| Object: Diabetes mellitus is a disease which cause and mechanism has not been clarified. There are many clinical types with high blood glucose as their common major marker. Absolutely and comparatively deficiency of insulin and decreased sensitivity of tissue and cell to insulin is the basement of developing into diabetes.In diabetic state, impaired glucose utilization due to insulin deficiency renders tissues more dependent on lipid oxidation for their energy instead of glucose. The synthesis of lipid is decreased and the mobilization and decomposition of fat is increased, causing an increased level of free fatty acid and triglyceride in blood. The fatty acid overload is accompanied by an increased β-oxidation of fatty acids .It has been established that β-oxidation of fatty acids occurs in both peroxisomes and mitochondria. But β-oxidation pathways in these two organelles are different at many aspects such as substrate, end product, enzymes. In addition, peroxisomes of livers in rodents can be induced to proliferate. Such induction is mediated with peroxisome proliferator-activated receptor-α(PPARα). A large number of chemicals, including hypolipidemic drug,chloride, and its structural analogs, as well as hypolipidemic agents structurally unrelated to chloride such as Wy-14,643 and fatty acids and their derivatives, can activate PPARα, producing a marked induction both of peroxisomes and of the synthesis of number of peroxisomal enzymes , particularly those of the peroxisomal pathway forβ-oxidation of fatty acids in livers of rodents.A variety of data accumulated has indicated that membrane of peroxisomes proliferated by chemical agents display physical properties which distinguish them from peroxisomes in untreated rodents. These differences include membrane phospholipid composition, integral membrane protein profile, membrane fluidity, membrane permeability etc. All these showed that the structure of proliferated peroxisomes is different from peroxisomes in physical state.In diabetes mellitus, strengthened fat mobilization and the β-oxidation pathway of fatty acids will produce many fatty acids and their deviations, the latter are the natural ligands for PPARα, they can also cause peroxisomes in livers of rats proliferated, the amount and activity of enzymes involved β-oxidation pathway is increased at the same time. However it is not yet know whether the membrane properties of liver peroxisomes proliferated in diabetic state are different from normal state.For this purpose, with the diabetic rat model induced by streptozotocin, we intended to study the membrane propertiesfrom two points, that is membrane fluidity and membrane permeability, and investigate peroxisomal function of liver in diabetic state in order to know more about the lipid metabolism of diabetes mellitus .Methods: Twenty eight Sprague-Dawlay rats aged six weeks, sex ratio one to one, weighting 200-250 grams, were divided randomly into sex-matched experimental and control groups. The experimental group were injected intraperitoneally with streptozotocin to induce diabetes. Diabetes was confirmed three days after injection by the presence of hyperglycemia (fasting blood glucose≥15mmol/L).Two weeks following induction of diabetes, fasting blood glucose were tested with rat tail vein blood and rats were exsanguinated , blood and liver tissue were used as materials for exeperiment. Perform morphological investigations for peroxisomes of rat liver under electron microscope. With type SYNCHRONLX20 automatic biochemistry analyzer, detect serum cholesterol, triglyceride with immune turbidimetry method, high density lipoprotein with enzymatic assay. Prepare erythrocytes membrane by lower osmotic pressure solution , isolate peroxisomes, mitochondria and microbodies by sucrose concentration density gradient centrifugation method; Using 1,6-diphenyl-1,3,5-hexatriene(DPH) as probe, detect fluorescence polarization to calculate membrane fluidity of erythrocytes, peroxisomes, mitochondria and...
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