Consumption of (+)-catechin and (−)-epicatechin is associated with beneficial effects on human health. However, their limited systemic circulation in native form suggests that their metabolites may contribute to these effects. The aim of this study was to produce and structurally characterize glucuronide metabolites of (+)-catechin and (−)-epicatechin, which are not commercially available, and to assess their presence in plasma from volunteers who consumed a blend of grape and wild blueberry extracts. Firstly, four monoglucuronides of each flavanol were produced using rat liver microsomes and characterized by UHPLC-DAD-MS/MS and NMR. Using these compounds, we were able to confirm the presence in human plasma of three glucuronides: one known (−)-epicatechin glucuronide and two previously unidentified (+)-catechin glucuronides. Further research is needed to understand their biological role.
Non-alcoholic fatty liver disease (NAFLD) is a growing global health burden with limited therapeutic options. This study investigated the protective effects of mulberry leaf glutelin (UDG) on NAFLD using free fatty acid-induced HepG2 cells and a high-fat diet (HFD) mouse model. UDG inhibited pancreatic lipase and cholesterol esterase activities in vitro, promoted fecal lipid excretion, and reduced triglyceride and cholesterol accumulation in cells and liver tissue. In vivo, UDG administration significantly alleviated HFD-induced weight gain, dyslipidemia, hepatic steatosis, and liver injury (p < 0.05). Serum biochemical analyses showed improvements in ALT, AST, lipid profiles, and lipopolysaccharide levels, accompanied by decreased expression of inflammatory cytokines (IL-6, IL-1β, TNF-α) and suppression of the TLR4/MyD88/NF-κB signaling pathway. Furthermore, untargeted serum metabolomics revealed that UDG markedly regulated metabolic profiles, with enrichment in pathways related to bile acid metabolism, amino acid metabolism, and central carbon metabolism. Notably, metabolites such as cholic acid and chenodeoxycholic acid were negatively correlated with NAFLD indicators and restored by UDG intervention. These findings show that UDG exerts lipid-lowering, hepatoprotective, and anti-inflammatory effects against NAFLD, potentially through modulation of bile acid biosynthesis and serum metabolic pathways. This study highlights mulberry leaf glutelin as a promising plant protein source with functional food potential for NAFLD prevention and management.
Methionine-containing cyclolinopeptide ([1–9-NαC]-linusorb B2, CLB) and α-linolenic acid (ALA), two anti-inflammatory flaxseed constituents, were investigated for their combined vascular benefits. CLB-enriched orbitides were prepared for long-term high-fat diet (HFD)-fed mouse studies, while high-purity CLB monomer (>97%) was isolated via preparative chromatography for acute in vivo and cell-based assays. Structural confirmation and purity validation were achieved via mass spectrometry and liquid chromatography. CLB-enriched orbitides co-administered with ALA in HFD-fed mice reduced body weight gain, serum trimethylamine N-oxide (TMAO), dyslipidemia, and vascular inflammation, histologically confirmed by reduced pro-inflammatory mediators and endothelial repair. Purified CLB combined with ALA further demonstrated efficacy in alleviating TMAO-induced acute vascular inflammation in mice. Mechanistically, CLB enhanced ALA metabolism by upregulating key enzymes (lipoxygenases and cytochrome P450) and directly binding to their catalytic pockets. Combined effect loss upon enzyme inhibition confirmed ALA metabolic modulation as the key mechanism. These findings highlight CLB's role in amplifying ALA's efficacy to combat vascular inflammation.
The field of personalised nutrition is growing and is based on the concept that delivering personalised dietary advice will be more effective than generic healthy eating guidelines for individuals to improve their diet and metabolic health. While there is substantial interest in the field, there is also a need to examine the evidence base. The objective of this review was to examine existing literature on the efficacy of personalised nutrition approaches and to identify research gaps and future needs. A literature search was conducted in PubMed for randomised controlled trials published between 2000 and 2025. Studies investigating the effects of personalised nutrition were included, and relevant papers were identified through the reference lists of existing papers. In total, 24 papers were included, with 12 studies investigating personalised nutrition based on current diet, phenotype, and metabolic biomarkers, five studies examining the effects of genotype-based personalised nutrition, and seven studies exploring approaches based on gut microbiome and machine learning algorithms. Overall, evidence from the included studies indicates that personalised nutrition approaches consistently improved dietary quality and led to significant improvements in metabolic markers, including HbA1c, triglycerides, and insulin sensitivity. However, few studies showed significant between-group differences in weight loss, and most studies did not find significant differences in blood pressure. While the results are promising, there are key challenges and research gaps that remain. Some approaches demonstrated potential for targeted improvements, but further high-quality research is needed to confirm their effectiveness and long-term impact. Future research should prioritise longer-term studies, better stratification of responders and non-responders, and cost-effectiveness evaluations to determine where and for whom personalised nutrition adds the most value.
