Food frontiers最新文献

Alcohol-associated liver disease (ALD) has become a serious public health issue worldwide. This study was conducted to investigate the protective role of Lactobacillus helveticus ZJUIDS12 (Z12) on ALD. Z12 (10⁹ CFU/day) significantly reversed alcohol-induced liver injury, hepatic steatosis, oxidative stress, and inflammation by restoring lipid metabolism and gut barrier integrity. Z12's effects, abolished in antibiotic-treated mice, involve gut microbiota, notably Clostridium sensu stricto 1, linked to Reg3γ upregulation. Clostridium butyricum (a representative strain of Clostridium sensu stricto 1) or butyric acid replicated Z12's benefits, which were absent in Reg3γ^−/− mice. Further studies revealed that the heat-inactivated postbiotics of Z12 and its secreted exopolysaccharides still significantly alleviated ALD, similar to the effects of the live Z12. Our present study suggests that Z12 probiotics and their postbiotics ameliorate alcohol-induced hepatic steatosis and liver injury in mice by enhancing butyrate production via C. butyricum, mediated through the Reg3γ pathway. These findings support the therapeutic potential of probiotic and postbiotic interventions for ALD.

This study examined the fermentation mechanism of Gansu starter cultures (GSSC) and Henan starter cultures (HNSC), each mixed with yeast, in enhancing the distinctive flavor of bread. High-throughput sequencing analysis revealed that 157 bacterial genera and 53 fungal genera were identified in the GSSC, while the HNSC comprised 29 bacterial genera and 35 fungal genera. The data confirmed that the levels of lactic acid and exopolysaccharides (EPS) increased during the mung bean sourdough fermentation process with GSSC and HNSC, contributing to improved dough fermentation properties. The results of scanning electron microscopy and disulfide bond analysis indicated improved gluten network formation in Gansu mung bean dough (GMD) and Henan mung bean dough (HMD). The FT-IR data revealed that Gansu mung bean sourdough bread (GMB) and Henan mung bean sourdough bread (HMB) each exhibited a stable protein secondary structure, which enhanced specific volume and texture property. Specifically, the specific volume of GMB and HMB increased by 35.38% and 67.69%, respectively, compared to the regular mung bean bread. Gas chromatography-ion mobility spectrometry (GC-IMS) analysis of bread identified 42 key volatile compounds. Correlation analysis showed that GMB developed citrus and burnt popcorn aromas, while HMB presented fruity and floral notes. These new findings would provide theoretical basis for using new starter cultures for enhancing both the quality and flavor of mung bean bread.

Dietary soluble fiber may alleviate renal damage in chronic kidney disease (CKD) by promoting intestinal urea excretion, though the underlying mechanisms remain unclear. This study investigated the digestion, fermentation, and renoprotective effects of Coix lachryma-jobi L. seed polysaccharides (CP) using in vitro systems and adenine-induced CKD mice. CP resisted gastric and small intestinal digestion but was effectively fermented by human gut microbiota, exhibiting effective urease inhibitory activity and reducing ammonia production in vitro. In CKD mice, CP treatment ameliorated renal histopathology, reduced serum creatinine, phosphorus, calcium, and fecal p-cresol, indole, while increasing urinary and fecal urea excretion and decreasing fecal ammonia. CP reshaped the gut microbiota, reducing Parabacteroides, Anaeroplasma, and other genera linked to amino acid metabolism (all p < 0.05), which positively correlated with p-cresol and serum creatinine. Conversely, Lactobacillus were enriched (p < 0.01) and negatively correlated with toxin levels, while positively correlated with the excretion of urea and ammonia in urine. These findings suggested CP improved renal function by modulating gut microbiota to suppress urease activity and aromatic amino acid metabolism, thereby reducing uremic toxin production and enhancing nitrogenous waste elimination via the gut–kidney axis.

