Armillaria luteo-virens Sacc (ALS) is a rare wild Chinese medicinal and edible basidiomycete. However, its protective effect on intestinal functions and the underlying mechanism is still unknown. This work explored the improvement of dextran sulfate sodium (DSS)-induced colitis by ALS. ALS supplementation markedly improved colitis symptoms, gut barrier integrity, and goblet loss in DSS-treated mice. In addition, ALS inhibited colonic inflammation through the inhibition/activation of the mitogen-activated protein kinases/NF-κB signaling pathway. The 16S rRNA gene-based microbiota analysis revealed that ALS altered the gut microbiota composition, decreasing the richness of Enterobacteriaceae and increasing the abundance of Lactobacillaceae. The bile-acid-targeted metabolomic analysis showed that ALS recovered the microbial bile acid metabolism in the gut, enabling the activation of the farnesoid X receptor signaling by these acids, thus maintaining the intestinal homeostasis. Importantly, broad-spectrum antibiotic treatment reduced the efficacy of ALS-induced protection from colitis. Overall, our findings suggest that ALS may represent a novel approach in the nutritional intervention to prevent colitis.

Obesity has become a major disease that endangers human health. Studies have shown that dietary interventions can reduce the prevalence of obesity and diabetes. Resistant starch (RS) exerts anti-obesity effects, alleviates metabolic syndrome, and maintains intestinal health. However, different RS types have different physical and chemical properties. Current research on RS has focused mainly on RS types 2, 3, and 4, with few studies on RS1. Therefore, this study aimed to investigate the effect of RS1 on obesity and gut microbiota structure in mice. In this study, we investigated the effect of potato RS type 1 (PRS1) on obesity and inflammation. Mouse weights, as well as their food intake, blood glucose, and lipid indexes, were assessed, and inflammatory factors were measured in the blood and tissues of the mice. We also analyzed the expression levels of related genes using PCR, with 16S rRNA sequencing used to study intestinal microbiota changes in the mice. Finally, the level of short-chain fatty acids was determined. The results indicated that PRS1 promoted host obesity and weight gain and increased blood glucose and inflammatory cytokine levels by altering the gut microbiota structure.

Background: Intestinal barrier problems cause obesity and related health issues. We focus on treatments that fix the gut lining and change gut bacteria. Soy oligosaccharides (SOSs) are prebiotics. They change gut bacteria and help lower fats. The mechanism by which SOS affects high-fat diet (HFD)-induced obesity remains to be fully elucidated. Objectives: We want to see if SOS improves the mucus barrier in the gut by investigating how mucus is produced, modified and released. We hypothesise that SOS can reduce obesity and associated health problems by regulating mucus and gut bacteria. Methods: Accordingly, HFD-fed mice were used in this study. Results: The results showed that SOS alleviated HFD-induced weight gain and glucose disorders. It also enhanced the gut mucus barrier by promoting goblet cell differentiation and regulating mucus-related genes. In addition, SOS intervention was associated with increased abundance of potentially beneficial gut taxa. These bacterial changes were linked to better health measures. In conclusion, our findings demonstrate that SOS confer metabolic protection against HFD-induced obesity, at least partially, by coordinately modulating the mucus–microbiota axis. Conclusions: These data suggest that SOS may alleviate obesity and related disorders by improving the intestinal mucus layer and gut microbiota.

Hypercholesterolemia is a major risk factor for cardiovascular diseases. Genistein, a major bioactive isoflavone, has shown cholesterol-lowering potential, but the mechanisms underlying this effect remain unclear. In this study, genistein was purified from fermented soybean meal, and ICR mice fed a high-cholesterol diet were treated with genistein (40 mg/kg body weight/day) from fermented soybean meal for eight weeks. Genistein reduced body weight gain without affecting food intake, and decreased serum total cholesterol and low-density lipoprotein cholesterol. Genistein increased fecal total bile acid excretion and decreased serum total bile acids, accompanied by elevated fecal ursodeoxycholic acid and muricholic acid derivatives. Gut microbiota analysis showed restored alpha diversity, a decreased Firmicutes/Bacteroidetes ratio, and enriched Akkermansia, Parabacteroides and norank_f__Muribaculaceae. Fecal short-chain fatty acids (SCFAs) were increased, especially butyrate and valerate, and propionate was restored to levels comparable to normal controls. At the mRNA level, genistein treatment reduced intestinal farnesoid X receptor and fibroblast growth factor 15 expression and increased hepatic cholesterol 7α-hydroxylase expression, accompanied by altered expression of genes involved in cholesterol synthesis and efflux. Correlation analysis linked genistein-enriched taxa with improved cholesterol, bile acid, and SCFA profiles. In conclusion, purified genistein may alleviate diet-induced hypercholesterolemia by affecting the bile acid pool, gut microbiota, and SCFA production. These findings provide mechanistic insights into the cholesterol-lowering effects of genistein and may offer a scientific basis for the future development of genistein-based functional ingredients from soybean-derived materials.