The mRNA of insulin receptor （IR）, the insulin receptor substrates （IRSs）, glucose transporter 2 （GLUT2） and glucokinase （GK） in alloxan-induced diabetic rat livers were amplified by RT-PCR. The protein of the...The mRNA of insulin receptor （IR）, the insulin receptor substrates （IRSs）, glucose transporter 2 （GLUT2） and glucokinase （GK） in alloxan-induced diabetic rat livers were amplified by RT-PCR. The protein of the insulin receptor in rat livers was determined by westem-blotting. The results show that IR expression level decreased at the level of mRNA and protein. The gene expressions of IRSs, GLUT2 and GK changed significantly. The hepatic glycogen content in alloxan-diabetic rats treated with insulin （（13.2 ± 0.4） mg·g^-1） did not restore to normal level （（17.0 ±0.4） mg·g^-1） by means of anthrone-H2SO4 methods. The results imply that insulin resistance is developed during inchoate phase of alloxan-induced diabetic rats.展开更多
基金Supported by the National Natural Science Foundation of China (20671037, 20371018)
文摘The mRNA of insulin receptor （IR）, the insulin receptor substrates （IRSs）, glucose transporter 2 （GLUT2） and glucokinase （GK） in alloxan-induced diabetic rat livers were amplified by RT-PCR. The protein of the insulin receptor in rat livers was determined by westem-blotting. The results show that IR expression level decreased at the level of mRNA and protein. The gene expressions of IRSs, GLUT2 and GK changed significantly. The hepatic glycogen content in alloxan-diabetic rats treated with insulin （（13.2 ± 0.4） mg·g^-1） did not restore to normal level （（17.0 ±0.4） mg·g^-1） by means of anthrone-H2SO4 methods. The results imply that insulin resistance is developed during inchoate phase of alloxan-induced diabetic rats.