Chronic kidney disease (CKD) is associated with impaired kidney function, intestinal barrier dysfunction, accumulation of uremic toxins, and gut microbiota dysbiosis. In this study, we used an adenine-induced CKD mouse model to evaluate the effects of Bifidobacterium longum subsp. longum CCFM1375 on CKD progression. Mice with CKD displayed increased serum creatinine and blood urea nitrogen (BUN) levels, kidney tissue histopathological injury, disrupted intestinal barrier integrity, elevated lipopolysaccharides (LPS) levels, and changes in gut microbiota composition. Intervention with B. longum subsp. longum CCFM1375 significantly alleviated these symptoms. Bifidobacterium longum subsp. longum CCFM1375 enhanced gut barrier function by upregulating tight junction proteins (ZO-1, ZO-2) and reducing pro-inflammatory cytokines (IL-6, TNF-α), thereby lowering serum LPS levels. Metagenomic analysis revealed that B. longum subsp. longum CCFM1375 restored the gut microbial structure, increasing beneficial species such as Faecalibaculum rodentium, Asaccharobacter celatus, Adlercreutzia equolifaciens, while reducing potential pathogens. Furthermore, metabolic analysis showed that gut microbiota metabolic functions shifted from urea production to amino acid biosynthesis, significantly increasing fecal tryptophan and tyrosine levels and elevating serum glutamate content, potentially alleviating CKD progression by reducing urea production and ammonia toxicity. The intervention also enhanced thiamine synthesis and increased fecal cholic acid levels, significantly reducing serum uremic toxin levels, including trimethylamine N-oxide, phenyl sulfate, and the indoleacetic acid precursor indole-3-pyruvic acid. In conclusion, B. longum subsp. longum CCFM1375 may delay CKD progression by repairing the intestinal barrier, modulating nitrogen metabolism pathways, and reducing uremic toxin accumulation, providing new evidence for the use of probiotics in kidney disease intervention.

Ulcerative colitis (UC) is a chronic intestinal inflammatory disease with complex pathogenesis. Previous studies have shown that probiotics alleviate UC by modulating the gut microbiome. Therefore, this study aimed to investigate the ameliorative effect of Lactobacillus plantarum 6C (L. plantarum 6C) on dextran sulfate sodium (DSS)-induced UC mice and to elucidate its specific mechanism. The results showed that L. plantarum 6C intervention ameliorated DSS-induced UC in mice, as evidenced by reduced colon shortening and weight loss, diminished levels of the pro-inflammatory cytokine IFN-γ, and increased the levels of the anti-inflammatory cytokine IL-4. Additionally, L. plantarum 6C reduced oxidative stress markers (MPO and MDA levels), enhanced the protein expression of E-cadherin, occludin, and ZO-1, and increased the abundance of beneficial bacteria such as Ligilactobacillus, Prevotella, and Dysosmobacter. Furthermore, L. plantarum 6C upregulated the Lama2 and Lamb2 genes, which are key genes in the PI3K-AKT pathway. In conclusion, our results indicate that L. plantarum 6C ameliorates DSS-induced colitis, its potential mechanism may be the increased abundance of Ligilactobacillus, which modulates Lama2 and Lamb2 expression, thereby suppressing the PI3K-AKT signaling pathway. Overall, this study demonstrates the beneficial role of L. plantarum 6C in alleviating ulcerative colitis and promoting intestinal homeostasis.

Safety incidents involving the presence of fluoroquinolones (FQs) residues in animal-derived food are frequently reported, posing a significant threat to human health. Here, we constructed a fluorescence sensing method using iron ions as a bridge for the detection of FQs in food. Iron ions significantly weakened the fluorescence intensity of N-CDs by forming a non-fluorescent substance through coordination with C = N on N-CDs, which caused a static burst by the electron transfer effect (ET), and the fluorescence changed from “on” to “off.” Since the FQs have a strong chelating effect with Fe³⁺, the quenched fluorescence is restored by the competitive binding of FQs with Fe³⁺, which results the fluorescence was “on.” The detection of FQs was achieved by the change of fluorescence intensity, for which the limit of detection (LOD) was 4.40 µmol/L. Compared with existing methods, the proposed method has a wider linear range of 5–900 µmol/L. For real samples including tap water, milk, and honey, the recoveries of FQs determination ranged from 91.31% to 107.50%. These results indicate that the fluorescence detection method constructed in this study offers a novel strategy for detecting FQs residues in real samples.

Arrhythmias account for approximately 80% of sudden cardiac deaths, posing a significant challenge to public health. Investigating the relationships between plasma metabolites and arrhythmia contributes to understanding disease etiology and informing therapeutic strategies. In this research, we accessed the causal links between 735 circulating metabolites and arrhythmias using Mendelian randomization (MR) across multiple genome-wide association studies (GWAS) datasets and meta-analyzed the results. Tyrosine showed the strongest putative causal association with arrhythmias and their risk factors. We further replicated this finding using independent GWAS data from FinnGen, providing additional support. Moreover, genetic loci associated with circulating tyrosine levels were significantly enriched for genes implicated in cardiovascular disease. To provide experimental support, we tested these predictions in an animal model. Transthoracic echocardiography demonstrated that tyrosine increased ejection fraction and fractional shortening, indicating enhanced cardiac systolic function. Transcriptomic analysis indicated that tyrosine activated adrenergic signaling in cardiomyocytes, which promotes cardiac conduction and muscle contraction. Consistently, tyrosine elevated serum epinephrine levels in a dose-dependent manner. Furthermore, metabolomic profiling showed that tyrosine altered serum metabolites previously linked to arrhythmias. In conclusion, convergent evidence from genetic analyses and animal experiments suggests that excessive dietary tyrosine induces cardiac hypercontractility, and circulating tyrosine may serve as a potential target for arrhythmia prevention.

