The Intervention Effect Of Broccoli On High-Fat-Induced Obesity And Metabolic Associated Fatty Liver Disease And Its Mechanism

With the continuous improvement of living standards,the dietary lipid intake of residents has been increasing,resulting in fat accumulation and overweight,thereby accelerating the occurrence of obesity and metabolic-associated fatty liver disease(MAFLD).Currently,nearly one-fifth of the world’s population suffers from obesity,and about 60-90% of obese patients will further develop MAFLD.As a common liver disease,without prompt treatment,MAFLD will have severe consequences on the liver,including malfunction,fibrosis,cirrhosis,and cancer.However,the main treatments for obesity and MAFLD are drugs and surgery,which have great side effects on the body.Therefore,dietary intervention has gradually become the focus of public attention.Many studies have reported that dietary intervention has a positive effect on obesity and MAFLD.Among them,broccoli,as the king of vegetables,is rich in a variety of nutrients and is sought after by people who are reducing fat and has become a research hotspot to improve lipid metabolism.In this thesis,we investigated the effects of broccoli on HFD-induced obesity and MAFLD mice and the underlying mechanisms.The main research results are as follows:1.Obesity model was established in C57BL/6J mice induced by HFD for 8 weeks,meanwhile,the mice were fed broccoli,and the alleviating effect of different doses of broccoli on obesity was analyzed.The results showed that different doses of broccoli intake could prevent the excessive increase of body weight,fasting blood glucose level,WAT weight,epididymal fat weight,fat index,fat volume,fasting insulin,TC,IL-1β and GPT levels to a certain extent,reduce liver fat storage and enhance the activities of CAT,GSH-Px,and SOD.In addition,high-dose broccoli also reduced leptin and LDLC levels and increased T-AOC levels compared to low-dose.These results suggested that high-dose broccoli may be more effective by enhancing antioxidant and antiinflammatory ability,reducing fat accumulation and liver damage,to effectively delaying the occurrence and development of obesity.2.To further explore the continuous influence of broccoli on lipid metabolism,based on the obesity model,high-fat induction was conducted for another 4 weeks to establish the MAFLD model,and the effects of different doses of broccoli on MAFLD mice were analyzed.The results showed that different doses of broccoli could both prevent the increase in body weight,pro-inflammatory factor levels(IL-1β and IL-6),liver damage enzymes(GOT and GPT)activities,and total bile acid levels of mice induced by HFD to a certain extent,as well as reduce the volume of adipocytes,improve blood and liver lipid,restore antioxidant capacity,and improve the structure of intestinal microbiota and fecal SCFAs.In addition,compared with low-dose,the highdose broccoli was more prominent in liver lipids(LDL-C and TC),antioxidants(CAT and T-AOC),and liver damage index enzymes(GPT).These results suggested that broccoli had a good preventing effect on high fat-induced MAFLD,and the effect became more significant with the increase in dose.3.The expressions of the bile-acid/fatty-acid metabolic pathway(FXR/LXRαpathway),inflammatory factor genes,and other important genes in the liver of obese and MAFLD mice were detected by Western blot and qPCR to explore the mechanism of the regulation effect of broccoli on obesity and MAFLD.The results showed that different doses of broccoli could affect the expression of genes in the FXR/LXRα signal pathway,inflammatory factor genes,and other important genes in both obesity and MAFLD models.Consistent with the apparent indicators,compared with low-dose broccoli,high-dose broccoli had a more significant down-regulation effect on the expressions of Lpin1 and SCD1 genes in the obesity model and a more significant upregulation effect on the expressions of PRDM16 and SIRT1 genes in MAFLD model.In summary,broccoli can prevent the effects of HFD-induced obesity and MAFLD by reducing inflammation,boosting antioxidant capacity,and controlling the expression of genes involved in the FXR/LXRα pathway.