Studies On The Mechanism Of Berberine In Improving Insulin Resistance Of Type1Diabetic Rats

Diabetes mellitus (DM) is a metabolic syndrome of chronic disorders resultingfrom absolute or relative lack of insulin. Insulin resistance occurs as a response tocontinuous high glucose, high fat and oxidative stress in the body, accelerating thedevelopment and deterioration of diabetes mellitus. Previous studies have indicatedthat berberine could improve the insulin resistance by lowering the blood glucose andfat, and reducing oxidative stress, but its underlying mechanism is not quite clear. Inthis study, we employed alloxan-induced diabetes rat model to study the effect ofberberine on the body weight and food intake, blood glucose and fat, and the level ofplasma triglycerides（TG）, Methyl Di Aide Hyde(MDA) and free fatty acid (FFA) inserum, TG and MDA in liver. According to the analysis of the effect of berberine onthe activity of AMPK and its downstream target ACC, and the translocation ofGLUT4in skeletal muscle, we explored the mechanism through which berberinecontributes to reduce blood glucose and fat, and improve insulin resistance in diabeticrats, which provides scientific evidence for treating diabetes with berberine.Our results demonstrated that the food intake of berberine-treated group ratsdecreased compared to that of diabetes model group after treated with berberine for9days. In contrast, the body weight of berberine-treated group increased. We alsofound that the fasting blood glucose, TG, FFA, MDA in serum and TG, MDA in liverof berberine-treated group declined significantly compared to diabetes model group.Furthermore, our data from western blot indicated that there was an evident decreasein the phosphorlation of AMPK and its downstream target ACC, and the translocationof GLUT4in skeletal muscle of diabetes model group compared to control group, butthey all increased and even recovered to the state of control group after treated withberberine.The results suggest that berberine could reduce fasting blood glucose, and inhibitexcessive lipid accumulation and oxidative stress, improve insulin resistance viaactivating the AMPK signaling pathway and its downsteam target ACC, and promotethe translocation of GLUT4to the cell membrane of sleletal muscle in diabetes rats.