The diversity and activity of the gut microbiota residing in humans and animals are significantly influenced by the diet. Quercetin, one of the representative polyphenols in human diets, possesses a wide range of biological properties. The aim of this study was to investigate the prebiotic effects of quercetin in antibiotic-treated mice. Gut dysbiosis was successfully induced in mice by treatment with an antibiotic cocktail. Gas chromatography and 16S rDNA high-throughput sequencing techniques were used to investigate short-chain fatty acid content and gut microbial diversity and composition. The results showed that quercetin supplementation significantly improved the diversity of the gut bacterial community in antibiotic-treated mice (P < 0.05). Meanwhile, intestinal barrier function was also recovered remarkably as indicated by a decrease in the content of serum D-lactic acid and the activity of serum diamine oxidase (P < 0.05). The length of intestinal villi and mucosal thickness were also significantly increased in response to quercetin treatment (P < 0.05). Furthermore, the production of butyrate in faeces was enhanced significantly in quercetin-treated mice (P < 0.05). In conclusion, quercetin is effective in recovering gut microbiota in mice after antibiotic treatment and may act as a prebiotic in combatting gut dysbiosis.

Riboflavin deficiency is widespread in many regions over the world, especially in underdeveloped countries. In this study, we investigated the effects of riboflavin deficiency on protein expression profiles in HepG2 cells in order to provide molecular information for the abnormalities induced by riboflavin deficiency. HepG2 cells were cultured in media containing different concentrations of riboflavin. Changes of cell viability and apoptosis were assessed. A comparative proteomic analysis was performed using a label-free shotgun method with LC–MS/MS to investigate the global changes of proteomic profiles in response to riboflavin deficiency. Immunoblotting test was used to validate the results of proteomic approach. The cell viability and apoptosis tests showed that riboflavin was vital in maintaining the cytoactivity of HepG2 cells. The label-free proteomic analysis revealed that a total of 37 proteins showing differential expression (±2 fold, p < 0.05) were identified after riboflavin deficiency. Bioinformatics analysis indicated that the riboflavin deficiency caused an up-regulation of Parkinson’s disease pathway, steroid catabolism, endoplasmic reticulum stress and apoptotic process, while the fatty acid metabolism, tricarboxylic citrate cycle, oxidative phosphorylation and iron metabolism were down-regulated. These findings provide a molecular basis for the elucidation of the effects caused by riboflavin deficiency.

This study investigated the effects of purple sweet potato anthocyanins (PSPA) in a type 2 diabetes mellitus (T2DM) mouse model. Sixty-five male mice were randomly divided into one control group and four experimental groups, which were fed with a high-fat diet and intraperitoneally injected with streptozotocin (STZ) to induce T2DM. The model mice were treated with 0 (M), 227.5 (LP), 455 (MP), or 910 (HP) mg/kg PSPA for ten days. ELISA, 16S rRNA sequencing, and hematoxylin and eosin staining were used to assess blood biochemical parameters, gut microbial composition, and liver tissue structure, respectively. The FBG concentration was significantly decreased in the LP (6.32 ± 1.05 mmol/L), MP (6.32 ± 1.05 mmol/L), and HP (5.65 ± 0.83 mmol/L) groups; the glycosylated hemoglobin levels were significantly decreased in the HP group (14.43 ± 7.12 pg/mL) compared with that in the M group (8.08 ± 1.04 mmol/L; 27.20 ± 7.72 pg/mL; P < 0.05). The PSPA treated groups also increased blood glutathione levels compared with M. PSPA significantly affected gut microbial diversity. The Firmicutes/Bacteroidetes ratio decreased by 38.9 %, 49.2 %, and 15.9 % in the LP, MP, and HP groups compared with that in the M group (0.62). The PSPAs treated groups showed an increased relative abundance of Lachnospiraceae_Clostridium, Butyricimonas, and Akkermansia and decreased abundance of nine bacterial genera, including Staphylococcus. PSPA reduced blood glucose levels, increased serum antioxidant enzymes, and optimized the diversity and structure of the gut microbiota in mice with T2DM.

Background: Dietary intervention could modulate gut microbiota, improve insulin resistance status, and play a key role in blood glucose regulation. Objective: This study investigated the regulatory effects of paeonidin- and cyanidin-rich fractions (PCs) on gut microbiota and serum metabolites in high-fat, high-sucrose diet/streptozotocin-induced type 2 diabetes mellitus (T2DM) rats. Method: Following a 14-day intragastric PC administration (25 mg/kg/day), non-targeted metabolomics and 16S rDNA sequencing were performed. Results: PC intervention significantly reduced water intake, and even the effects on lipids were limited. Among 83 differential serum metabolites, PC restored 28, including tauroursodeoxycholic acid (TUDCA) and lysophosphatidylcholines, while decreasing glycated branched-chain amino acid derivatives. PC-enriched Bifidobacterium, Sediminibacterium, SC-I-84, and Fusicatenibacter, which positively correlated with TUDCA. Additionally, PC upregulated insulin secretion and p53 signaling pathways with increased RYR2 and FAS, while downregulating pentose and glucuronate interconversion enzymes (UxaC, XylB). Conclusions: These findings suggest that the amelioration of glycolipid metabolic disorders and insulin secretion defects by PC may be associated with a synergistic gut microbiota-metabolite-enzyme axis, potentially involving Bifidobacterium-mediated TUDCA elevation and downstream modulation of metabolic enzymes.