AIM: To study the effect of insulin sensitivity agonist—
rosiglitazone on protein kinase B (PKB) expression of insulin resistant
rats skeletal muscle. METHODS: Insulin resistant rat model was induced by high fat diet feeding. Thirty-nine male SD rats were randomly divided into two groups feeding either normal chow (NC, n=9) or high-fat diet(HF, n=30). After 2 mo, rats in group HF were randomly divided into three groups, high fat diet group (HFF, n=9), normal chow intervention group (HFN, n=9) and
rosiglitazone intervention group (HFR, n=12). After 1 mo intervention treatment, all rats were fasted for 12 h. The rats were killed and skeletal muscles were isolated rapidly ten minutes after insulin (10 U·kg -1 body weigh) intraperitoneal injection. The PKB expressions were tested with Western blotting. RESULTS: The rats in group HFF developed obvious
insulin resistance, their PKB expression of skeletal muscle (OD value 8.24±s 0.11 vs 9.36±0.18, P<0.01) decreased significantly compared with normal control group. Rats treated with rosiglitazone in group HFR and normal chow intervention in group HFN improved insulin resiatance obviously. Compared with group HFF, their PKB expression (OD value 8.89±0.08, 8.40±0.09 vs 8.24±0.11, P<0.01) increased significantly. CONCLUSION: Development of insulin resistance of rats which fed with high fat diet is obviously associated with suppression of insulin-stimulated PKB expression of skeletal muscle. Rosiglitazone can increase PKB expression of skeleted muscle and partially restore the impaired insulin signal transduction, and further improve insulin resistance. This may be one of the mechanisms which decreases the insulin resistance.