Polysaccharides from Tumorous stem mustard prevented high fructose diet-induced non-alcoholic fatty liver disease by regulating gut microbiota, hepatic lipid metabolism, and the AKT/FOXO1/MAPK signaling pathway

Ingestion of 30 % fructose water (HF) for eight weeks caused non-alcoholic fatty liver disease (NAFLD) in mice and manifested in prominent weight gain, insulin resistance, abnormal lipid metabolism, oxidative stress, and liver damage. Biochemical analysis suggested that treatment with non-starch polysaccharides extracted from Tumorous stem mustard (NSPTSM) at 25-50 mg/kg center dot bw prevents these symptoms in HF-induced NAFLD. 16S rRNA sequencing revealed that NSPTSM balanced the HF-perturbed colonic microbiota and significantly increased the relative abundance of Akkermansia in mice. Metabonomics results indicated that the hepatic biomarkers were LPE (18:1/0:0) and LPC (16:1/0:0), which were negatively related to cecal 23-nordeoxycholic acid. Transcriptome and western blot analysis suggested that protein kinase B (AKT)/forkhead box protein O-1 (FOXO1)/mitogen-activated protein kinase (MAPK) signaling pathway played an important role in prevention of HF-induced NAFLD by NSPTSM. These findings indicated that NSPTSM protected mice against HF-induced NAFLD and underscored the efficacy of utilizing NSPTSM as a possible prebiotic.