Marjan Tajik kord, Fatemeh Poorrajab
*, Javad Mohiti Ardekani, Manizheh Azari, Alireza Raeissi
1 Departement of Biochemistry, Shahid Sadoughi University of Medical Science, Yazd, Iran
Abstract
Backgrounds and Objectives: Diabetes type 2 is a metabolic disorder that affects many organs through chronic high blood levels of glucose. The GLUT4 translocation from cytosolic component to the cell membrane is the most important mechanism and strategy to compensate this situation. At the present study, we aimed to investigate the molecular mechanism of anti-diabetic and hypoglycemic effects of ginger, through evaluating the translocation of GLUT4 in C2C12 myotubes.
Material and Methods: In an experimental study, the C2C12 cells were treated with 50µgr/mL concentration of ethyl acetate ginger extract for 3 hours. Sub-cellular fractions were made by centrifugation from homogenized myotubes. After preparation of cytosolic and membrane fractions, the amount of GLUT-4 (an important glucose transporter) was determined using sodium dodecyl sulfate polyacrylamide gel (SDS PAGE) electrophoresis, western blotting and chemiluminescent methods. Finally, gel documents software gene tools were used to analyze sub-cellular expression of the transporter.
Results: The expression of GLUT4 was considerably higher in the ginger-treated cells (112.2±2.41) compared to the control (the DMSO-treated cells) (98.62±3.92) (P value < 0.05). Also, the amount of GLUT4 in membrane fraction of cells treated with ginger extract (100±0) was higher compared to the DMSO-treated cells (78.46±5.84). The amount of GLUT4 in cytosolic fraction of cells treated with ginger extract (12.22±2.41) was lower compared to the control (the DMSO-treated cells) (20.15±2.56). These results show an enhanced translocation of GLUT4 from cytosolic fraction to the cell membrane fraction in the ginger-treatments.
Conclusion: One of the mechanisms and also the most important anti-diabetic effects of ginger would be to decrease insulin resistance increasing GLUT4 translocation to the cell membrane, which declines following diabetic complications.