Bayberry (BB) fruits contain high levels of polyphenols and possess good bioactivities. However, there are no specific studies to illustrate the impact of human gut microbiota fermentation (HGMF) on BB polyphenols subjected to gastrointestinal digestion (GID). Therefore, in this study, BB was subjected to simulated GID and HGMF (0–48 h) in order to study the fate of BB bioactive components. Phenolic gut metabolites were identified and quantified by relevant standards using HPLC. Cyanidin-3- O -glucoside was the only anthocyanin in BB and could be detected in its free form even after gut fermentation for 24 h. Gut metabolites of BB showed better hypoglycemic activity by improving hepatic glucose consumption and glycogen content. Furthermore, gut metabolites significantly ameliorated glucolipotoxicity induced oxidative stress. Since BB gut metabolites showed good hypoglycemic and antioxidant activities, BB can be considered as a functional food and dietary supplementation of BB could help in maintenance of good health.
Type 2 diabetes (T2DM) is induced by the abundance of glucose and lipids , which causes glucolipotoxicity to the pancreatic β-cells. Silibinin is a natural flavonoid possessing the regulatory activity on insulin production and therapeutic activity in diabetic mice; however, its effect on glucolipotoxicity is not fully explained. This in vitro study investigates the effects of silibinin on palmitic acid (PA) and high glucose (HG)-induced cell loss and ferroptosis of rat insulinoma INS-1 cells. In the cells treated with PA and HG, expressions of glucose transporter 4 (Glut4) and carnitine acyltransferase I (CPT1) for β-oxidation of fatty acids are reduced. Mitochondria are the metabolic organelles for glucose and fatty acids. The mitochondrial membrane potential (MMP) and ATP production were decreased, while the ROS level was elevated in the cells treated with PA and HG, indicating an induction of mitochondrial disorder . Cell loss was partially rescued by ferroptosis inhibition, suggesting an involvement of ferroptosis in the cells treated with PA and HG. More importantly, the increases in total iron, lipid ROS, MDA and COX-2, and the decrease in ferroptosis inhibitory molecules GSH, GPX4 and FSP1 appeared in the cells treated with PA and HG, confirming the occurrence of ferroptosis. Moreover, PINK1/parkin-mediated mitophagy , a vital process for selective elimination of damaged mitochondria, was blocked. Interestingly, silibinin rescued the mitochondria, restricted the ferroptosis and restored the mitophagy. By using the pharmacological stimulator and inhibitor of mitophagy, and si-RNA transfection to silence PINK1 expression, silibinin's protective effect against ferroptosis caused by PA and HG treatment was found to depend on mitophagy. Collectively, our current study reveals the new mechanisms for the protection of silibinin against the injury of INS-1 cells treated with PA and HG, elucidates the participation of ferroptosis in glucolipotoxicity, highlighting the involvement of mitophagy in defense against ferroptotic cell death.
危险品化学品经营许可证（带存储）