Figure 1.
Effect of BDSW on fasting blood glucose levels (A) and glucose tolerance (B) in STZ-induced diabetic mice, for 4 weeks.
Each color curve represents normal (dark blue), STZ diabetes control (Red), STZ with BDSW 0 (green), 1000 (purple), 2000 (deep Sky Blue), 4000 (yellow) group, respectively. Each value represents the mean ± SE (n = 8 per group). *P<0.05, **P<0.01: significant difference vs. STZ diabetic group. Nor, normal group; Con, STZ diabetic group; STZ, streptozotocin; BDSW, balanced deep-sea water.
Figure 2.
Effects of BDSW on adipokines (A) and cytokines (B) levels in plasma of STZ-induced diabetic mice, for 4 weeks.
Each value represents the mean ± SE (n = 8 per group). *P<0.05, **P<0.01: significant difference vs. STZ diabetic group. Nor, normal group; Con, diabetic control group; STZ, streptozotocin; BDSW, balanced deep-sea water.
Figure 3.
Effects of BDSW on pancreatic islet morphology and insulin and glucagon production in pancreas of STZ-induced diabetic mice, for 4 weeks.
Representative hematoxylin and eosin, insulin, and glucagon staining of the islets of Langerhans are shown at ×400 magnification (n = 8 per group). Scale bar, 50 µm. STZ, streptozotocin; BDSW, balanced deep-sea water.
Figure 4.
Effects of BDSW on the expression of genes involved in gluconeogenesis (A), glucose oxidation (B), and glycogen metabolism (C), in the liver of STZ-induced diabetic mice for 4 weeks.
Each value represents the mean ± SE (n = 8 per group). *P<0.05, **P<0.01: significant difference vs. STZ diabetic group. STZ, streptozotocin; BDSW, balanced deep-sea water.
Figure 5.
Effects of BDSW on the expression of genes involved in glucose uptake (A), glucose oxidation (B), and β-oxidation (C) in the muscles of STZ-induced diabetic mice for 4 weeks.
Each value represents the mean ± SE (n = 8 per group). *P<0.05, **P<0.01: significant difference vs. STZ diabetic group. STZ, streptozotocin; BDSW, balanced deep-sea water.
Figure 6.
Effects of BDSW on 2-NBDG uptake in C2C12 myotubes.
For the glucose-uptake assay at different levels of BDSW hardness (A), C2C12 myotubes were preincubated in DMEM with low glucose for 1 h. They were then incubated in DMEM containing BDSW at different levels of hardness, or 1 mM AICAR (AC), and 100 nM insulin (Ins) with 20 µM 2-NBDG for 1 h. For the glucose-uptake assay using several inhibitors (B), after preincubation in DMEM with low glucose in the presence or absence of 10 µM LY294002, 10 µM compound C (Comp C), 10 µM rapamycin (Rapa), 2 mM nicotinamide (NA), and 1 mM AICAR (AC) for 1 h, the cells were incubated in DMEM containing BDSW 2000 ppm hardness only, or with inhibitors, with 20 µM 2-NBDG for 1 h. After incubation was completed, cells were lysed, and the glucose uptake was measured using a fluorometer. Each value represents the mean ± SE (n = 8 per group). *P<0.05, **P<0.01: significant difference vs. CON group (A) or BDSW 2000 group (B). CON, non-treated control group; BDSW, balanced deep-sea water.
Figure 7.
Effects of BDSW on the phosphorylation of IRS-1, LKB, AMPK, and mTOR in C2C12 myotubes (A, B) and the muscles (C) of STZ-induced diabetic mice.
C2C12 myotubes were preincubated in DMEM with low glucose for 1 h. They were then incubated in DMEM containing BDSW at different levels of hardness and 1 mM AICAR (AC) for 1 h. For inhibitors assay, after preincubation in DMEM with low glucose in the presence or absence of 10 µM LY294002, 10 µM compound C (CC), 10 µM rapamycin (RP), and 2 mM nicotinamide (NA) for 1 h, the cells were then incubated in DMEM containing BDSW of 2000 ppm hardness with or without inhibitors for 1 h. Subsequently, lysates (20 µg) of C2C12 myotubes were subjected to SDS-PAGE and western blotting analyses using anti-phospho IRS-1, anti-phospho LKB1, anti-phospho AMPK, anti-phospho mTOR, anti-AMPK, and anti-β-actin antibodies. NOR, normal group; STZ, streptozotocin; BDSW, balanced deep-sea water.