Food & Function最新文献

Spanish mackerel is an important economic fish species in China, but corruption undermines its overall economic value. Fermentation serves as a crucial technique for preserving perishable fish in developing countries. This study aimed to examine the dynamic changes in the gel properties, physicochemical properties, microbial diversity, and volatile flavor compounds (VFCs) of Spanish mackerel sausages inoculated with Lactiplantibacillus plantarum CY1-2 during fermentation. The correlation between key microorganisms and VFCs was explored using a two-way orthogonal partial least squares analysis. The results showed that the group inoculated with strain CY1-2 exhibited significant improvements compared with the control group after 40 h of fermentation. Specifically, gel strength increased by 207.7%, total free amino acids increased by 37.49%, DPPH and ABTS radical scavenging rates increased by 34.12% and 58.73%, and TVB-N levels decreased by 54.2%, respectively. In addition, using gas chromatography-mass spectrometry, 36 VFCs were detected in fermented sausages, including 9 aldehydes, 9 hydrocarbons, 7 alcohols, 4 acids, 2 ketones, and 5 esters. High-throughput sequencing demonstrated that the bacterial profiles were altered in sausages inoculated with strain CY1-2 during fermentation. Enhydrobacter dominated initially but was quickly replaced by Macrococcus after 8 h of fermentation, while Lactobacillus became the dominant genus after 40 h. Correlation analysis revealed that Lactobacillus and Staphylococcus played important roles in the production of VFCs in the fermented sausages. Notably, Lactobacillus was positively associated with 2-undecanone, pentadecane, and hexanal. This study confirmed that strain CY1-2 inoculation could enable the production of high-quality fermented fish sausages.

Dietary polyphenols have been associated with many beneficial cardiovascular effects. However, these effects are rather attributed to small phenolic metabolites formed by the gut microbiota, which reach sufficient concentrations in systemic circulation. 4-Methylcatechol (4-MC) is one such metabolite. As it is shown to possess considerable vasorelaxant effects, this study aimed to unravel its mechanism of action. To this end, experimental in vitro and in silico approaches were employed. In the first step, isometric tension recordings were performed on rat aortic rings. 4-MC potentiated the effect of cyclic nucleotides, but the effect was not mediated by either soluble guanylyl cyclase (sGC), modification of cyclic adenosine monophosphate levels, or protein kinase G. Hence, downstream targets such as calcium or potassium channels were considered. Inhibition of voltage-gated K⁺ channels (K_V) markedly decreased the effect of 4-MC, and vasodilation was partly decreased by inhibition of the K_V7 isoform. Contrarily, other types of K⁺ channels or L-type Ca²⁺ channels were not involved. In silico reverse docking confirmed that 4-MC binds to K_V7.4 through hydrogen bonding and hydrophobic interactions. In particular, it interacts with two crucial residues for K_V7.4 activation: Trp242 and Phe246. In summary, our findings suggested that 4-MC exerts vasorelaxation by opening K_V channels with the involvement of K_V7.4.

This study examined the relationship between total vegetable intake, including specific vegetable types with long-term late-life dementia (LLD) risk in older Australian women. 1206 community-dwelling older women aged ≥70 years were included. Consumption of total vegetable intake and vegetable types (yellow/orange/red [YOR], cruciferous, allium, green leafy vegetables [GLV], and legumes) were estimated using a validated food frequency questionnaire at baseline (1998). LLD was considered any form of dementia occurring after 80 years of age. LLD events (comprising hospitalisation and/or death) were obtained from linked health records. Associations were examined using restricted cubic splines within multivariable-adjusted (including APOE4 genotype) Cox proportional hazard models. Over 14.5 years of follow-up (∼15 134 person-years) there were 207 (17.2%) LLD events, 183 (15.25%) with LLD hospitalisations and 83 (6.9%) with LLD deaths. Compared to women in the lowest Quartile (Q1) of total vegetable intake, those with higher intakes (Q3, but not Q4) had 39% lower hazard for a LLD death. Compared to Q1, women in the highest quartile of YOR intake (Q4) consistently recorded lower hazards for a LLD event (47%), hospitalisation (46%), and death (50%). Similarly, women with the highest allium intake (Q4), had lower hazards for LLD events (36%) and deaths (49%), compared to Q1. Women with the highest GLV intake (Q4) also recorded 45% lower hazards for a LLD death. Whilst total vegetable intake may be important, allium, GLV and especially YOR vegetables may be most beneficial when considering LLD risk. These results require further validation in other cohorts, including men. The clinical trial registry numbers are https://anzctr.org.au/Trial/Registration/TrialReview.aspx?id=368778&isReview=true, CAIFOS: ACTRN12615000750583, and https://anzctr.org.au/Trial/Registration/TrialReview.aspx?id=372818&showOriginal=true&isReview=true, PLSAW: ACTRN12617000640303.

