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Objective: To establish a model of non-alcoholic fatty liver disease (NAFLD) in rats to explore the mechanism of the endotoxemia enterogenic formation and its role in NAFLD, plasma adiponectin levels, hepatic peroxisome proliferator-activated expression and glycine receptor γ (peroxisome proliferators-activated receptors gamma, PPARγ) expression in rat plasma adiponectin levels and liver tissue PPARγ and its mechanism to provide new ideas for clinical treatment of nonalcoholic fatty liver disease . Methods: 54 of clean male Wistar rats were randomly divided into three groups: control group (normal diet feeding); model group (fatty liver group) (84% of the normal diet, 14% lard, cholesterol feeding); treatment group (glycine group) (79% of the ordinary feed, lard 14%, 2% cholesterol, 5% glycine feeding). Rats were killed respectively in the first 8,10,12 weekend, measurement of body weight and liver weight, liver index, detection of plasma insulin, glucose, tumor necrosis factor α (TNFα), transaminase (ALT), triglyceride (TG), lipid adiponectin and portal vein plasma endotoxin (ET), calculated insulin resistance index (IRI); Liver HE staining to observe the morphological changes of the liver; liver tissue PPARγ expression was detected by RT-PCR method. Results: (1) each group body weight of rats showed a growth model group, liver index was significantly higher than the control group and the treatment group (P lt; 0.05), and tended to increase with time; (2) model fasting blood glucose tended to increase compared with the same period in the control group, 12 weeks was significantly higher (P lt; 0.05), blood sugar is lower than the same period of the treatment group, the control group, the difference was not statistically significance (P gt; 0.05); (3) insulin and IRI model group compared with the control group over the same period of 8 weeks was significantly higher (P lt; 0.05), the treatment group were significantly lower than the same period in the model group (P lt; 0.05); (4) and normal control group, model rats eight weeks of TNFα, ET was significantly higher (P lt; 0.05), 10 weeks of TG was significantly higher (P lt; 0.01); compared with the same period in the model group significantly reduced the treated rats TNFα and TG ( P lt; 0.05), 12 ET was significantly lower (P lt; 0.05); (5) compare eight weeks from the model of the control group rats ALT elevated, 10 weeks, the difference was statistically significance (P lt; 0.05), a 12-week treatment group was significantly lower than the same period in the model group (P lt; 0.05); (6) three time periods adiponectin model group were significantly lower than the same period in the control group (P lt; 0.01) with the same period in the model group In comparison, the treatment group was significantly higher (P lt; 0.05); (7) liver histological change: control group liver cells arranged rules, hepatic cords clear, no fat droplet formation and inflammatory cell infiltration. Model group increased, with time lesions visible cytoplasm loose, cell swelling, liver cord disorders, lipid droplets to form nuclei pushed to one side, almost all liver cells in the liver tissue appears to bullous lipid droplets as The main mixed steatosis part inflammatory cell infiltration. The treatment group compared with the same period in the model group lesions alleviate; (8) Linear correlation analysis showed: of TNFα portal vein serum ET correlation analysis: r = 0.819, P = 0.001 lt; 0.01, were highly correlated; insulin resistance index and plasma lipid associated prime correlation analysis: r = -0.787, P = 0.001 lt; 0.01, a high negative correlation; plasma TNFα and adiponectin correlation analysis: r = -0.673, P = 0.002 lt; 0.01, a high negative correlation; Insulin Resistance index and plasma TNFα correlation analysis: r = 0.712, P = 0.001 lt; 0.01, are highly correlated; (9) RT-PCR showed that liver PPARγ expression increased with the modeling time in 12 weeks peak (P lt; 0.01), glycine can be lowered PPARγ gene expression. Conclusion: in NAFLD development process associated with intestinal endotoxemia hyperlipidemia. Glycine alleviate fatty liver insulin resistance to protect the liver. Glycine increase plasma adiponectin lowered by reducing the level of endotoxin liver tissue PPARγ gene expression to relieve of NASH.
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