In recent years, research on the interaction between flavonoids and intestinal microbes have prompted a rash of food science, nutriology and biomedicine, complying with future research trends. The gut microbiota plays an essential role in the maintenance of intestinal homeostasis and human health, but once the intestinal flora dysregulation occurs, it may contribute to various diseases. Flavonoids have shown a variety of physiological activities, and are metabolized or biotransformed by gut microbiota, thereby producing new metabolites that promote human health by modulating the composition and structure of intestinal flora. Herein, this review demonstrates the key notion of flavonoids as well as intestinal microbiota and dysbiosis, aiming to provide a comprehensive understanding about how flavonoids regulate the diseases by gut microbiota. Emphasis is placed on the microbiota-flavonoid bidirectional interaction that affects the metabolic fate of flavonoids and their metabolites, thereby influencing their metabolic mechanism, biotransformation, bioavailability and bioactivity. Potentially by focusing on the abundance and diversity of gut microbiota as well as their metabolites such as bile acids, we discuss the influence mechanism of flavonoids on intestinal microbiota by protecting the intestinal barrier function and immune system. Additionally, the microbiota-flavonoid bidirectional interaction plays a crucial role in regulating various diseases. We explain the underlying regulation mechanism of several typical diseases including gastrointestinal diseases, obesity, diabetes and cancer, aiming to provide a theoretical basis and guideline for the promotion of gastrointestinal health as well as the treatment of diseases.

Whole-wheat flour (WWF) is increasingly popular because of the health benefits of whole grains. This study investigated the effect of WWF particle size on dough properties, bread quality and in vitro starch digestibility. WWF was made from intact whole grain directly. Three WWF particle sizes were examined, including coarse, medium and fine with a mean size of 1315, 450 and 199 μm, respectively. The dough made from WWF of a larger particle size exhibited lower extensibility and stability, and subsequently the bread had a more compact structure (i.e. lower open porosity and thicker cell thickness), smaller specific volume and harder texture, which were regarded as poor quality attributes. On the other hand, the bread made from the fine WWF exhibited a higher amount of released glucose than those made from the coarse and medium WWFs. Moreover, the particle size of bread bolus showed no significant effect on in vitro starch digestion. The whole study demonstrated that the particle size of WWF plays a critical role in determining both bread quality and digestibility.

Non-alcoholic fatty liver disease (NAFLD) is one of the chronic liver diseases with high incidence in the world. This study aimed to investigate whether total flavonoids from Chimonanthus nitens Oliv. leaves (TFC) can ameliorate NAFLD. Herein, a high-fat diet (HFD)-induced NAFLD mice model was established, and TFC was administered orally. The results showed that TFC reduced the body weight and liver index and decreased the serum and hepatic levels of triglyceride (TG) and total cholesterol (TC). TFC significantly reduced the activity of liver functional transaminase. Aspartate aminotransferase (AST) and alanine aminotransferase (ALT) decreased by 34.61% and 39.57% in serum and 22.46% and 40.86% in the liver, respectively. TFC regulated the activities of oxidative-stress-related enzymes and upregulated the protein expression of nuclear factor E2-related factor (Nrf2)/heme oxygenase (HO-1) pathway in NAFLD mice, and the activities of total superoxide dismutase (T-SOD) and glutathione peroxidase (GSH-PX) in serum were increased by 89.76% and 141.77%, respectively. In addition, TFC reduced the levels of free fatty acids (FFA), endotoxin (ET), and related inflammatory factors in mouse liver tissue and downregulated the expression of proteins associated with inflammatory pathways. After TFC treatment, the levels of tumor necrosis factor-α (TNF-α), interleukin (IL)-6 and IL-1β in the liver tissues of NAFLD mice were downregulated by 67.10%, 66.56%, and 61.45%, respectively. Finally, TFC reduced liver fat deposition, oxidative stress, and inflammatory response to repair liver damage and alleviate NAFLD. Further studies showed that TFC regulated the expression of intestinal-barrier-related genes and improved the composition of gut microbiota. Therefore, TFC reduced liver inflammation and restored intestinal homeostasis by regulating the gut–liver axis. Overall, our findings revealed a novel function of TFC as a promising prophylactic for the treatment of NAFLD.