Food & Function最新文献

Ulcerative colitis (UC) is characterized by chronic intestinal inflammation and impaired mucosal barrier function. Myrica rubra contains polyphenols and flavonoids, but the mechanisms underlying its potential protective effects in colitis remain unclear. We evaluated Myrica rubra juice (MRJ) in a dextran sulfate sodium (DSS)-induced mouse model of colitis and a TNF-α-injured colonic organoid model. The study combined 16S rRNA gene sequencing, untargeted serum and fecal metabolomics, and molecular docking. MRJ treatment attenuated disease severity and was associated with increased expression of occludin and MUC2 in DSS-treated mice. MRJ also altered microbial diversity and taxonomic composition in a taxon-specific manner. Serum and fecal metabolomic profiles differed after MRJ treatment, including pathways related to amino acid and bile acid metabolism. Integrated analyses identified associations among microbial taxa, putatively annotated metabolites, and host inflammatory and barrier-related variables. Direct exposure to 20% (v/v) whole MRJ increased occludin immunofluorescence in TNF-α-injured colonic organoids cultured without a gut microbial community. This single-marker result is consistent with an epithelial response to whole MRJ under the applied in vitro conditions. Molecular docking generated predicted poses and docking scores for selected parent compound-protein pairs. These calculations did not demonstrate physical binding, functional inhibition, or target engagement in vivo. Together, the findings support a direct epithelial response and identify concurrent microbiota-associated changes. However, the present design could not determine whether these microbial changes contributed to protection. It also could not separate or quantify the host-directed and microbiota-mediated contributions or identify the active chemical species.

Obesity is a growing global health challenge associated with dysregulated appetite, impaired gut function, and metabolic disorders. Glucomannan and resistant starch are functional dietary fibers that may influence obesity-related pathways through distinct but interconnected mechanisms. This systematic review aimed to synthesize current evidence regarding their effects on satiety and appetite regulation, gut fermentation and microbiota-related pathways, and weight-related and metabolic outcomes. A systematic search of Scopus, PubMed/MEDLINE, ScienceDirect, and the Cochrane Library was conducted without publication-date restrictions, with the final search performed on 25 August 2026. Eligible randomized and crossover trials, non-randomized intervention studies, and animal studies investigating glucomannan, resistant starch, or relevant formulations were included when they reported predefined obesity-related outcomes. Twenty studies met the inclusion criteria, comprising six randomized or crossover trials, three non-randomized intervention studies, and eleven animal studies. Several studies reported improvements in satiety, hunger, food or energy intake, body weight, adiposity, or metabolic outcomes, although findings were heterogeneous across interventions, populations, and study designs. Glucomannan-containing interventions were generally associated with viscosity-related satiety effects, whereas resistant starch was more frequently associated with gut fermentation, microbiota modulation, and short-chain fatty acid production. Mechanistic and metabolic evidence was predominantly derived from animal studies, and several human studies reported null findings. Overall, the findings suggest potential complementarity between glucomannan and resistant starch at the mechanistic level, but direct evidence supporting synergistic effects of their combined use remains limited.

