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Takayuki Fujii - One of the best experts on this subject based on the ideXlab platform.

Chen Guo-rong - One of the best experts on this subject based on the ideXlab platform.

  • mRNA expression of insulin receptor and leptin receptor in Liver of nonalcoholic Fatty Liver disease from diabetic rats
    Chinese Journal of Pathophysiology, 2009
    Co-Authors: Chen Guo-rong
    Abstract:

    AIM:To observe the pathologic changes of Liver in diabetic rats and to investigate the role of mRNA expression of insulin receptor and leptin receptor in the pathogenesis of nonalcoholic Fatty Liver disease (NAFLD). METHODS:Twenty male Sprague-Dawley rats were divided randomly into two groups:normal control group and diabetic group. After fed with high-fat diet for 4 weeks,diabetic rats were injected with streptozotocin at a dosage of 30 mg/kg intraperitoneally to induce NAFLD model of type 2 diabetes mellitus. Then the diabetic animals were fed with high-fat diet continuously for 12 weeks. At the end of the experiment,the rats were sacrificed,the concentrations of blood glucose,serum lipid,ALT and AST were measured biochemically. The levels of serum leptin and serum insulin were detected by enzyme-linked immunosorbent assay (ELISA) and radio immunoassay (RIA),respectively. The pathologic changes of Liver were observed under light microscopy (LM) stained with HE,Sudan Ⅲ and Masson trichrome staining,respectively. The ultra-structural changes of Liver were observed under transmission electron microscopy (TEM). Additionally,the mRNA expressions of PEPCK,G6Pase,insulin R and leptin R from rat Livers were assayed by semi-quantitative RT-PCR. RESULTS:The levels of blood glucose,serum insulin,serum TG,ALT and AST increased significantly (P0.01),serum TC elevated (P0.05),and the levels of serum leptin decreased (P0.01) in diabetic group compared to those in normal control group. Obvious Liver Fatty Degeneration,piecemeal necrosis with accompanying inflammatory infiltration and fibrosis were found under LM. Hepatocytes pyknosis,lots of lipid deposits in cytoplasm of hepatocytes,proliferation of collagen in space of Disse were observed under TEM in diabetic group. The expression of insulin R and leptin R mRNA in Liver from diabetic rats increased significantly (P0.01) while the expression of PEPCK and G6Pase mRNA remained unchanged. CONCLUSION:Insulin resistance plays an important role in the pathogenesis of NAFLD. Low level of serum leptin,up-regulation of mRNA expression of insulin R and leptin R in Liver caused by insulin resistance may be involved in this process.

  • Effect of gingko biloba extract on Liver from experimental type 2 diabetic rats
    Chinese Journal of Pathophysiology, 2007
    Co-Authors: Chen Guo-rong
    Abstract:

    AIM: To study the protective effect of the ginkgo biloba (EGB) extract on Liver from experimental type 2 diabetic rats and to explore its possible mechanism. METHODS: Thirty-nine male Sprague-Dawley rats were divided randomly into four groups: normal control group, high-fat group, diabetic group and EGB-treated group. After fed with high-fat diet for 4 weeks, the later two groups were injected with streptozotocin intraperitoneally to induce type 2 diabetes mellitus. EGB-treated group was injected intraperitoneally with EGB at a dose of 8 mg·kg-1·d-1, and the other three groups were treated with normal saline of the same volume. After 8 weeks, the morphologic change of hepatic tissue was observed under transmission electron microscope (TEM) and light microscope (LM), respectively. In addition, the activity of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-PX), total nitric oxide synthase (TNOS), inducable nitric oxide synthase (iNOS) and the content of malondialdehyde (MDA), nitric oxide (NO) in Liver homogenate were detected biochemically. RESULTS: Obvious Liver Fatty Degeneration, apparent decrease of glycogen granules in cytoplasm of hepatocytes under light microscope and hepatocytes pyknosis, lots of lipid deposits in cytoplasm of hepatocytes, proliferation of hepatic stellate cells and collagen under TEM were observed in diabetic group. The activity of SOD, CAT, GSH-PX decreased but the activity of tNOS, iNOS and the content of MDA, NO-2/NO-3 increased in diabetic group compared with normal control group. The pathological change was relieved in EGB-treated group. The activity of SOD, CAT, GSH-PX increased, the activity of tNOS, iNOS and the content of MDA, NO-2/NO-3 decreased in the Liver of rats in EGB-treated group compared with diabetic group. CONCLUSION: EGB exerts a beneficial effect on Liver in experimental type 2 diabetic rats. Anti-lipid peroxidation and suppression of NO production may be involved in this process.

Ji Zhonghe - One of the best experts on this subject based on the ideXlab platform.

