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Aim to build a high -sugar diet nonalcoholic fatty liver disease (NAFLD) model , through the different time points in rat liver tissue ACC ﹑ ChREBP and its target gene expression of FAS mRNA and protein levels , ChREBP and ACC ﹑ FAS gene promoter sub- carbohydrate response element (ChRE) binding of assay to investigate ChREBP and its target genes ACC ﹑ FAS in high glucose nonalcoholic fatty liver disease (NAFLD) pathogenesis role. Methods 32 SD rats were randomly divided into control group and high glucose group . High glucose group were sacrificed at 4,8,12 weekend , the control group were sacrificed at 12 weeks . Each group were sacrificed after 12 hours of fasting before abdominal aortic blood test triglycerides (TG), total cholesterol (TC), alanine aminotransferase (ALT), aspartate aminotransferase (AST), HE staining of liver steatosis , RT- PCR and Western blot were measured at different time points in rat liver tissue ChREBP, ACC, Fan mRNA expression and protein levels , chromatin immunoprecipitation method to analyze the different time points ChREBP and ACC ﹑ FAS gene promoter carbohydrate response element ( ChRE) combined with the situation . Was successfully constructed high-sugar diet rat model of NAFLD , with modeling time, serum biochemistry (TG,, TC, ALT, AST) index was significantly higher (P lt; 0.01), has been increasing the degree of liver fat , 4 , 8 and 12 week high glucose liver tissue ChREBP, ACC, Fan mRNA, protein and ChREDNA expression levels compared with the control group difference was significant (P lt; 0.01), and with the modeling time extension , and its expression increased significantly . Conclusion The high carbohydrate diet can enhance the expression of ChREBP and ChREBP ACC ﹑ by upregulating the expression of FAS involvement of non- alcoholic fatty liver formation . Therefore, high-sugar diet ChREBP may be caused by non- alcoholic fatty liver important pathogenic factor , ChREBP may become the treatment of non -alcoholic fatty liver new role of targets.
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