Food & Function最新文献

Pectinase-assisted processing may enhance the functional value of immature citrus peel (Qingpi, QCP), but the links between matrix degradation, metabolite remodeling, and bioactivity remain unclear. QCP aged for 1, 3, 7, and 10 years and their corresponding pectinase hydrolysates (QCPEH) were evaluated using antioxidant assays, an ethanol-injured HepG2 model, metabolite profiling, chemical-space analysis, network pharmacology, molecular docking, single-compound validation, and RT-qPCR. Pectinase hydrolysis enhanced DPPH, ABTS, and FRAP responses at all aging periods, with 10-QCPEH showing the strongest overall activity. In HepG2 cells, 10-QCPEH reduced LDH release, ALT and AST activities, ROS and MDA levels, restored SOD activity, and partially recovered ADH and ALDH activities. Changes in IL-1β, IL-6, and TNF-α were not statistically significant. Pectinase treatment decreased pectin molecular weight and remodeled both VOC and NVOC profiles, supporting increased metabolite accessibility. Tangeretin, thymol, and nobiletin each reduced ROS accumulation and LDH release. Aromaticity was positively correlated with DPPH, ABTS, and FRAP activities (ρ = 0.90-0.95, q < 0.05). Network and docking analyses highlighted targets related to redox regulation, metabolism, inflammation, and cell survival. RT-qPCR further showed increased HMOX1 and PPARA and decreased PPARG, RELA, TNF, and PTGS2 expression, whereas AKT1 was not significantly altered. These findings support pectinase hydrolysis as a strategy to improve the functional potential of aged QCP through matrix depolymerization and metabolite remodeling.

Although dietary guidelines emphasize consuming foods rich in eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), intakes remain below recommended levels in many populations worldwide. To address this concern, we developed an algae oil-fortified soymilk beverage and assessed its short-term chronic bioavailability compared to algae oil capsules. In a 4-week, open-label, randomized parallel trial, 21 healthy adults consumed either an algae oil-fortified soymilk beverage (200 mg EPA, 320 mg DHA) or a closely matching dose of algae oil-fortified capsules (230 mg EPA, 380 mg DHA) daily. The primary endpoint was the change in red blood cell (RBC) EPA and DHA, with plasma and peripheral blood mononuclear cell (PBMC) profiles assessed secondarily. Both groups exhibited significantly increased EPA and DHA across all blood compartments over the 4-week intervention. Although the capsule group showed a greater unadjusted increase in RBC and plasma DHA, no significant difference in EPA or DHA accumulation remained after normalizing for dose and compliance. Therefore, fortified soymilk is a well-tolerated delivery vehicle for algae oil which increases RBC EPA and DHA offering a comparable food-based alternative to traditional capsules.

Coffee pulp (CP) and silverskin (SSK), two major coffee industry by-products, were recently shown to ameliorate metabolic syndrome (MetS) features induced by high-fructose feeding in rats. This work investigated, using proteomic analysis, whether CP and SSK induce changes in the hypothalamus and hippocampus relevant to fructose-induced MetS. In the hippocampus, high fructose consumption altered pathways related to the extracellular matrix (ECM), ECM-receptor interaction, cell-cell adhesion, synaptic transmission, and neuronal excitability. A highly coherent functional module centered on basement membrane (BM) proteins (COL4A1, COL4A2, LAMA2, LAMA4 and LAMA5) was identified. CP and SSK produced proteomic signatures suggestive of structural remodeling, particularly involving BM-related proteins associated with age-dependent changes in BM stability, neurovascular function, and cognitive trajectories. Of note, changes in the abundance of three proteins associated with neurodegenerative diseases observed following fructose feeding were not observed in animals co-treated with CP (VCCG3) or SSK (RETSAT and S100A6). In the hypothalamus, fructose consumption altered proteins involved in neuronal signaling and calcium dynamics, metabolism and stress response, gene regulation, cytoskeletal organization, and membrane-associated processes. CP mainly affected pathways associated with the neuronal cell body, whereas SSK predominantly influenced GTP binding and membrane-bounded organelles. Overall, fructose induced specific proteomic alterations in the hippocampus and hypothalamus and, in the hippocampus, CP and SSK altered proteins associated with neurovascular function and cognitive trajectories, consistent with a potential association with neuroprotective processes in the context of fructose-induced MetS. Distinct proteomic signatures observed with CP and SSK under standard and high-fructose diets further indicate specific protective mechanisms of these coffee by-products.

