Objective To observe the effect and mechanism of epigallocatechin-3-gallate (EGCG) on insulin resistance in type 2 diabetic rats.
Methods Totally 90 Sprague-Dawley rats were randomly divided into a normal control group (10 rats) and a model group (80 rats). The rat model of type 2 diabetes mellitus (T2DM) was established with high fat and sugar diet combined with intraperitoneal injection of 35 mg/kg streptozotocin (STZ). Fifty T2DM model rats were randomly divided into five groups (10 in each group): a positive control group (with distilled water), metformin group (300 mg/kg), low-, moderate-, and high-EGCG group (25, 50, 100 mg/kg). By the end of 6-week intragastric treatment, the body weight, fasting blood glucose (FBG) and serum insulin (INS) level were measured, and insulin sensitivity index (ISI) and homeostatic model assessment of insulin resistance (HOMA-IR) were calculated. The mRNA and protein expression of phosphoenolpyruvate carboxykinase (PEPCK) in liver tissue and glucose transporter 4 (GLUT4) in skeletal muscle were detected with real-time fluorescence quantitative PCR (real time-PCR) and Western blot.
Results Significantly decreased body weight but increased FBG and HOMA-IR were detected in T2DM model rats compared to those in the normal control rats (P < 0.05 for all). Significantly lower serum INS but higher ISI and HOMA-IR were observed in the rats of moderate-EGCG group than those in the T2DM model rats (all P < 0.05). In comparison to the normal control rats, the T2DM model rats had significantly increased PEPCK mRNA expression in liver tissues but decreased GLUT4 mRNA expression in skeletal muscles (both P < 0.05); while, the rats treated with high-EGCG had significantly lower PEPCK mRNA expression in liver tissues but higher GLUT4 mRNA expression in skeletal muscles than the T2DM model rats (both P < 0.05).
Conclusion EGCG can improve insulin resistance to a certain extent in type 2 diabetic rats and the effect may be related to the enhancement of insulin sensitivity, the inhibition of hepatic gluconeogenesis, and the increase of glucose transport in skeletal muscle.
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