Ginsenoside CK regulates non-alcoholic fatty liver disease by regulating liver fat metabolism and gut microbiota.

CK intervention significantly attenuated body weight gain in HFHC diet-induced NAFLD mice.

• The body weight of mice in the CK-L group (60 mg/kg) decreased by approximately 11.7% compared to the HFHC diet group.
• A high-fat-high-cholesterol (HFHC) diet-induced mouse model was used.
• Two doses of CK were tested, with the low dose being 60 mg/kg.

CK reduced hepatic inflammation in HFHC diet-induced NAFLD mice.

• Hepatic inflammation was reduced by about 35%-45% following CK intervention.
• CK exhibits hepatoprotective and anti-inflammatory activities as previously established.
• Inflammation reduction was assessed in the context of the HFHC diet-induced mouse model.

CK improved hepatic lipid deposition in HFHC diet-induced NAFLD mice.

• Lipid deposition was improved by roughly 50%-60% with CK intervention.
• NAFLD is characterized by hepatic lipid metabolism disorder, which CK was found to ameliorate.
• Lipid deposition improvement was observed in the context of the HFHC diet-induced mouse model.

CK activates the PPAR signaling pathway to regulate lipid metabolism-related genes and proteins.

• CK activates the peroxisome proliferator-activated receptor (PPAR) signaling pathway.
• This activation regulates the expression of lipid metabolism-related genes and proteins.
• Activation of the PPAR pathway was identified as the mechanistic basis for CK's amelioration of lipid metabolism disorder.

CK reverses HFHC diet-induced gut microbiota dysbiosis in NAFLD mice.

• CK upregulated the abundance of the beneficial bacterium Akkermansia.
• CK increased the proportion of Bacteroidetes and decreased the proportion of Firmicutes at the intestinal phylum level.
• These changes represent a reversal of HFHC diet-induced gut microbiota dysbiosis.
• CK modulated intestinal phylum composition in NAFLD mice.

CK regulates NAFLD via the gut-liver axis.

• The mechanism by which CK regulates the occurrence and development of NAFLD involves the gut-liver axis.
• Both lipid metabolism regulation and gut microbiota modulation contribute to CK's protective effects.
• The findings provide experimental evidence for subsequent mechanistic research on NAFLD prevention and treatment and exploration of candidate drugs.