The oral mucosa is the first site of contact with food allergens, yet the influence of food matrices and oral processing on allergen release remains poorly understood. This study investigated the roles of bread matrix and mastication behaviors in the oral bio-accessibility of wheat allergens. Volunteers consumed breads with distinct structural profiles (baked, steamed, baguette; with/without shortening) under video monitoring. Results showed that the bread matrix did not alter the types of released proteins but significantly modulated their IgE-reactivity. The addition of shortening enhanced IgE-binding capacity, suggesting a lipid-mediated modulation of allergen release is likely through emulsion formation. Oral processing parameters correlated strongly with bolus properties and allergen immunoreactivity, highlighting that individual mastication behaviors personalize the exposure dose. High-molecular-weight (MW) and low-MW glutenin, serpin, GAPDH, and α-amylase inhibitors were identified as the primary bio-accessible wheat allergens released in the oral phase. This study provides a new perspective on the initial exposure pathway of wheat allergens from the novel lens of allergen–matrix interactions.
Cold-pressed almond oil is considered a premium product due to its solvent-free extraction and sensory quality. Its industrial production produces large volumes of a nutrient-rich by-product, namely almond press cake (APC). In this study, this by-product was submitted to supercritical fluid extraction (SFE) with CO2 using two different pressure conditions for extracting residual oil in APC, further generating two residues (APC20 and APC24, from extraction at 20 and 24 MPa, respectively). Except for fat, which, as expected, was reduced in APC20 and APC24, and available carbohydrates, which were higher in the SFE-derived samples, the three residues showed similar contents of the remaining macronutrients (p > 0.05). The residues were particularly rich in total dietary fiber (from 73.7 to 76.2 g per 100 g), presenting also relevant quantities of protein (from 9.3 to 9.5 g per 100 g). APC20 and APC24 showed a strong retention of phenolic compounds, with only about a 10% decrease of total phenols compared to APC. In vitro digestion using the INFOGEST protocol revealed that some phenolic compounds exhibited high bioaccessibility values, with taxifolin, amygdalin, caffeic acid, vanillic acid, protocatechuic acid, and quercetin-3-O-glucoside exceeding 100% bioaccessibility. Moreover, the antioxidant potential of bioaccessible fractions after simulated digestion was superior to that exhibited by non-digested samples. Furthermore, the prebiotic potential of digested residues was evident through the promotion of Lactobacillus and Bifidobacterium growth, comparable to inulin. Altogether, these results highlight the value of almond oilcake and its extraction residues as promising and sustainable functional food ingredients.
The impact of zinc deficiency on systemic mineral homeostasis remains unclear. This study investigated the effects of zinc deficiency on mineral homeostasis by quantifying sixteen minerals across nineteen tissues, along with their intake, excretion, and distribution. Principal component analysis revealed distinct differences in the mineral composition profiles of serum, whole blood, heart, spleen, testis, urine, and feces between the low-zinc and normal-zinc diet groups. Specifically, zinc deficiency enhanced intestinal absorption of Ca, Co, V, Ni, and Mo, and decreased their excretion, leading to elevated concentrations in the blood, heart, kidneys, testes, and cecal contents. Conversely, zinc deficiency increased the excretion of As, Mg, Se, and K, resulting in reduced concentrations of these minerals in the kidneys, testes, spleen, and femur. Additionally, zinc deficiency directly influenced the distribution of Mn, Cr, Cu, Na, and Pb, causing significant alterations in their concentrations across multiple tissues. Correlation analysis revealed that changes in mineral concentrations may contribute to a spectrum of adverse health outcomes. Our findings revealed that zinc deficiency disrupts systemic mineral homeostasis through four key pathways: intake, absorption, distribution, and excretion.
