Daidzin decreases blood glucose and lipid in streptozotocin-induced diabetic mice

摘要

Purpose: To investigate the ameliorative effect of daidzin (DZ) on diabetes in streptozotocin (STZ)-induced diabetic Institute of Cancer Research (ICR) mice, with a view to determining its usefulness in the treatment of diabetes. Methods: The effect of DZ (100, 200 and 400 mg/kg) on blood glucose was investigated in both normal and STZ-induced diabetic mice with glibenclamide (3 mg/kg) and metformin (400 mg/kg) as positive control, respectively. Serum or hepatic levels of lipid, proinflammatory factors, malondialdehyde (MDA) and superoxide dismutase (SOD) were measured. Glucosidase activity assay and glucose uptake by C2C12 myotubes were performed in vitro and the ex pression of glucose transporter 4 (GLUT4) in C2C12 cells was determined by western blot. Results: DZ (200 and 400 mg/kg) did not decrease fasting blood glucose in normal mice but inhibited starch-induced postprandial glycemia. Oral administration of 400 mg/kg of DZ for 14 days significantly decreased mouse blood glucose (p 0.01), as well as serum total cholesterol (TC, p 0.01), triglycerides (TG, p 0.01), low-density lipoprotein cholesterol (LDL-c, p 0.01) levels in STZ-induced hyperglycemic mice and improved oral glucose tolerance. The serum and hepatic activity of SOD was enhanced (p 0.01 and p 0.001, respectively) while MDA level decreased (p 0.001). Blood concentrations of interleukin-6 (IL-6, p 0.001), tumor necrosis factor α (TNF-α, p 0.01), monocyte chemotactic protein 1 (MCP-1, p 0.01) were also significantly reduced. In vitro glucosidase activity results showed that DZ inhibited α-glucosidase with IC50 values of 82, 98 and 389 μg/mL for α-glucosidase from S. cerevisiae, Rhizopus sp. and rat intestines, respectively. It also stimulated glucose uptake and GLUT4 membrane translocation in C2C12 myotubes at 20 μM (p 0.05). Conclusion: Oral administration of DZ is effective in alleviating diabetic hyperglycemia, dyslipidemia and inflammation. Inhibition of α-glucosidase and stimulation of glucose consumption by muscles may account for its inhibitory effect on blood glucose.