Left To Hypoglycemic Fat Eliminating Improve Mkr Control Ppar Alpha, Cyp2e1 Expression Of Transgenic Mice With Type 2 Diabetic Fatty Liver Function Research

Purpose:Genetically modified type2diabetic patients with nonalcoholic fatty liver in mice as a model (referred to as the fat MKR mouse), a high-fat feeding of MKR the observed Zuogui hypoglycemic CLT side of the high-fat MKR mice fasting glucose, impaired glucose tolerance, serum insulin liver function, blood lipids, peripheral organizations (skeletal muscle, fat, liver) in the nuclear transcription factor of PPAR-alpha and CYP2E1expression of affect, and then explore the left normalized hypoglycemic clear fat side through the regulation of nuclear transcription factor of PPAR-alpha and CYP2E1expression to improve the MKR mice type2diabetic patients with nonalcoholic fatty liver mechanism.Meathods:1. High-fat group MKR mice at8weeks, fasting glucose, AST, and AST, TG and the TC and LDL-C, HDL-C content than those in the wild of C57BL/6mice and MKR&P food group was significantly increased (p<0.05), serum insulin increased (p<0.05), impaired glucose tolerance (p<0.05).2. Left normalized hypoglycemic the CLT side group has a significantly lower blood glucose, improve glucose tolerance (p<0.05), improve insulin resistance (p<0.05), improve fat MKR mouse liver dysfunction (p<0.05) compared with MKR model group, lower lipid levels (p<0.05), the regulation of pancreatic islets in peripheral tissues (fat, skeletal muscle, liver, etc.) of nuclear factor of PPAR-alpha a CYP2E1table (p<0.05) of metformin simvastatin group, no statistically significance (p>0.05).Results:1. MKR mice and non-fat-fed high fat diet MKR mice and C57mice, control experiments show that the MKR transgenic type2diabetic rats there is significant insulin resistance, impaired glucose tolerance, high-fat feeding can further increase the lipid disorders, resulting in impaired liver function2. Zuo Gui the hypoglycemic clear fat side with lowering blood glucose, improve glucose tolerance and improve insulin resistance and improve liver function, regulating the role of lipids.3. Zuo Gui hypoglycemic CLT, has raised islets in peripheral tissues (fat, skeletal muscle, liver, etc.) the nuclear transcription factor PPAR-alpha and down-regulated the expression of CYP2E1metabolic enzymes, the improvement of type2diabetic patients with non-alcoholic fatty liver disease the role of mechanism may be through regulation of nuclear transcription factor PPAR-a and CYP2E1metabolic enzyme expression, thereby improving insulin resistance, regulates in vivo glucose and lipid metabolism, reduced hepatic lipid accumulation, mitigation of the development of fatty liver, liver function indicators improved, thereby protecting the liver.