Effect Of High-carbohydrate Diets On Aggravating In Rats With Nonalcoholic Steatohepatitis

Objective to explore the effects of sucrose on progress in rats with nonalcoholic steatohepatitis .Methods Experiment 1 24 wistar rats were randomly divided into three groups: (1)normal control (Control)group, high saturated fatty acid(HF)group, high glucose and high fat(HGF)group. After 9 weeks, the HF and HGF groups were induced the model of nonalcoholic fatty liver and nonalcoholic steatohepatitis via diet of high glucose and high fat.Everygroup animals were all freely eaing and drinking. And every group animals were bred with divided caging. All of models were formed for 9 weeks. Check fasting plasma glucose of rats; Observe free fatty acid(FFA) , malondialdehyde(MDA) , Alanine aminotransferase(ALT) of the plasma and TG of the liver tissue homogenate ; Assay tumor necrosis factor-α(TNF-α). Observe the change of liver histology with naked eye and light microscope. According to criterion of the steatosis and inflammation of liver histology, definite the type of NAFLD. Grouping and breeding of animals of Experiment 2—5 are same as Experiment 1. Detect the insulin of the serum with method ofradio-immunity, and calculate insulin resistance index(IRI) so as to judge the degree of IRI in every group . Observe the TNF-αof liver with the immunohistochemisty by SP methed . Detect the expression of uncoupling protein-2(UCP-2) and P38mitogen activated protein kinase(MAPK) of the rats with the way of Western blotting so as to judge the change of crista mit-ochondriales of the liver cells and degree of inflammation of liver histology. Last, detect the change of LPS in the blood with the methods of tachypleus amebocyte lysate and proceed the correlation test so as to judge the relationship between IETM and NASH.Results Blood fasting sugar between three groups were not significant difference and were in the normal limit. The levels of plasma FFA, MDA, ALT, TNF-αin model grou-ps were obviously higher than in Control(P<0.01) , and group HGF was higher than gr-oup HF (P<0.05). There were cellular infiltration of steatosis and phlogocyte in the liver tissue, and the group HGF was more grave than group HF. The expression of UCP-2 of groups HF were higher than HGF, meanwhile both HGF and HF were higher than group control; The expression of MAPKP38 of groups HGF were higher than gr-oup HF, but expression of group control was only microcontent expression . The level of LPS of blood plasma in grou-p model was higher than group control ,and group HGF was higher than group HF,and LPS was relevant to every index.Conclusion Exorbitancy cane sugar can enhance the progress of the nonalcoholic fatty liver and NASH. Sugar toxicity, IRI , IETM and factor of inflammation were produced via signal transmiting which play a important role in the progress of NASH induced by high cane sugar diet.