Zinc deficiency is a prevalent micronutrient disorder, and probiotic intervention has emerged as a promising strategy to improve zinc bioavailability. However, the strain-specific characteristics and genetic basis underlying the zinc-promoting effects of probiotics remain poorly understood. Therefore, this study aimed to identify the key physiological properties and functional genes associated with the zinc-promoting capacity of Heyndrickxia coagulans (H. coagulans, formerly Bacillus coagulans). A Caco-2 intestinal epithelial cell monolayer model and a zinc-deficient mouse model were established to evaluate the zinc-promoting effects of H. coagulans. Male BALB/c mice were fed a zinc-deficient diet and orally administered H. coagulans spores (10⁷ CFU per mouse per day) combined with zinc gluconate (0.15 mg Zn per mouse per day) for 4 weeks. Serum zinc concentration, alkaline phosphatase activity, organ indices, and intestinal zinc homeostasis-related gene expression were evaluated. Furthermore, comparative genomic analysis was performed to identify candidate genomic features potentially associated with strain-dependent differences in zinc-promoting capacity. Among the tested strains, H. coagulans CCFM1539, CCFM1540, and CCFM1541 exhibited distinct zinc-promoting capacities. In vitro, CCFM1539 significantly enhanced zinc transmembrane transport and modulated the transcription of zinc transporter genes. In vivo, supplementation with H. coagulans spores combined with zinc gluconate more effectively restored serum zinc concentration, alkaline phosphatase activity, organ indices, and intestinal zinc homeostasis-related gene expression (Zip4, Znt1, Znt2, and Vdr) than zinc supplementation alone. Notably, CCFM1541 showed the strongest overall zinc-promoting phenotype, with superior restoration of serum zinc concentration and Vdr expression. Comparative genomic analysis revealed that strain-specific zinc-promoting effects were associated with genes involved in ion transport, stress adaptation, carbohydrate metabolism, and cellular regulation. Among the CCFM1541-specific genes, ABC transporter-related genes, particularly gsiB, gsiC, gsiD, oppD, and oppF, were identified as candidate genes potentially associated with its superior zinc-promoting phenotype. In conclusion, the zinc-promoting effects of H. coagulans are strain-specific and are associated with changes in intestinal zinc homeostasis and bacterial genomic features. These findings provide genomic insights into probiotic-mediated mineral bioavailability and identify candidate genes for future functional validation.

Correction for 'Improving insulin resistance by sulforaphane via activating the Bacteroides and Lactobacillus SCFAs-GPR-GLP1 signal axis' by Sicong Tian et al., Food Funct., 2024, 15, 8644-8660, https://doi.org/10.1039/d4fo01059k.

Type 2 diabetes mellitus (T2DM), a highly prevalent chronic metabolic disorder, is primarily defined by persistent hyperglycemia due to defects in insulin secretion or action. In this study, a hypoglycemic peptide-containing fraction was prepared from oysters via liquid fermentation using Bacillus subtilis (CGMCC no. 28507). Following optimization of fermentation conditions and ultrafiltration separation, a fraction (FOP) with a molecular weight below 3 kDa was obtained, demonstrating the highest inhibitory potency against α-glucosidase. In vivo experiments using mice with T2DM confirmed that FOP markedly reduced fasting blood glucose, glycated haemoglobin levels, and insulin resistance and simultaneously improved glucose tolerance and lipid metabolism profiles, downregulating pro-inflammatory cytokines and alleviating pathological damage to the liver and pancreas. Following gel chromatography purification, three bioactive peptides (KSYFPT, VGGQGFF, and LRFPGQ) were identified by LC-MS/MS. According to molecular docking experiments, these peptides exhibited stable binding interactions with the α-glucosidase active site. All synthesized peptides exhibited significant inhibitory activity. This study delineates an eco-friendly protocol for the sustainable valorization of oyster proteins, simultaneously providing a theoretical basis for the formulation of food-derived functional agents with significant hypoglycemic potential.

Phenethyl isothiocyanate (PEITC), a dietary compound from cruciferous vegetables, is known for its chemopreventive activity, but its effects on liver fibrosis remain largely unexplored. In this study, we show that PEITC administration attenuated carbon tetrachloride (CCl₄)-induced hepatic injury and fibrosis in mice, as evidenced by reduced collagen deposition, hydroxyproline content and fibrotic marker expression, and improved liver function. PEITC inhibited cell survival and fibrogenic phenotypes in transforming growth factor β (TGF-β)-stimulated LX-2 human hepatic stellate cells (HSCs) while exhibiting minimal cytotoxicity towards normal hepatocytes. Mechanistically, PEITC depleted glutathione, inhibited glutathione peroxidase 4 (GPX4), and elevated reactive oxygen species (ROS), lipid peroxidation, and malondialdehyde, thereby triggering ferroptosis, as also confirmed by transmission electron microscopy showing mitochondrial shrinkage, increased membrane density, and cristae loss. Additionally, PEITC activated autophagy and promoted nuclear receptor coactivator 4 (NCOA4)-mediated ferritinophagy, leading to ferritin degradation. The involvement of autophagy was further validated by co-treatment with autophagy inhibitors, which partially reversed PEITC-induced ferritin heavy chain (FTH1) downregulation and NCOA4 upregulation. In vivo immunofluorescence staining revealed that PEITC suppressed antioxidant defense and promoted ferritin degradation in activated HSCs, as shown by reduced GPX4 and FTH1 fluorescence signals within α-smooth muscle actin (α-SMA)-positive areas in mouse liver sections. Collectively, these findings elucidate that PEITC alleviates liver fibrosis by promoting ferroptosis-related processes in activated HSCs, mainly through the NCOA4/FTH1 axis, positioning it as a promising nutraceutical candidate for antifibrotic therapy.