Insufficient selenium intake can lead to serious health problems. However, most research on the functional properties of selenium-enriched probiotics has focused on sub-health conditions or disease models, with limited studies involving healthy subjects. Additionally, previous research has primarily explored the direct effects of selenium itself, neglecting its influence on gut microbiota and metabolism. This study aimed to explore whether long-term intake of Pichia kudriavzevii enriched with selenium affected gut microbiota and host metabolism in mice and to identify microbiota and metabolites related to beneficial outcomes. Results demonstrated that selenium-enriched P. kudriavzevii (SeY) exhibited non-toxic properties, did not cause colon or liver damage, enhanced antioxidant capacity, and reduced inflammation in a selenium dose-dependent manner. Additionally, SeY supplementation significantly altered the gut microbiota. High-dose SeY (HSeY) elevated the abundance of beneficial bacteria such as Lactobacillus and suppressed harmful bacteria such as Eubacterium nodatum group, Prevotellaceae_NK3B31_group, and unclassified_f__Lachnospiraceae. Low-dose SeY (LSeY) increased the abundance of Faecalibaculum. The strain without enriched selenium exhibited higher levels of Akkermansia compared to selenium-enriched strains. Both strains, with or without enriched selenium, stimulated the production of short-chain fatty acids. Non-targeted metabolomics analysis revealed that HSeY treatment regulated various metabolic pathways, such as tryptophan metabolism, tyrosine metabolism, and arginine biosynthesis. LSeY treatment modulated tyrosine metabolism, secondary bile acid metabolism, bile secretion, and primary bile acid metabolism. P. kudriavzevii regulated the metabolism of purine, arginine, proline, and tryptophan. Our study highlights the promise of SeY supplementation in regulating host metabolism and the gut microbiota, offering insights into its implications for promoting health.

Obesity has become a serious epidemic problem in the world, and probiotics and prebiotics have been used to treat obesity. The effectiveness of diet therapy such as Clostridium butyricum (CB) and inulin supplementation in obesity and whether they can cooperate to produce better effects are still unclear. And during this process, intestinal flora play an important role, while the bacteria involved and the metabolic mechanism need to be explored. In this study, we successfully established a mouse obesity model with a high-fat diet (HFD) and divided it into three experimental groups: 7% CB (CB7), 7% CB + 1% inulin (C7G1), and 10% CB + 1% inulin (C10G). Dietary supplementation with CB and inulin could improve the glucose tolerance and intestinal microbial composition of obese mice, among which the simultaneous supplementation with 7% CB and 1% inulin (C7G1) has the most significant effect on obese mice fed with a HFD. It could significantly reduce the amount of total cholesterol, triglyceride, and low-density lipoprotein, improve abnormal glucose tolerance, and reduce abnormal blood glucose in obese mice. The intestinal flora of obese mice changed significantly, among which Lachnospiraceae_unclassified, Porphyromonaceae_unclassified, Olsenella, Bacteria_unclassified and Clostridiales_unclassified decreased due to the HFD, while Megamonas and Clostridium XIVa increased. After the supplementation with CB and inulin, the enrichment of three kinds of beneficial bacteria, Parabacteroides, Bacteroides, and Ruminococcaceae unclassified increased. The high-fat diet could upregulate the expression of FGF21, and the Clostridium butyricum and inulin supplemented diet could decrease the upregulation.