Cortical thickness, assessed by magnetic resonance imaging (MRI), is a biomarker of age-related neurodegeneration. Walnut ellagitannins may influence brain structure via gut microbiota-derived urolithins. We examined whether longitudinal changes in urinary urolithins are associated with concurrent changes in cortical thickness in cognitively healthy older adults. This longitudinal MRI sub-study was conducted within the Walnuts and Healthy Aging study, a two-center (Barcelona, Spain and Loma Linda, California) randomized controlled trial testing the effects of 2-year daily walnut consumption vs. a control diet on age-related health outcomes in older individuals. A subset of participants from the Barcelona center underwent structural MRI at baseline and after 2 years. Urinary urolithin concentrations were quantified by liquid chromatography-high-resolution mass spectrometry, and their changes were related to concurrent changes in cortical thickness using multivariable-adjusted linear regression models, with analyses stratified by urolithin metabotype to account for inter-individual variability. A total of 104 participants were included. Among those allocated to the walnut diet (n = 55), greater increases in urolithin A (β = 0.023 [95% CI, 0.003-0.043] per 1-SD), urolithin C (β = 0.015 [95% CI, <0.001-0.029] per 1-SD), and its glucuronide conjugate (β = 0.017 [95% CI, 0.002-0.031] per 1-SD) were associated longitudinally with preservation of cortical thickness, predominantly in right-hemisphere regions. Associations were more pronounced among metabotype B individuals. These findings provide novel clinical evidence linking microbiota-derived (poly)phenol metabolites to brain aging and support a precision nutrition framework. Trial registration: Clinical trials.gov as NCT01634841.

Objective: To investigate the association between the dietary inflammatory index (DII) and sarcopenia risk in older adults and identify cross-species microbial signatures linking dietary inflammatory burden with muscle phenotypes. Methods: A total of 1048 older adults were enrolled, and multivariable logistic regression models were applied to evaluate the association between the DII and sarcopenia risk. A sub-cohort of representative participants (n = 86) underwent fecal 16S rRNA gene sequencing. In parallel, a 10-week pro-inflammatory dietary intervention in naturally aged mice was conducted, followed by gut microbiome and skeletal muscle untargeted metabolomic profiling. Cross-species microbial signatures were identified by integrating human and mouse microbiome data. Results: Higher DII scores were associated with a greater prevalence of sarcopenia (OR = 1.305, 95% CI: 1.128-1.509). No significant difference in gut microbial α-diversity was observed between participants with and without sarcopenia, whereas β-diversity differed significantly between the two groups (p = 0.005). In aged mice, pro-inflammatory dietary intervention reduced grip strength and lean body mass and altered gut microbiota composition and skeletal muscle metabolic profiles. Group-by-time interaction effects for forelimb and all-limb grip strength remained significant after FDR correction (q < 0.05). Metabolomic changes were mainly enriched in lipid and amino acid metabolism pathways. Cross-species integration identified conserved microbial signatures, including the Family XIII AD3011 group, Akkermansia, and Fusobacterium. Conclusions: Higher dietary inflammatory burden is associated with increased sarcopenia risk and impaired muscle function in older adults. Gut microbiota alterations and skeletal muscle metabolic remodeling may contribute to this association. The identified cross-species microbial signatures provide potential targets for future mechanistic studies and nutritional interventions.

