Type 2 diabetes mellitus (T2DM) is a chronic metabolic disease which seriously affects public health. Gut microbiota remains a dynamic balance state in healthy individuals, and its disorder may affect health status and even results in metabolic diseases. Quercetin, a natural flavonoid, has been shown to have biological activities that can be used in the prevention and treatment of metabolic diseases. This study aimed to explore the mechanism of quercetin in alleviating T2DM based on gut microbiota. db/db mice were adopted as the model for T2DM in this study. After 10 weeks of administration, quercetin could significantly decrease the levels of body weight, fasting blood glucose (FBG), serum insulin (INS), the homeostasis model assessment of insulin resistance (HOMA-IR), monocyte chemoattractant protein-1 (MCP-1), D-lactic acid (D-LA), and lipopolysaccharide (LPS) in db/db mice. 16S rRNA gene sequencing and untargeted metabolomics analysis were performed to compare the differences of gut microbiota and metabolites among the groups. The results demonstrated that quercetin decreased the abundance of Proteobacteria, Bacteroides, Escherichia-Shigella and Escherichia_coli. Moreover, metabolomics analysis showed that the levels of L-Dopa and S-Adenosyl-L-methionine (SAM) were significantly increased, but 3-Methoxytyramine (3-MET), L-Aspartic acid, L-Glutamic acid, and Androstenedione were significantly decreased under quercetin intervention. Taken together, quercetin could exert its hypoglycemic effect, alleviate insulin resistance, repair the intestinal barrier, remodel the intestinal microbiota, and alter the metabolites of db/db mice.

Red palm oil (RPO) has been investigated for preventing or alleviating vitamin A deficiency (VAD). Previous data has offered inconclusive and inconsistent results about the effects of RPO in patients with VAD. Our objective was to undertake a meta-analysis to assess the effects of RPO in preventing VAD in the population. After conducting a comprehensive literature search, nine randomized controlled trials (RCTs) were included. Overall, when trial results were pooled, the results indicated that RPO reduced the risk of VAD (relative risk (RR) (95% confidence interval (CI)) = 0.55 (0.37, 0.82), p = 0.003), increasedserum retinol levels in both children (p < 0.00001) and adults (p = 0.002), and increased β-carotene levels (p = 0.01). However, RPO supplementation did not have a significant overall effect on serum α-carotene levels (p = 0.06), body weight (p = 0.45), and haemoglobin levels (p = 0.72). The results also showed that low level of PRO intake (≤8 g RPO) could increase serum retinol concentrations whereas PRO intake above 8 g did not lead to further increase of serum retinol concentrations. This meta-analysis demonstrated that RPO might be effective for preventing or alleviating VAD.

Cognitive impairment is associated with aging; however, the underlying mechanism remains unclear. Our previous study found that polyphenol-rich blueberry–mulberry extract (BME) had an antioxidant capability and effectively alleviated cognitive impairment in a mouse model of Alzheimer’s disease. Thus, we hypothesized that BME would improve cognitive performance in naturally aging mice and assessed its effects on related signaling pathways. Eighteen-month-old C57BL/6J mice were gavaged with 300 mg/kg/d of BME for 6 weeks. Behavioral phenotypes, cytokine levels, tight junction protein levels, and the histopathology of the brain were assessed, and 16S ribosomal RNA sequencing and targeted metabolome analyses were used for gut microbiota and metabolite measurements. Our results showed that the cognitive performance of aged mice in the Morris water maze test was improved after BME treatment, neuronal loss was reduced, IL-6 and TNF-α levels in the brain and intestine were decreased, and the levels of intestinal tight junction proteins (ZO-1 and occludin) were increased. Further, 16S sequencing showed that BME significantly increased the relative abundance of Lactobacillus, Streptococcus, and Lactococcus and decreased the relative abundance of Blautia, Lachnoclostridium, and Roseburia in the gut. A targeted metabolomic analysis showed that BME significantly increased the levels of 21 metabolites, including α-linolenic acid, vanillic acid, and N-acetylserotonin. In conclusion, BME alters the gut microbiota and regulates gut metabolites in aged mice, which may contribute to the alleviation of cognitive impairment and to inflammation inhibition in both the brain and the gut. Our results provide a basis for future research on natural antioxidant intervention as a treatment strategy for aging-related cognitive impairment.