Abstract: The aim of this study is to investigate the effect and mechanism of Dicliptera chinensis polysaccharide (DCP) on glucose and lipid metabolism in rats with high fat diet.After feeding for 8 weeks with high-fat diet,40 rats with successful modeling were randomly divided into normal group,model group and DCP groups (100 and 200 mg/kg) with 10 rats in each group.Starting from the 9th week,the DCP dose groups were intragastrically administered,and the rats of normal group and the model group were given an equal volume of distilled water for 6 weeks,and then sacrificed to collect blood and liver samples.Determination of serum triglyceride (TG),total cholesterol (TC),low density lipoprotein cholesterol (LDL-C),low density lipoprotein cholesterol (HDL-C),free fatty acid (FFA),advanced glycation end product-peptide (AGE-P),glycated hemoglobinan (HbAlc),hepatic glycogen and TG content by biochemical methods;The fasting blood glucose (FBG) level were measured by glucose oxidase method;The serum fasting insulin (FINS) content were tested by enzyme immunoassay(ELISA) to calculate insulin resistance index (HOMA-IR);Observation of fatty deposition in liver tissue by oil red O staining;Real-time quantitative PCR (RT-PCR) detection of sterol regulatory element-binding protein 1(SREBP-1) mRNA and Adenosine 5′-monophosphate (AMP)-activated protein kinase(AMPK)mRNA level;Western blot analysis of SREBP-1,AMPK and p-AMPK expression in rat liver tissue.The results showed that the DCP (100,200 mg/kg) dose group significantly down-regulated the contents of TC,TG,LDL-C,FBG,FINS,AGE-P,HbAlc and HOMA-IR,up-regulated the HDL-C and hepatic glycogen content,reduction of fat deposits,and significantly up-regulated the p-AMPK and inhibited SREBP-1 protein and its mRNA in liver tissue.The results of this study suggest that the mechanism by which DCP regulates glucose and lipid metabolism in rats may be related to inhibition of the AMPK/SREBP-1 pathway.

Key words: Dicliptera chinensis polysaccharide (DCP), high fat diet, glucolipid metabolism, AMPK/SREBP-1 signaling pathway