Enhancing textural properties through structural design is a significant direction in food science. This study focused on the development and functionality of Pickering type bigel-based low-fat spreads, using whey protein microparticles (WPM) as interfacial stabilizer. Pickering type bigels-based low-fat spreads were characterized using fluorescence microscopy, rheological analysis, friction properties, and sensory evaluations. The formulated fat mimetic could be spread on a sandwich with acceptable spreadable character, suggesting the successful preparation of bigel-based spread. Results demonstrated that lower WPM content (1.0%∼4.0%) led to lower initial G′, G″, yield stress, shear viscosity, and higher spreadability of bigels-based spreads. Whereas Pickering bigel-based low-fat spread with the highest WPM concentration (8.0%) exhibited the highest visual viscosity and stiffness with the lowest initial release amount of salt iron. The kinetics of salt release showed that the highest WPM concentration resulted in a burst release while proper WPM content (2.0% and 4.0%) triggered sustained release of salt from the bigel-based spread. Moreover, low-fat spreads stabilized by the highest WPM concentration achieved the best spreadability and lubrication sensation. Principal component analysis (PCA) and correlation analysis indicated that the coefficient of friction at 50 mm/s was an indicative of spreadability, while the coefficient of friction at 3 mm/s provided insights into visual stickiness, yield strain, and salt ion release from the bigel. This study enhances our understanding of how Pickering bigels can be engineered to adjust the quality of low-fat spreads, paving the way for the development of low-fat spreads with tunable sensory attributes.

Selenium is an essential trace element for human health, and the selenium content in selenium-enriched matcha meets the official criteria for selenium-enriched foods in China. In the present work, hepatoprotective effects of selenium-enriched matcha against alcohol-induced liver injury were systematically investigated, and its mechanism was explored by label-free proteomic technique for the first time. When fed with selenium-enriched matcha, selenium was distributed in various organs and tissues (heart, liver, spleen, lung, kidney, serum, and muscle), and the selenium content in the liver was significantly higher than that in other organs and tissues (p < 0.05). Levels of alanine transaminase, aspartate transaminase, total cholesterol, triglyceride, total bilirubin, and malondialdehyde in selenium-enriched matcha intervention groups were lower than those in the alcohol model (AM) group, while levels of glutathione peroxidase, superoxide dismutase, and glutathione in selenium-enriched matcha intervention groups were higher than those in the AM group. A total of 376 differentially expressed proteins (DEPs) were identified, in which 35 key DEPs were involved in 26 biological processes, 14 cellular components, and 14 molecular functions. Intervention with selenium-enriched matcha notably downregulated cytochrome P450 (Cyp2c40 and Cyp2c54), which specifically modulated pathways of chemical carcinogenesis-DNA adducts, arachidonic acid, and retinol metabolisms. These results provide evidence for the use of selenium-enriched matcha in alleviating alcohol-induced liver injury.

Ulcerative colitis (UC) is a chronic inflammatory bowel disease characterized by persistent inflammation and ulceration of the colon. This research investigated the protective effects of Clitocybe squamulosa fruiting body polysaccharide (CSFP) and purified polysaccharides named CE on dextran sulfate sodium (DSS)-induced UC in mice. CSFP and CE significantly alleviated clinical symptoms and histopathological damage, enhanced the activity of antioxidant enzymes (catalase [CAT], superoxide dismutase [SOD], and glutathione peroxidase [GSH-Px]), and regulated inflammatory markers (TNF-α, IL-6, IL-1β, and IL-10). Importantly, both polysaccharides reinforced intestinal barrier integrity by upregulating tight junction proteins (ZO-1, occludin, claudin-1) and mucins (MUC2/3). Mechanistically, CSFP and CE enhanced the expression of autophagy-related proteins Beclin1, autophagy-related gene-5/7 (Atg5/7), and LC3-II, while reducing the accumulation of p62. Further studies confirmed that CSFP and CE may be novel targets for alleviating DSS-induced colitis through the inhibition of PI3K/Akt/mTOR pathway. In parallel, CSFP and CE remodeled gut microbiota composition, enriching beneficial bacteria such as Akkermansiaceae, Muribaculaceae, Bifidobacteriaceae, and Dubosiella, while suppressing harmful Lachnospiraceae. These microbial shifts promoted short-chain fatty acid (SCFA) production and upregulated SCFA receptors (GPR41/43/109A), further contributing to intestinal homeostasis. These results indicate that CSFP and CE can improve colitis by regulating autophagy and modulating the gut microbiota, thus exerting a protective effect against DSS-induced colitis, and providing a promising basis for their development as functional food ingredients or nutraceuticals for intestinal health.