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Objective: To investigate the preventive effect of Radix Astragali on tumor necrosis factor-α(TNF-α). induced insulin resistance. Methods: Rats were treated orally with Radix Astragali before TNF-α intravenous injection. The changes of K value in glucose-insulin tolerance test, the concentrations of glucagon(GC), ACTH and lipids in serum and the contents of glycogen, triglyceride (TG) in liver and red quadricepswere tested 4 hours after the injection and compared with the control. Results: Exogenous TNF-α can inducehyperinsulinemia in normal rats, and the K value decreased, the concentration of serum ACTH, GC and lipidsall increased, the glycogen contents in liver and red quadriceps muscle decreased, and the liver TG depots increased. Radix Astragali can improve all the parameters significantly except the serum lipids level and livertriglyceride dePOts. Conclusions: Radix Astragali has preventive effect on insulin resistance induced by TNF-αand is useful in the treatment of type 2 diabetes. The mechanism may be due to the decrease of insulin-antagonistic hormones and the increase of tissue glycogen contents.
Objective: To investigate the preventive effect of Radix Astragali on tumor necrosis factor-α(TNF-α).induced insulin resistance. Methods: Rats were treated orally with Radix Astragali before TNF-α intravenous injection. The changes of K value in glucose- Plasma tolerance test, the concentrations of glucagon(GC), ACTH and lipids in serum and the contents of glycogen, triglyceride (TG) in liver and red quadricepswere tested 4 hours after the injection and compared with the control. Results: Exogenous TNF-α Can inducehyperinsulinemia in normal rats, and the K value decreased, the concentration of serum ACTH, GC and lipidsall increased, the glycogen contents in liver and red quadriceps muscle decreased, and the liver TG depots increased. Radix Astragali can improve all the parameters significantly except The serum lipids level and livertriglyceride dePOts. Conclusions: Radix Astragali has preventive effect on insulin resistance induced by TNF-αand is useful in the treatment of type 2 The mechanism may be due to the decrease of insulin-antagonistic hormones and the increase of tissue glycogen contents.