1,25(OH)₂D₃ attenuates hepatic insulin resistance in rats with streptozotocin-induced diabetes via antioxidation

Abstract

Aim: This study was conducted to explore the mechanism by which 1,25(OH) 2 D 3 ameliorates hepatic insulin resistance in rats with streptozotocin (STZ)-induced type 2 diabetes. Methods: Sprague Dawley (SD) rats were randomly divided into five groups: normal, control, and 1,25(OH) 2 D 3 administered at 0.075, 0.15, and 0.3 μg/kg/d. Tissue and blood samples were obtained from all five groups after 4 and 12 weeks of treatment. Morphological changes in the livers were observed with HE staining. The levels of fasting blood glucose (FBG), insulin, and lipids were determined using an automatic biochemistry analyzer. The levels of hepatic glycogen, superoxide dismutase (SOD), malondialdehyde (MDA), aspartate aminotransferase (AST), and alanine aminotransferase (ALT) were analyzed by spectrophotometry. Protein expression of AKT and GLUT2 was examined by western blotting. Results: 1,25(OH) 2 D 3 treatment reduced the FBG content as well as hepatic MDA, AST, and ALT levels, improved the activity of SOD, and enhanced the expression of GLUT2 and AKT in diabetic rats. These findings suggest that 1,25(OH) 2 D 3, exerts antioxidant effects and ameliorates insulin resistance in the liver. Conclusion: 1,25(OH) 2 D 3 is a potential agent that could be used in the treatment of insulin resistance in the liver.