  • Experimental Research of the Therapeutic Effect of Silibinin Capsule on Fatty Liver in Rats
    The Journal of Medical Theory and Practice, 2007
    Co-Authors: Ji Zhonghe
    Abstract:

    Objective: To investigate the therapy effect of dangfeiliganning capsules(silibinin) on Fatty Liver in experimental rats.Methods: 60 Wistar rats were divided into 3 groups randomly: The rats of model control group were subcutaneously injected the mixture of carbon tetrachloride(40%) and plant oil(60%) according to its weight(0.5ml/100g) with two consecutive days per week for 3 weeks.The rats of normal control group were also subcutaneously injected the saline solution with the same dosage.At the third weekend,part of the rats of the model control group were divided into 4 therapy groups according to the dosage,they were stopped injecting the mixture(carbon tetrachloride and plant oil) and given different therapy drugs by gastric lavage every day for 3 weeks,the rest of the model control group and the normal control group were all stopped injecting the mixture(carbon tetrachloride and plant oil) but given saline by gastric lavage every day for 3 weeks.At the end of the sixth week,all these experimental rats were anaesthetised with sodium pentobarbital and killed for obtaining their blood and Liver tissue,then the levels of ALT,TG,CHO,LDL,VLDL,Cr,BUN and GS in the sera was tested and the Liver tissues were examined by pathologic methods.Results:In the group treated with silibinin,the serum levels of ALT,TG,CHO,LDL,VLDL,Cr,BUN and GS was reduced significantly(P0.05),but the pathological examination suggested that the degree of Liver Fatty Degeneration and Liver fibrosis was obviously relieved after the treatment of silibinin.Conclusion: Silibinin has therapeutical effect on the formed Fatty Liver in experimental rats.

Fei Zou - One of the best experts on this subject based on the ideXlab platform.

  • Green tea polyphenol epigallocatechin-3-gallate ameliorates insulin resistance in non-alcoholic Fatty Liver disease mice
    Acta pharmacologica Sinica, 2015
    Co-Authors: Lu Gan, Zijun Meng, Ri-bo Xiong, Jin-qiang Guo, Zhi-wei Zheng, Yan-ping Deng, Bing-de Luo, Fei Zou
    Abstract:

    Epigallocatechin-3-gallate (EGCG) is a major polyphenol in green tea. In this study, we investigated the effects of EGCG on insulin resistance and insulin clearance in non-alcoholic Fatty Liver disease (NAFLD) mice. Mice were fed on a high-fat diet for 24 weeks. During the last 4 weeks, the mice were injected with EGCG (10, 20 and 40 mg·kg−1·d−1, ip). Glucose tolerance, insulin tolerance and insulin clearance were assessed. After the mice were euthanized, blood samples and tissue specimens were collected. Glucose-stimulated insulin secretion was examined in isolated pancreatic islets. The progression of NAFLD was evaluated histologically and by measuring lipid contents. Insulin-degrading enzyme (IDE) protein expression and enzyme activity were detected using Western blot and immunocapture activity assays, respectively. The high-fat diet significantly increased the body weight and induced grade 2 or 3 Liver Fatty Degeneration (steatosis, lobular inflammation and ballooning) accompanied by severe hyperlipidemia, hyperglycemia, hyperinsulinemia and insulin resistance in the model mice. Administration of EGCG dose-dependently ameliorated the hepatic morphology and function, reduced the body weight, and alleviated hyperlipidemia, hyperglycemia, hyperinsulinemia and insulin resistance in NAFLD mice. Furthermore, EGCG dose-dependently enhanced insulin clearance and upregulated IDE protein expression and enzyme activity in the Liver of NAFLD mice. EGCG dose-dependently improves insulin resistance in NAFLD mice not only by reducing body weight but also through enhancing the insulin clearance by hepatic IDE. The results suggest that IDE be a potential drug target for the treatment of NAFLD.

Zhao He-ping - One of the best experts on this subject based on the ideXlab platform.

  • Effect of Jiangzhiyigan granula on nonalcoholic Fatty Liver disease
    Journal of Shanxi Medical University, 2008
    Co-Authors: Zhao He-ping
    Abstract:

    Objective To investigate the effect of Chinese medicine Jiangzhiyigan granula on nonalcoholic Fatty Liver disease(NAFLD)in rats. Methods Twenty-four male Wistar rats were randomly divided into three groups(n=8 in each group).The rats were fed with standard diet in normal group and with high-fat diet in model group and treated group.Then the rats were given Jiangzhiyigan granula in treated group at the beginning of experiment,while the same volume of life drinking water in normal group and model group.After eight weeks,the rats were executed.The pathological changes were observed,and the levels of Liver total cholesterol(TC),triglyeride(TG),HDL-C,LDL-C,TXB2,6-Keto-PGF1α and TXB2/6-Keto-PGF1α were determined. Results Hepatosteatosis in treated group was obviously improved.The levels of HDL-C and 6-Keto-PGF1α in treated group were significantly higher than that in model group,while the levels of TC,TG,LDL-C and TXB2 and the ratio of TXB2/6-Keto-PGF1α were significantly lower than that in model group. Conclusion Jiangzhiyigan granula may lessen Liver Fatty Degeneration,increase the levels of HDL-C and 6-Keto-PGF1α and decrease the levels of TC,TG,LDL-C,TXB2 and TXB2/6-Keto-PGF1α,which may be one of the mechanisms of anti-nonalcoholic Fatty Liver disease.