Hyperglycemia and reduced adiposity of streptozotocin-induced diabetic mice are not alleviated by oral benzylamine supplementation

Figure 1 Influence of Bza supplementation on body weight gain, food intake and water consumption in normoglycemic and STZ-induced diabetic mice. A: Body weight of diabetic (squares) and nondiabetic mice (circles) drinking water (open symbols) or 0.5% Bza (Bza-drinking, closed symbols). Mean ± SEM of n = 8 males in each group. Significant difference at: ^aP < 0.001 between diabetic and nondiabetic mice, irrespective of the treatment; B: Average daily food intake and water intake. The mean daily consumption calculated throughout the treatment is expressed as g or mL/mouse, for each of the following groups: nondiabetic (white columns), nondiabetic Bza-drinking (red columns), STZ diabetic (yellow columns), STZ diabetic Bza-drinking (black columns). Each column is the mean ± SEM of at least 16 determinations. Different from nondiabetic rats at: ^aP < 0.01. Different from respective control significant at: ^bP < 0.01; ^cP < 0.001. STZ: Streptozotocin; Bza: Benzylamine.

Figure 2 Non-fasting and fasting blood glucose in normoglycemic and STZ-induced diabetic mice during Bza supplementation. A: Blood glucose measured every three days at 12:00 in diabetic (squares) and nondiabetic mice (circles) drinking water (open symbols) or Bza 0.5% (Bza-drinking, closed symbols) for 24 d; B: Overnight fasted blood glucose levels at the end of experiment for the same groups of mice. Mean ± SEM of n = 8 males in each group. Different from nondiabetic mice at: ^aP < 0.001. No significant difference was found between Bza drinking and respective controls. STZ: Streptozotocin; Bza: Benzylamine; Expt end: The end of experiment.

Figure 3 Lack of influence of Bza supplementation on organ weight in normoglycemic and STZ-induced diabetic mice. Mean ± SEM of the wet weight of subcutaneous or visceral white adipose tissues, and of liver for eight males in each group. Different from nondiabetic mice at: ^aP < 0.001. No significant difference was found between Bza-drinking and respective controls. STZ: Streptozotocin; Bza: Benzylamine; WAT: White adipose tissues.

Figure 4 Direct stimulation by insulin and Bza of hexose uptake in adipocytes: lack of influence of Bza supplementation and invitro inhibition by phenelzine. A: Radiolabeled 2-deoxyglucose (2-DG) uptake was determined in basal condition or in response to increasing doses of insulin in adipocytes from nondiabetic mice of the water-drinking (open circles) or Bza-drinking (red circles) group, while it could not be determined in diabetic mice due to the scarcity of adipocytes isolated from their emaciated fat depots, in both control and Bza-drinking groups. Mean ± SEM of eight adipocyte preparations. B: 2-DG uptake was determined after 45 min incubation without (basal) or with 200 nmol/L insulin and 0.1 mmol/L Bza. The stimulated hexose uptake was significantly different from basal at: ^aP < 0.001; ^bP < 0.01. Phenelzine was added at 0.1 mmol/L in the incubation medium of adipocytes from control nondiabetic mice (blue columns) or from Bza-drinking nondiabetic mice (purple columns). Phenelzine inhibited significantly Bza-induced hexose uptake at: ^cP < 0.01. STZ: Streptozotocin; Bza: Benzylamine; WAT: White adipose tissues.

Figure 5 Bza oxidation in adipose tissue of normoglycemic and STZ-induced diabetic mice: lack of influence of dietary Bza consumption. Radiolabeled Bza was present at 0.1 mmol/L during 30 min incubation at 37°C with WAT homogenates from nondiabetic (white columns), nondiabetic Bza-drinking (red columns), STZ diabetic (yellow columns), STZ diabetic Bza-drinking (black columns). Mean ± SEM of eight determinations for nondiabetic mice and four determinations for lipoatrophic STZ diabetic mice. Different from nondiabetic at: ^aP < 0.02. No significant influence of Bza-treatment was detected. STZ: Streptozotocin; Bza: Benzylamine; WAT: White adipose tissues.