, hypoglycemic function of DDN in db/db mice. The animals were starved for 12 h and then orally injected with vehicle (0.5% methylcellulose) or DDN (5 mg/kg). Human insulin (1 unit/kg) was injected intraperitoneally as a positive control. Blood glucose was monitored before and after drug administration at 1-h intervals (*, p < 0.05; **, p < 0.01, n = 5; two-way analysis of variance versus vehicle). D, DDN improves the glucose tolerance in ob/ob mice. The animals were starved for 12 h and then orally dosed with vehicle (0.5% methylcellulose) or DDN (5 mg/kg). Human insulin (1 unit/kg) was injected intraperitoneally as a positive control. A bonus of glucose (2 gm/kg) was injected intraperitoneally 1 h later. Blood glucose was measured at 30-min intervals (*, p < 0.05; **, p < 0.01, n = 5; two-way analysis of variance versus vehicle control).