Anti-diabetic effect of Alpinia oxyphylla extract on 57BL/KsJ db-/db- mice.

Diabetes mellitus is characterized by high blood glucose levels. Increased levels of reactive oxygen species (ROS) may disrupt insulin signaling and result in insulin resistance. The Alpinia oxyphylla extract (AOE) possesses powerful antioxidant activity and may therefore inhibit the development of insulin resistance. The objective of the present study was to determine the effects of AOE on blood glucose, insulin and lipid levels in a type II diabetic nephropathy animal model (C57BIKsj db-/db-). All experiments were performed on male C57BL/Ks DB/DB and db-/db- mice that were left to acclimatize for 1 week prior to the experimental period. AOE was administered to these mice at different dosages (100, 300 and 500 mg/kg) for 8 weeks. The results demonstrated that AOE did not affect mouse weight, while blood glucose concentrations were found to significantly decrease in a dose-dependent manner (P<0.05). The effect of administering 500 mg/kg AOE (AOE500) to db-/db- mice was tested further. Treatment with AOE500 for 8 weeks led to improved glucose tolerance and reduced plasma insulin concentrations (P<0.05), as well as a significant decrease in triglyceride concentrations (P<0.05) and levels of total cholesterol (P<0.05) in db-/db- mice. Furthermore, treatment with AOE500 decreased the concentration of malondialdehyde, elevated the concentration of glutathione and increased the activities of the antioxidant enzymes superoxide dismutase and peroxidase (P<0.05) in the livers of db-/db- mice. Meanwhile, AOE-treated mice exhibited significantly reduced urine albumin, creatinine and blood urea nitrogen excretion (P<0.05). In parallel, the upregulated expression of phosphatase and tensin homolog (PTEN) in the liver and kidneys of db-/db- mice was impaired following AOE500 treatment. The results of the present study suggest that AOE regulates blood glucose and lipid levels and improves renal function by mediating oxidative stress and PTEN expression at the onset of type II diabetes mellitus.