Epidemiological and animal studies have indicated that calcium and boron are essential for bone development and metabolism. However, limited information is available regarding the effects of boron supplementation on bone development and metabolism in newly weaned infants with either calcium deficiency or calcium sufficiency. This study assessed the effects of dietary boron supplementation (0 and 3 mg kg^-1) on bone development and metabolism, in a newly weaned mouse model, under both calcium deficiency and sufficiency feeding conditions. The results show that mice fed a calcium sufficient diet exhibited lower fat percentage and final body weight than those fed a calcium deficient diet. Boron supplementation reduced the serum high-density lipoprotein cholesterol level and up-regulated the mRNA levels of FABP3, PPAR-γ, and CaMK in the intestinal mucosa. Importantly, boron supplementation increased the tibial weight in mice on a calcium-sufficient diet and enhanced the tibial volume in those on a calcium-deficient diet. Metabolomic analysis highlighted calcium and boron's impact on metabolites like carboxylic acids and derivatives, fatty acyls, steroids and steroid derivatives, benzene and substituted derivatives, organonitrogen compounds, organooxygen compounds, and phenols, and were related to lipid metabolism and the neural signaling pathway. Transcriptomic analysis corroborated the role of calcium and boron in modulating bone metabolism via the JAK-STAT, calcium signaling, lipid metabolism, and inflammatory pathways. Multi-omics analysis indicated a strong correlation between calcium signaling pathways, lipid metabolism signaling, and dietary calcium and boron contents. This research provides insights into these complex mechanisms, potentially paving the way for novel interventions against calcium and boron deficiencies and bone metabolism abnormalities in clinical settings.

Background: Prior investigations identified correlations between dietary habits and the risk of prostate cancer (PCa); however, the causative dynamics are unclear. Methods: Utilizing the Mendelian randomization (MR) framework, we investigated the causal links between dietary habits, daily nutrient intakes, and risk of PCa (79 148 cases and 61 106 controls). Exposure and outcome data were obtained from the UK Biobank and the Prostate Cancer Association Group to Investigate Cancer-Associated Alterations in the Genome (PRACTICAL) consortium, respectively. Univariable and multivariable MR analyses were employed. Sensitivity analyses were performed to detect outliers, evaluate heterogeneity, and discern potential pleiotropic effects. Utilizing data from the National Health and Nutrition Examination Survey (NHANES) database (2009-2010), we selected 1294 and 1778 men aged ≥40 years from a pool of 10 537 participants, ensuring no missing information. Regression analyses examined the associations between leafy/lettuce salad intake, daily nutrient intake, and the odds of PCa. Results: Univariable MR (UVMR) analysis reveals that the intake of pork and salad/raw vegetable correlated with an elevated PCa risk. Subsequent to confounder adjustment via multivariable MR (MVMR) analysis, a causal link was established between salad/raw vegetable intake and an increased risk of PCa (odds ratio [OR]: 1.658, 95% confidence interval [95% CI]: 1.037-2.644, P = 0.046). The analysis based on NHANES datasets demonstrated a link between leafy/lettuce salad intake and heightened odds of PCa (OR: 1.025, 95% CI: 1.003-1.049, P = 0.038). Increased daily intakes of β-carotene (original OR: 1.00006, 95% CI: 1.00001-1.00011, P = 0.024) and vitamin B1 (OR: 1.474, 95% CI: 1.104-1.967, P = 0.014) were associated with a higher likelihood of PCa. Conclusions: These MR analyses substantiate the causal nexus between salad/raw vegetable intake and PCa risk. Similarly, leafy/lettuce salad intake and the odds of PCa were significantly correlated in the cross-sectional observational study. Moreover, higher daily intakes of β-carotene and vitamin B1 were linked to an increased likelihood of PCa. These findings provide practical dietary recommendations for PCa prevention and enhance early identification and diagnosis.

