Regulation Of Ginsenoside Compound K On Fat Metabolism In Liver Tissues Of Db/db Mice

Objective:The effects of Compound K,a bacterial metabolite of Ginsenoside in intestinal tract,on lipid metabolism in liver tissue of db/db mice were studied at animal,tissue and protein levels by using the non-alcoholic fatty liver model of db/db mice with leptin receptor gene mutation.Methods:There were 6 BKS mice and 12 db/db mice in 6-8 weeks.BKS mice served as normal control group,model group(leptin receptor gene mutated db/db obese mice)and treatment group(leptin receptor gene mutated db/db obese mice and ginsenoside Compound K treatment).Three groups of animals were given normal diet.The mice in the treatment group were fed with ginsenoside Compound K solution at a dose of 20 mg/kg daily.The food intake,body weight and liver weight of mice were collected through experiments.Fasting blood glucose(FBG)of db/db mice after fasting for 12 hours was measured by an electronic blood glucose meter.Fat deposition and pathological changes of liver were observed by oil red O staining and HE staining.Western blot(WB)was used to detect the activity changes of GRK-2,mTOR,SIRT-3,AMPK and downstream lipid metabolism-related proteins in liver tissues.Results:The following results were obtained that ginsenoside Compound K could inhibit appetite,weight loss,liver weight,fasting blood glucose(FBG)and triglyceride content of liver in db/db mice with fatty liver by using leptin receptor gene mutation;Primary,ginsenoside CK could reduce intrahepatic fat deposition and formation of fat vacuoles,and inhibit fatty liver development.Thirdly,protein level showed that ginsenoside CK inhibited GRK-2 and mTOR,activated SIRT-3 protein,finally activated AMPK,up-regulated CYPT7A1,AOX-1 protein and inhibited SREBP-1 protein expression.Conclusions:First at all,ginsenoside Compound K(20mg/kg)could improve obesity in db/db mice with leptin receptor gene mutation and delay non-alcoholic fatty liver in db/db mice.Second,ginsenoside Compound K may activate AMPK and regulate the expression of downstream lipid metabolism related proteins by regulating the expression of GRK-2,mTOR and SIRT-3 proteins,further inhibiting the accumulation of triglycerides in the liver of db/db mice.