Erucic acid is a monounsaturated omega-9 fatty acid with reported immunomodulatory activity. This study evaluated its protective effects against cyclophosphamide (CTX)-induced immunosuppression in mice. Thirty animals were divided into six groups: normal control, CTX (80 mg kg−1), erucic acid (10 and 20 mg kg−1), levamisole (20 mg kg−1), and an erucic acid-only group (20 mg kg−1). Immune organ indices, hematological parameters, cytokines, oxidative stress markers, IgG levels, and splenic lymphocyte proliferation were measured, along with histological assessment of the spleen and thymus. Network pharmacology was used to predict immune-related targets and docking affinities. CTX reduced the spleen index from 7.26 ± 0.75 mg g−1 to 3.04 ± 0.21 mg g−1 and the thymus index from 3.60 ± 0.32 mg g−1 to 1.50 ± 0.21 mg g−1. Lymphocyte proliferation dropped from 100.0 ± 3.28% to 37.50 ± 3.07%. WBC and RBC counts declined to 2.53 ± 0.30 × 103 µL−1 and 4.33 ± 0.69 × 106 µL−1, respectively. CTX also lowered IFN-γ (3.50 ± 0.19 to 1.80 ± 0.19 ng mg−1), TNF-α (105.0 ± 5.56 to 52.0 ± 5.56 pg mL−1), and IgG levels (12.00 ± 0.54 to 4.70 ± 0.54 pg mL−1), while increasing MDA (1.42 ± 0.16 to 4.88 ± 0.41 nmol mg−1) and NO (0.10 ± 0.01 to 0.24 ± 0.01 µmol g−1). Erucic acid at a 20 mg kg−1 dose increased the spleen index to 6.63 ± 0.60 mg g−1, the thymus index to 3.00 ± 0.22 mg g−1, and the lymphocyte proliferation to 61.67 ± 3.44%. It improved WBC counts to 4.72 ± 0.29 × 103 µL−1 and restored IFN-γ (3.28 ± 0.22 ng mg−1), TNF-α (87.0 ± 5.56 pg mL−1), and IgG (9.03 ± 0.87 pg mL−1). Antioxidant markers also improved, with SOD rising from 5.55 ± 0.52 to 10.22 ± 1.02 U mg−1 and GSH from 3.13 ± 0.35 to 6.45 ± 0.46 µmol g−1. Histology showed reduced splenic and thymic damage in treated groups. Docking analysis indicated strong interactions between erucic acid and key immune-regulatory targets. Overall, erucic acid, particularly at a dose of 20 mg kg−1, counteracted cyclophosphamide-induced immune suppression and oxidative stress, with effects comparable to those of levamisole.
Enterotoxigenic Escherichia coli (ETEC) is a leading cause of diarrhea in infants and young children. lysophospholipid (LPL) has been shown to enhance lipid and nutrient absorption while improving intestinal morphology and function in animals. Owing to the close similarity between their gastrointestinal physiology and that of human infants, weaned piglets are widely employed as the animal model for gastrointestinal disease research. This study investigated the effects of dietary LPL (containing 6% active ingredient) supplementation on intestinal health and diarrhea mitigation under ETEC challenge. Thirty-two weaned barrows (Duroc × Landrace × Yorkshire, 7.24 ± 0.07 kg BW, 25 days of age) were randomly assigned to four groups based on body weight. The dietary treatments included: (1) basal diet (CON), (2) basal diet + ETEC K88 (CON + ETEC), (3) basal diet + 0.3% LPL (CON + LPL), and (4) basal diet + 0.3% LPL + ETEC K88 (LPL + ETEC). The results demonstrated that LPL significantly improved the apparent total-tract digestibility of nutrients in piglets (P < 0.05) without affecting growth performance (P > 0.05). In addition, LPL significantly reduced diarrhea incidence in piglets before and after ETEC challenge (P < 0.05). LPL effectively ameliorated ETEC-induced intestinal morphological damage, including improvements in villus height and crypt depth (P < 0.05). LPL also upregulated expressions of intestinal barrier-related genes (MUC1, Occludin and LPA2) in different intestinal segments (P < 0.05) while counteracting ETEC-induced CFTR upregulation and MUC2 downregulation. Furthermore, LPL enhanced antioxidant capacity by reducing serum malonaldehyde (MDA) content (P < 0.05) and increasing ileal total superoxide dismutase (T-SOD) and glutathione peroxidase (GSH-Px) activities (P < 0.05), while mitigating inflammatory responses through decreasing serum IL-1β and IL-6 levels (P < 0.05). In summary, LPL enhances nutrient digestion and absorption to alleviate nutritional diarrhea and, via the LPA2/CFTR pathway, preserves intestinal barrier structure and function during ETEC infection while exerting anti-inflammatory and antioxidant effects to reduce diarrhea and improve gut health, demonstrating strong translational potential for preventing and treating ETEC induced diarrhea.