Chronic kidney disease (CKD) is increasingly recognised as a systemic disorder extending beyond renal impairment to include cognitive decline. The present review focuses on the mechanisms through which CKD and cognitive impairment are connected in the gut-kidney-brain axis, especially when considering the role played by nutrition as a possible target for interventions. Sources of literature were identified in PubMed, Scopus, Web of Science, and Google Scholar up until 2026 and included in the present analysis clinical trials, systematic reviews and studies in peer-reviewed journals related to nutritional, microbial and cognitive outcomes in CKD. From both interventional and observational data, CKD is characterised by a reduction in short-chain fatty acid (SCFA)-producing bacteria such as Faecalibacterium prausnitzii and Roseburia spp., as well as an increase in proteolytic organisms responsible for uremic toxin production with a consequent elevation in indoxyl sulphate (IS) and p-cresyl sulphate (PCS). Metabolic abnormalities in IS and PCS have been linked to the disruption of blood-brain barrier (BBB), microglial activation, and impaired attention, executive function and memory in human subjects, while animal studies suggest additional impairments including neuronal cell death and learning impairment in hippocampus, although causality cannot be confirmed in humans. Deficiencies of proteins, vitamin B, vitamin D, magnesium, and polyunsaturated fatty acids (PUFAs) are frequently found in CKD and contribute to the above-mentioned problems. Renal-adapted Mediterranean diet, supplementation with micronutrients guided by biomarkers and synbiotics reduce levels of PCS and inflammation, while prebiotics and synbiotics perform better than probiotics, although no cognitive endpoints were defined in most studies.

Lutein and zeaxanthin are carotenoids that play a significant role in maintaining eye health and must be obtained from dietary sources, as humans cannot synthesise them de novo. However, their concentrations in foods are generally very low. This study evaluates the role of fermentation in enhancing the bioaccessibility of xanthophylls in twelve commonly consumed fruits and vegetables. In addition, it investigates the cellular uptake and bioactivity of raw and fermented kale and corn, which contain detectable levels of both lutein and zeaxanthin. The Lutein and zeaxanthin contents increased by 30-50% in fermented vegetables after five days of spontaneous fermentation. Similarly, cellular uptake of those compounds increased by 35% and 38% in kale and corn, respectively. Fermented kale and corn also demonstrated a 45-50% reduction in cytokine production in response to induced inflammatory and oxidative stress in Caco-2 cells, indicating enhanced anti-inflammatory and antioxidant properties. Full-length 16S rRNA sequencing revealed that Leuconostoc mesenteroides, Lactiplantibacillus plantarum, Lactococcus lactis and Weissella confusa were the dominant bacteria in fermented corn and kale. The consistent increase in lutein and zeaxanthin observed during the controlled fermentation of kale and corn using bacteria isolated from their respective spontaneously fermented samples further supports the beneficial role of spontaneous and controlled fermentation in enhancing xanthophylls in plant foods.

Antimicrobial resistance and the demand for effective food-preservation strategies have increased interest in fatty acids (FAs) and their derivatives as potential antibacterial agents. FAs can affect bacterial membranes, cellular energetics, biofilm-associated phenotypes, and, in some organisms, specific metabolic pathways. However, these effects vary considerably with FA structure, concentration, ionization state, pH, formulation, bacterial species, and assay conditions. Additionally, microbiota-derived short-chain FAs may also contribute to host defense by influencing epithelial integrity, immune signalling, microbiome composition, and colonization resistance. Still, researchers should distinguish these indirect effects from direct bacterial killing. Evidence from laboratory media cannot necessarily predict performance in complex foods, where proteins, lipids, processing conditions, oxidation, and sensory limitations can alter antibacterial activity. Next, monoglycerides, conjugates, and delivery systems may improve stability or availability, although their efficacy, safety, and regulatory status require formulation-specific evaluation. This review critically examines direct antibacterial activity, host- and microbiome-mediated effects, food-matrix applications, resistance-related considerations, and emerging formulation approaches. Current evidence supports the potential of selected FAs in defined applications, while emphasizing the need for standardized assays, appropriate food-matrix validation, and stronger animal and human evidence.

