Increasing evidence has confirmed that whole grain oats are effective in regulating hyperlipidemia. However, which specific ingredient is crucial remains unclear. This study focused on which whole grain components, oat phenolic compounds (OPC) or oat β-glucan (OBG), can regulate lipid metabolism and gut microbiota. The experiment unveiled that OPC and/or OBG not only reduced the body weight and fasting blood glucose (FBG) but also regulated serum and hepatic lipid levels in high-fat-diet (HFD) fed mice. There was no significant difference in the regulatory effects of OPC and OBG (p > 0.05). The combination of OPC and OBG (OPC + OBG) significantly decreased the body weight (p < 0.01) and reduced the blood glucose (p < 0.01) and lipid profile levels (p < 0.01). The real-time quantitative PCR (RT-qPCR) study revealed that OPC + OBG significantly altered mRNA expression related to lipid metabolism. Histopathological analysis showed that OPC + OBG improved liver lipid deposition as well as liver oxidative stress (p < 0.05). In addition, OPC + OBG combination regulated the gut microbiota community phenotype and increased probiotics. OPC + OBG significantly increased the abundance of Bacteroidetes and reduced the abundance of Firmicutes (p < 0.05) compared with the OPC and OBG fed mice. In conclusion, OPC + OBG has a synergistic effect in alleviating hyperlipidemia via lipid metabolism and gut microbiota composition. This finding also provided a potential justification for the advantages of whole grains in preventing hyperlipidemia.

Advanced glycation end products (AGEs) are formed in non-enzymatic reaction, oxidation, rearrangement and cross-linking between the active carbonyl groups of reducing sugars and the free amines of amino acids. The Maillard reaction is related to sensory characteristics in thermal processed food, while AGEs are formed in food matrix in this process. AGEs are a key link between carbonyl stress and neurodegenerative disease. AGEs can interact with receptors for AGEs (RAGE), causing oxidative stress, inflammation response and signal pathways activation related to neurodegenerative diseases. Neurodegenerative diseases are closely related to gut microbiota imbalance and intestinal inflammation. Polyphenols with multiple hydroxyl groups showed a powerful ability to scavenge ROS and capture α-dicarbonyl species, which led to the formation of mono- and di- adducts, thereby inhibiting AGEs formation. Neurodegenerative diseases can be effectively prevented by inhibiting AGEs production, and interaction with RAGEs, or regulating the microbiota-gut-brain axis. These strategies include polyphenols multifunctional effects on AGEs inhibition, RAGE-ligand interactions blocking, and regulating the abundance and diversity of gut microbiota, and intestinal inflammation alleviation to delay or prevent neurodegenerative diseases progress. It is a wise and promising strategy to supplement dietary polyphenols for preventing neurodegenerative diseases via AGEs-RAGE axis and microbiota-gut-brain axis regulation.

Obesity is associated with increased risk of many types of cancer and can be induced by various high-fat diets (HFD) from different fat sources. It remains unknown whether fatty acid composition in different HFD influences obesity-associated tumor development. Here we report that consumption of either a cocoa butter or fish oil HFD induced similar obesity in mouse models. While obesity induced by the cocoa butter HFD was associated with accelerated mammary tumor growth, consumption of the fish oil HFD uncoupled obesity from increased mammary tumor growth and exhibited a decrease in protumor macrophages. Compared with fatty acid (FA) components in both HFDs, n-3 FA rich in the fish oil HFD induced significant production of reactive oxygen species (ROS) and macrophage death. Moreover, A-FABP expression in the protumor macrophages facilitated intracellular transportation of n-3 FA and oxidation of mitochondrial FA. A-FABP deficiency diminished n-3 FA–mediated ROS production and macrophage death in vitro and in vivo. Together, our results demonstrate a novel mechanism by which n-3 FA induce ROS-mediated protumor macrophage death in an A-FABP–dependent manner. Significance: This study provides mechanistic insight into dietary supplementation with fish oil for breast cancer prevention and advances a new concept that not all HFDs leading to obesity are tumorigenic.