| Objective:1.To study the effect of Rehmannia glutinosa oligosaccharides(ROS) on the key enzymes of the hepatic glucose metabolism and the related gene expression in type 2 diabetic and dexamethasoneinduced insulin resistant rats.2.To study the ameliorative effect and mechanism of ROS on the glucose metabolism in high lipid food-induced insulin resistant rats.Methods:1.To induce the model of type 2 diabetic rats which were injected intraperitoneally with STZ(30 mg·kg-1) after fed with high lipid food for two months.The rats were divided into the control group,type 2 diabetic model group,ROS(100,200 mg·kg-1·d-1) treated group and metformin(200 mg·kg-1·d-1) treated group.All drugs were administered by intragastric administration(i.g.).The ameliorative effects of ROS on glucose metabolism in type 2 diabetic rats were evaluated through the changes of the body weight,plasma glucose,quantity of ingestion,quantity of drinking,content of the hepatic glycogen, content of the muscle glycogen and index of organs.2.Studying the effect of ROS on the activity and gene expression of hepatic key enzymes in type 2 diabetic rats.Taking the liver to determine the activity and gene expression of GK and G-6-Pase,the skeletal muscle to determine the gene expression of GLUT4 and the fat to determine the gene expression of TNF-α,PPAR-γand adiponectin by RT-PCR.3.The insulin resistance model was induced by both high lipid food and dexamethasone(1 mg·kg-1, i.p.every other day).The rats were divided into the control group,insulin resistance model group,ROS (100,200 mg·kg-1·d-1) treated group and rosiglitazone(3.4 mg·kg-1·d-1) treated group.All drugs were administered by intragastric administration(i.g.).The glucose tolerance test was taken every other week. The tats were killed after they had been administered for six weeks.The ameliorative effects of ROS on insulin resistance were measured through the glucose tolerance,body weight and organ index.4.Studying the effect of ROS on the activity and gene expression of hepatic key enzymes indexamethasone-induced insulin resistant rats.Taking the liver to determine the activity and gene expression of GK and G-6-Pase,the skeletal muscle to determine the gene expression of GLUT4,the fat to determine the gene expression of TNF-α,PPAR-γand adiponectin by RT-PCR.5.Studying the ameliorative effect and mechanism of ROS on the insulin resistance in high lipid food-induced insulin resistant rats.The insulin resistance rats were induced by feeding with high lipid food for two months,the rats were divided into the control group,insulin resistance model group,ROS (100,200 mg·kg-1·d-1) treated group and rosiglitazone(3.4 mg·kg-1·d-1) treated group.All drugs were administered by intragastric administration(i.g.).The glucose tolerance test was taken every other week. The rats were killed after they had been administered i.g for six weeks.The ameliorative effects of ROS on insulin resistance were measured through the glucose tolerance,body weight,hepatic glycogen, plasma lipids,organ index and HK activity.Results:1.The hypoglycemic effect and mechanism of ROS in type 2 diabetic rats:The concentration of the fasting plasma glucose(P＜0.05),quantity of ingestion(P＜0.05)and drinking(P＜0.01)can be reduced significantly by ROS in type 2 diabetic rats.And the organ index can be ameliorated.On the respect of the mechanism,the content of the hepatic glycogen(P＜0.01) can be improved significantly,the activity (P＜0.01) and gene expression(P＜0.05) of GK can be increased,and the activity(P＜0.01) and gene expression(P＜0.05) of G-6-Pase can be reduced.The gene expression of PPAR-γ(P＜0.05),adiponecti (P＜0.01) and GLUT4(P＜0.05) can be increased by ROS.2.The ameliorative effect and mechanism of ROS on the insulin resistance in dexamethasoneinduced insulin resistant rats:the concentration of the fasting plasma glucose can be reduced by ROS in insulin resistant rats.The plasma glucose level of the high dose of ROS treated group was decreased 6.8%(P＜0.05) compared with that of the model group.The low dose group was 9.1%(P＜0.05).The glucose tolerance and organ index of insulin resistant rats can be ameliorated.On the respect of the mechanism,the activity(P＜0.05) and gene expression(P＜0.05) of GK can be increased,the activity (P＜0.05) of G-6-Pase can be reduced by ROS.The gene expression of PPAR-γ(P＜0.05)and GLUT4 (P＜0.05) can be increased by ROS.3.The ameliorative effect and mechanism of ROS on the insulin resistance in high lipid foodinduced insulin resistant rats:the glucose tolerance of insulin resistant rats can be ameliorated by ROS.Its ameliorative effect on the glucose metabolism maybe have a close relationship with increasing the index of the thymus(P＜0.05) and adrenal gland(P＜0.05),reducing the concentration of TC,TG and FFA, reducing the contend of the hepatic glycogen(P＜0.01) and muscle glycogen and increasing the activity of HK in the muscle.Conclusion:1.ROS has the hypoglycemic effect,meanwhile reduces the quantity of ingestion and drinking.It has the ameliorative effect on the hepatic glucose metabolism through increasing the content of the hepatic glycogen,increasing the activity and gene expression of GK and reducing the activity and gene expression of G-6-Pase and they can active the gene expression of PPAR-γ,adiponectin and GLUT4 in type 2 diabetic rats.2 ROS can reduce the concentration of the fasting plasma glucose and ameliorate the glucose tolerance of insulin resistant rats.It has the ameliorative effect on the hepatic glucose metabolism through increasing the activity and gene expression of GK and reducing the activity of G-6-Pase and can active the gene expression of PPAR-γand GLUT4 in dexamethasone-induced insulin resistant rats.3.ROS can ameliorate the glucose tolerance of insulinresistant rats.It can increase the index of the thymus and adrenal gland,reduce the concentration of TC,TG and FFA,decrease the content of the hepatic glycogen and muscle glycogen;meanwhile increase the activity of HK in the muscle.
|
PDF Full Text Request