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The first part of the high fat diet-induced insulin resistance in a rat model of purpose: the establishment of a high fat diet-induced insulin resistance rat models. Methods: 60 male Wistar rats, 8 weeks old, weighing 180-200g. The rats were randomly divided into normal control group, 12, fed a normal diet; fat diet group (n = 48), fed with high fat feed. Experiment Weigh weight, serum lipids (TC, TG, HDL-c, LDL-c) and blood sugar, glucose tolerance test, insulin tolerance test to determine glucose metabolism; enzyme-linked immunosorbent assay serum insulin levels, calculated Insulin sensitivity index and insulin resistance index for assessing insulin sensitivity. Results: The high-fat diet group weight, TC, TG and LDL-c water average significantly higher than the normal diet group (P lt; 0.01), HDL-c, fasting blood glucose compared with the normal diet group had no significant difference (P gt; 0.05) ; the glucose tolerance test and insulin tolerance test, the area under the blood glucose levels and glucose curve after the load of the high fat diet group were higher than the normal diet group (P lt; 0.05 or P lt; 0.01); while the group fasting serum insulin, insulin resistance index were higher than the normal diet group (P lt; 0.05 or P lt; 0.01), insulin sensitivity index was lower than the normal diet group (P lt; 0.05). Conclusion: The high fat diet can be successfully established insulin resistance rat models, performance similar to the model of human obesity due to insulin resistance, suitable for the study of insulin resistance. The second part of ursolic acid on insulin resistance in rats sugar, lipid metabolism, and liver glucokinase Objective: To observe the ursolic acid on insulin resistance in rats sugar, lipid metabolism, and liver glucokinase. Methods: high-fat diet group, 48 rats were randomly divided into model control group (PBS solution gavage), metformin (metformin 200mg/kg · d gavage), the ursolic acid high dose group (ursolic acid 300mg/kg. d orally), ursolic acid low-dose the group (150mg/kg.d gavage), 12 in each group, continue to feed a high fat diet. The normal control group 12 fed a normal diet and orally with PBS solution. Experiment Weigh weight, medication 4 weeks and 8 weeks, serum lipids (TC, TG, HDL-c, LDL-c) and glucose; oral glucose tolerance test, insulin tolerance test to determine glucose metabolism; anthrone method detection of liver glycogen content; enzyme-linked immunosorbent assay serum insulin levels and insulin sensitivity index and insulin resistance index for assessing insulin sensitivity; HE staining of liver pathological changes; enzyme-linked immunosorbent assay glucokinase content, real-time PCR assay glucokinase mRNA expression, immunohistochemical assay glucokinase protein expression. Results: The weight of the treated rats, TC, TG, LDL-c, load blood glucose, glucose area under curve, fasting serum insulin, insulin resistance index were lower than those in the untreated control group (P lt; 0.05 or P lt; 0.01 ), while the treated group, insulin sensitivity index and liver glycogen content higher than that in the untreated control group (P lt; 0.05 or P lt; 0.01). Treated group near normal part of the liver, model group obviously hepatic steatosis. Glucokinase content of the treated group, the protein and mRNA expression is higher than the model control group (P lt; 0.05 or P lt; 0.01). Conclusion: Ursolic acid by reducing weight, improve glucose and lipid metabolism, increased liver glycogen content of glucokinase and glucokinase mRNA and protein expression to improve insulin resistance.
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