Neonatal necrotizing enterocolitis (NEC) is a severe inflammatory bowel disease that commonly affects premature infants. Breastfeeding has been proven to be one of the most effective methods for preventing NEC. However, the specific role of lipids, the second major nutrient category in human breast milk (HBM), in intestinal development remains unclear. Our preliminary lipidomic analysis of the HBM lipidome revealed that dioleoyl phosphatidylethanolamine (DOPE) is not only abundant but also shows high solubility in lipids, endowing it with significant biological utility. Experimental results confirmed that DOPE significantly reduces the mortality of neonatal rats, ameliorates impairment of intestinal barrier function, and alleviates the expression of intestinal inflammatory factors IL-1β and IL-6. Furthermore, DOPE promotes the migration and proliferation of intestinal epithelial cells, thereby enhancing the integrity of the intestinal barrier function in vitro. The progression of NEC is linked with the onset of ferroptosis. Our cellular-level analysis of lipid peroxide and iron ion concentrations revealed that DOPE significantly reduces the indicators of ferroptosis, while also modulating the expression of pivotal ferroptosis-associated factors, including SLC7A11, GPX4, and ACSL4. Hence, this research on DOPE is expected to provide novel insights into the bioactive lipids present in HBM.

Diabetes ranks among the top 10 causes of death globally, with over 90% of individuals diagnosed with diabetes having type 2 diabetes mellitus (T2DM). It is acknowledged that a high-fat diet (HFD) poses a serious risk for T2DM. The imbalance of intestinal flora, mediated by HFD, can potentially exacerbate the onset and progression of T2DM. However, the impact of HFD on pathological indicators and the intestinal microbiome in the development of T2DM has not been systematically investigated. Therefore, a HFD mouse model and a T2DM mouse model were established, respectively, in this study. The role of HFD as a driving factor in the development of T2DM was assessed using various measures, including basic pathological indicators of T2DM, lipid metabolism, liver oxidative stress, intestinal permeability, levels of inflammatory factors, gut microbiota, and short-chain fatty acids (SCFAs). The findings indicated that HFD could influence the aforementioned measures to align with T2DM changes, but the contribution of HFD varied across different pathological metrics of T2DM. The impact of HFD on low-density lipoprotein cholesterol, glutathione peroxidase, malondialdehyde, and tumor necrosis factor-α did not show a statistically significant difference from those observed in T2DM during its development. In addition, regarding gut microbes, HFD primarily influenced the alterations in bacteria capable of synthesizing SCFAs. The notable decrease in SCFA content in both serum and cecal matter further underscored the effect of HFD on SCFA-synthesising bacteria in mice. Hence, this research provided a systematic assessment of HFD's propelling role in T2DM's progression. It was inferred that gut microbes, particularly those capable of synthesizing SCFAs, could serve as potential targets for the future prevention and treatment of T2DM instigated by HFD.

Ulcerative colitis (UC), an inflammatory bowel disease, seriously affects people's quality of life. Diet-derived active peptides and Lactobacillus plantarum have shown promise for mitigating symptoms of UC. This investigation explored the combined effects of α-lactalbumin (α-LA) hydrolysate, which boasts a high antioxidant capacity, and L. plantarum 69-2 (L69-2) on a colitis mouse model. The results showed that α-LA hydrolysate with a molecular weight <3 kDa obtained with neutral protease had excellent antioxidant activity and potential to enhance probiotic proliferation. Furthermore, the synergistic application of α-LA hydrolysate and L69-2 could alleviate the adverse impact of colon inflammation by reducing oxidative stress and regulating immune disorders. It maintains the intestinal epithelial barrier, thereby reducing immune system over-activation, promoting the colonization of beneficial bacteria, and regulating intestinal immune responses. Simultaneously, it remodels the structure of the disrupted intestinal flora. The increase in the richness and diversity of the flora leads to the production of beneficial metabolites, which in turn inhibits the activation of the TLR4/NF-κB inflammatory pathway. This study provides a novel perspective on milk-derived peptide synergism with probiotics in alleviating UC.