Molecular Nutrition & Food Research最新文献

Dietary interventions represent safe and healthy strategies for reducing cholesterol levels and improving metabolic health. This study aimed to investigate the effects of the probiotic Schleiferilactobacillus harbinensis Z171, its extracellular polysaccharides (EPS), and postbiotics on cholesterol metabolism in the gut of mice fed a high-fat diet. The analysis focused on total cholesterol and bile acid levels in intestinal contents and serum, as well as bile acid reabsorption, short-chain fatty acid (SCFA) levels, gut microbiota composition, and metabolomic profiles. The results showed that high-dose EPS (400 mg/kg body weight), live S. harbinensis Z171, and postbiotics significantly increased fecal bile acid excretion to 86.49, 79.94, and 85.20 µmol/L, and SCFA production to 33.12, 28.71, and 29.01 µmol/g, respectively. Conversely, they decreased fecal cholesterol levels to 7.96, 8.26, and 5.93 µmol/L, respectively. Fecal metabolomics revealed an enrichment of metabolites related to bile acid biosynthesis. Gut microbiota analysis showed an increase in beneficial bacterial species associated with SCFA production, which improved lipid metabolism and gut health. Specifically, high-dose EPS enriched Faecalibaculum and Enterorhabdus in the gut, S. harbinensis Z171 increased Bifidobacterium abundance, and postbiotics elevated Dubosiella and Akkermansia levels. These findings suggest these interventions are promising strategies for regulating cholesterol metabolism through gut-liver axis mechanisms.

Gluten protein generates an immunogenic 33-mer peptide upon incomplete digestion, leading to induced cytotoxic and inflammatory responses in intestinal epithelial cells of susceptible individuals with Celiac disease (CeD). The present study investigates the protective effects of gluten hydrolyzing probiotic strains-Bacillus subtilis AJG10 and Bacillus tequilensis AJG23 on gliadin and 33-mer peptide in the Caco-2 cell model. The effect of probiotics on further degradation of 33-mer peptide and pepsin-trypsin digested gliadin was analysed using SDS-PAGE and mass spectrometry. The effect of all fractions on Caco-2 cell viability, nitric oxide (NO) production, and expression of pro-inflammatory cytokines was evaluated. A significant degradation of immunogenic peptide fragments after probiotic treatments resulted in 44%-53% reduction in NO production and a decrease of 27%-37% in cytokine expression and overall improvement in cell viability. The results suggested the potential of probiotic interventions in reducing the toxic effects of digested gliadin and immunogenic peptides.

This study examined the metabolic effects of wheat flour intake on body weight regulation in mice. Male and female C57BL/6 mice were given free access to standard chow and wheat-based foods, including bread and baked wheat flour, and food preference, energy expenditure, hepatic gene expression, and blood metabolite profiles were analyzed. Mice showed a strong preference for wheat-based foods, leading to significant body weight gain despite comparable caloric intake. Wheat flour consumption was associated with reduced energy expenditure, increased adiposity, and elevated circulating insulin and leptin levels. Blood metabolomic analysis revealed increased fatty acid levels and reduced essential amino acids, suggesting enhanced lipogenesis and a potential imbalance in amino acid intake. Consistently, hepatic expression of genes involved in fatty acid synthesis and lipid transport was upregulated. Importantly, withdrawal of wheat flour rapidly attenuated body weight gain and reversed the associated metabolic alterations. These findings demonstrate that wheat flour intake promotes obesity in mice primarily by decreasing energy expenditure and altering metabolic pathways independent of excess calorie consumption, highlighting wheat flour as a dietary factor that strongly influences energy homeostasis and body weight regulation.

Chemotherapy-induced senescence-associated tumor microenvironment (S-TME) facilitates colorectal cancer (CRC) progression. This study elucidates the mechanism by which Tianma granule (TMG), a traditional Chinese medicine formula, remodels the S-TME and inhibits CRC, specifically investigating the role of the miR-29a-5p/P53 axis. Liquid chromatography–tandem mass spectrometry (LC–MS/MS) identified 18 bioactive components in TMG, and network pharmacology highlighted P53 as a core target. Functional assays, including Cell Counting Kit-8 (CCK-8), β-galactosidase staining, flow cytometry, wound-healing, and Transwell migration tests, were conducted using doxorubicin (DOX)–induced senescent human umbilical vein endothelial cells (HUVECs) and CRC lines. TMG suppressed CRC cell proliferation, motility, and invasiveness while promoting apoptosis. TMG reduced P53/cyclin-dependent kinase inhibitor 1A (P21) and senescence-associated secretory phenotype (SASP) factors (IL-6, IL-8, CCL20), while upregulating miR-29a-5p in senescent HUVECs. miR-29a-5p inhibition enhanced senescence and increased P53/P21/SASP, whereas P53 silencing lowered P21 and decreased miR-29a-5p, indicating mutual regulation. In azoxymethane/dextran sulfate sodium (AOM/DSS)-CRC mice, TMG reduced tumor burden and improved survival, accompanied by lower P53/P21 and restored miR-29a-5p in tissues. TMG remodels the chemotherapy-induced S-TME and suppresses CRC progression by modulating the miR-29a-5p/P53 axis, enhancing apoptosis in senescent cells, and counteracting S-TME-mediated tumor growth and metastasis. This highlights TMG's therapeutic potential.