Cognitive decline is a growing global public health concern in aging populations, with genetic and dietary factors contributing to individual differences in cognitive trajectories. Dietary choline, as a precursor of acetylcholine and a key regulator of methylation and membrane integrity, may protect cognitive function. However, epidemiological evidence remains inconsistent, and the optimal intake for neuroprotection remains unclear. This study aimed to evaluate the association between dietary choline intake and cognitive decline and related outcomes, and a dose-response meta-analysis was performed. Eligible studies reporting risk estimates for cognitive decline, mild cognitive impairment (MCI), or related outcomes according to dietary choline intake were included. Study characteristics and outcomes were extracted. Pooled odds ratios (ORs) were estimated using a random-effects model and dose-response associations were assessed using a two-stage generalized least-squares framework. Eleven articles were included, of which nine independent cohorts involving 218 378 participants contributed to the primary meta-analysis. Higher dietary choline intake was significantly associated with a lower risk of adverse cognitive outcomes (pooled OR = 0.76, 95% CI: 0.63-0.92) and cognitive impairment/decline (pooled OR = 0.67, 95% CI: 0.47-0.95). A significant inverse association was also observed for Alzheimer's disease (AD) (pooled OR = 0.74, 95% CI: 0.55-0.99), whereas the association with dementia was not statistically significant. Dose-response analyses revealed significant nonlinear associations for adverse cognitive outcomes and cognitive impairment/decline, with the lowest risk observed at approximately 350-400 mg day^-1 of dietary choline intake. Dietary choline intake was associated with lower risks of adverse cognitive outcomes, cognitive impairment/decline, and AD, with the lowest risks observed at moderate intake levels. These findings highlight the potential importance of adequate choline intake for cognitive health.

Correction for 'Effects of different galactans on DSS-induced colitis and the gut microbiota' by Xuefei Wei et al., Food Funct., 2026, 17, 4171-4184, https://doi.org/10.1039/d6fo00058d.

Nutrigenomics explores how nutrients interact with the genome to influence metabolic and physiological functions through microbial and molecular mechanisms. Nutrients and bioactive food compounds act as biochemical modulators that regulate gene expression and immune responses, sustaining physiological stability. On the other hand, the gut microbiota create a balanced, complex ecosystem that is vital for maintaining host physiology and metabolic balance. The type and composition of diet directly shape gut microbial communities and populations, which, in turn, influence host gene expression. Disruption of this balance can contribute significantly to various health issues. In this context, the gut microbiota act as both allies and adversaries in human health. This review discusses the current state of nutrigenomics, focusing on the complex interplay among dietary metabolites, microbiota, and genes, and linking this interplay to the genesis and prevention of several chronic diseases. This review provides an overview of the unique composition of the intestinal microbiota and its role in mediating nutrigenomic interactions.

Circadian disruption (CD) is an important risk factor for cognitive impairment and neurodegenerative diseases, potentially through disturbances in tryptophan (TRP) metabolism. This study investigated the protective effects of orally administered vanillin in a mouse model of CD. CD impaired spatial learning and recognition memory, whereas vanillin improved cognitive performance and corrected abnormal changes in TRP-related metabolites, including tryptophan, kynurenine (KYN), and kynurenic acid (KYNA). Vanillin also modulated the composition and diversity of the gut microbiota, enhanced intestinal barrier function, and improved immune homeostasis. Immunofluorescence staining and western blot analysis further showed that vanillin regulated hippocampal proteins associated with neuronal and synaptic function and reduced astrocyte activation. These findings suggest that vanillin alleviates CD-induced cognitive impairment, accompanied by alterations in gut microbiota composition, TRP-kynurenine metabolism, intestinal barrier function, and neuroinflammatory responses.