This study employs an in vitro model to investigate the pH-dependent interfacial complexation of gallic acid (GA) with mucin, a key molecular mechanism underlying astringency, through systematic analysis of phase behavior, electrokinetics, adsorption dynamics, and lubrication properties. Results show that GA induces concentration-dependent mucin aggregation, with the hydrodynamic diameter increasing 2.8-fold (152 ± 3 nm to 423 ± 12 nm) at pH 3.5, while remaining largely stable at pH 7.5. A critical aggregation threshold emerged at a 60 : 40 w/w GA : mucin ratio at pH 3.5, coinciding with peak turbidity (OD₅₀₀ = 0.69 ± 0.05) and sedimentation (88 ± 2% mass recovery). At this ratio, electrokinetic measurements revealed near-complete charge neutralization (-0.8 ± 0.3 mV at pH 3.5 vs. -22.4 ± 0.5 mV for mucin alone), indicating that aggregation is driven by reduced electrostatic repulsion in conjunction with other noncovalent interactions. QCM-D analysis displayed that, at pH 3.5, GA formed a highly dissipative (ΔD₅ ≤ 6.76 ± 0.01 × 10^-6), thick (Δt = 14.41 ± 0.02 nm), and water-rich viscoelastic adlayer with substantial mass uptake (Δm = 633.67 ± 0.09 ng cm^-2). Conversely, at pH 7.5, GA adsorption yielded a thinner (Δt = 3.81 ± 0.01 nm), less dissipative (ΔD₅ ≤ 0.87 ± 0.01 × 10^-6), and more rigid film with markedly lower mass accumulation (Δm = 380.37 ± 0.10 ng cm^-2). ΔD-Δf plots confirmed more extensive viscoelastic changes at pH 3.5, indicating a pronounced interfacial restructuring. Tribology directly linked this structural change to lubrication loss; mucin alone exhibited low friction (μ ∼ 0.002-0.003), GA increased friction roughly 7-fold (μ ∼ 0.022) at pH 3.5, while medium-chain triglyceride partially restored lubrication, reducing μ to ∼0.010 (∼54.5% decrease) at pH 3.5 and to ∼0.009 (∼30.8% decrease) at pH 7.5. These results confirm that pH-dependent GA-mucin aggregation and adlayer restructuring coincide with increased friction, linking interfacial changes to astringency-related lubrication loss.

Tiger nut (Cyperus esculentus L.), a highly promising oil crop, produces oil rich in unsaturated fatty acids and contains various natural bioactive components. However, the role of these accompanying lipid constituents in the health effects of tiger nut oil has been insufficiently investigated. In this study, tiger nut oil unsaponifiables (TNU) were prepared via saponification followed by solvent extraction, and their chemical composition was identified by GC-MS. The effects of TNU on metabolic dysregulation and cognitive impairment were assessed in a high-fat diet (HFD)-induced obese mouse model. The refined tiger nut oil was found to contain 1.247 ± 0.021% unsaponifiable matter, with phytosterols, tocopherols, and squalene as the major constituents. TNU supplementation resulted in significant attenuation of HFD-induced weight gain and lipid accumulation, improvement in glucose homeostasis and insulin sensitivity, and reduction in hepatic lipid deposition and adipose tissue pathology. Moreover, the hepatic expression of lipogenic genes Srebp-1, Fas, and Acc was markedly downregulated by TNU. In parallel, TNU effectively rescued learning and memory deficits and spatial cognitive impairment in obese mice, suppressed aberrant microglial activation in the hippocampus, alleviated neuroinflammation, and upregulated the mRNA expression of the synaptic protein PSD-95 as well as the neurotrophic factors Bdnf, Ngf, and Ntf-3. In summary, TNU may ameliorate HFD-induced cognitive dysfunction by modulating disorders of glucose and lipid homeostasis and inhibiting the metabolic inflammation-neuroinflammation axis. This study contributes to a theoretical basis for the development of tiger nut oil as a functional dietary lipid resource.