Food & Function最新文献

The imbalance between pyroptosis and mitophagy constitutes a key pathogenic axis in radiation-induced intestinal injury (RIII). Lactoferrin (Lf), a multifunctional glycoprotein with well-recognized antioxidant and anti-inflammatory properties, has not been fully characterized in relation to RIII. This study investigated the potential protective effects of Lf on RIII using rat intestinal epithelial IEC-6 cells exposed to 4 Gy X-ray irradiation and male C57BL/6J mice subjected to 10 Gy total-abdominal irradiation. Radiation induced pyroptosis and mitochondrial dysfunction in vitro and in vivo. Lf pretreatment reduced radiation-induced ROS accumulation, inhibited activation of the NOD-like receptor protein 3 (NLRP3)/caspase-1/gasdermin-D (GSDMD) pyroptosis pathway, and activated mitophagy to remove damaged mitochondria in irradiated IEC-6 cells. Consistently, Lf protected against RIII in irradiated mice by promoting mitophagy and suppressing pyroptosis. Mechanistically, these effects involved activation of ubiquitin-dependent (PINK1/Parkin-mediated) and ubiquitin-independent (FUNDC1/BNIP3/NIX receptor-driven) mitophagy pathways. The mitophagy-promoting effect of Lf was more pronounced on day 3.5 after radiation than on day 14. Notably, pharmacological inhibition of mitophagy with 3-Ma and Mdivi-1 abolished the protective effects of Lf. Collectively, our in vivo and in vitro findings demonstrate that Lf mitigates RIII by facilitating early clearance of damaged mitochondria, thereby inhibiting NLRP3 inflammasome activation and suppressing pyroptosis.

This study employed ultrasonic-assisted DES technology to extract jujube polysaccharides (ZJP) and investigated the effects of α-galactosidase modification on their structural characteristics and prebiotic functions. The modified polysaccharide (α-ZJP) exhibited significant alterations in physicochemical properties, including reduced neutral sugar and protein content, increased reducing sugars and uronic acids, and a shifted molecular weight distribution due to selective cleavage of galactose and rhamnose residues. Structural analysis confirmed the retention of key functional groups and revealed a transformed morphology from smooth sheets to a porous, sponge-like architecture. In vitro fermentation demonstrated that α-ZJP promoted rapid initial microbial growth and short-chain fatty acid (SCFA) production, by enriching Firmicutes and Lachnospiraceae. In contrast, unmodified ZJP showed sustained fermentation, yielding higher total SCFAs and selectively promoting butyrate-producing bacteria like Coriobacteriaceae. Both polysaccharides enhanced microbial diversity and SCFA accumulation, indicating their potential as prebiotics for gut health through distinct structure-dependent mechanisms.

Shifting to a plant-based diet naturally alters protein source choices. In many countries, protein from yellow pea is widely used as a main ingredient in meat alternatives. Still, its biological effects, especially regarding gastrointestinal health, remain incompletely understood. The aim of our study was to investigate how a weekly increase in the intake of a well-characterized pea protein isolate affects surrogate markers of health, fecal short-chain fatty acids and gut microbiota composition in healthy individuals. Male and female adults (N = 29) participated in this exploratory intervention study. A 4-week pre-intervention period for questionnaires and fecal samples collection was followed by a 4-week supplementation. Participants consumed isolated pea protein in weekly increasing amounts, starting from 0.25 g per kg body mass per day in week 5 to 1.00 g per kg body mass per day in week 8. Questionnaire data, fecal samples as well as fasting blood and 24 h urine samples were collected weekly. Data from biological samples and questionnaires confirmed a healthy study population and compliance. Fecal calprotectin levels significantly increased only in a subset of participants, which was accompanied by higher fecal water cytotoxicity in vitro. Short-chain fatty acids mainly rose in those subjects with stable calprotectin levels. Relative abundances of Limosilactobacillus frumenti, Odoribacter splanchnicus and Lactobacillus crispatus increased significantly in the total population during the intervention while the relative abundance of Bifidobacterium longum and Bifidobacterium catenulatum decreased. Our results indicate that an increased intake of pea protein isolate affects the growth of certain beneficial bacterial strains and differentially influences markers related to gut inflammation in healthy individuals.

3′-Hydroxypterostilbene (OHPt), a hydroxylated derivative of pterostilbene (Pt) naturally occurring in dietary plant sources, was evaluated for its anti-prostate cancer potential. In PC-3 cells, OHPt markedly reduced viability in a dose- and time-dependent manner, exhibiting stronger growth inhibition than Pt, implying that hydroxyl substitution at the 3′ position enhances anti-proliferative activity. Mechanistic studies revealed that OHPt triggered both intrinsic and extrinsic apoptosis, evidenced by mitochondrial membrane depolarization, activation of caspase-8, -9, and -3, and an increased Bax/Bcl-xL ratio. Additionally, OHPt promoted autophagic cell death, upregulating Beclin-1, LC3-II expression, and autophagosome formation. In a PC-3 xenograft nude mouse model, OHPt administration significantly suppressed tumor growth without apparent toxicity, accompanied by reduced COX-2 and MMP-9 protein levels and increased LC3-II expression. These findings suggest that OHPt displays strong anti-tumor activity in vitro and in vivo, achieved via coordinated activation of apoptotic and autophagic mechanisms, thereby supporting its potential as a therapeutic candidate for prostate cancer.

Type 2 diabetes mellitus (T2DM) poses a global threat to public health. While dietary fiber and plant extracts have been individually shown to exert hypoglycemic effects, the potential synergistic impact of their combined intervention on T2DM has yet to be fully elucidated. T2DM model control (MC) mice were established by administering mice with high-fat diets and streptozotocin. Resistant dextrin and mulberry leaf extract (MR) significantly decreased fasting blood glucose (FBG) and hemoglobin A1c (HbA1c) levels compared with MC. Notably, MR lowered the FBG and HbA1c levels better than resistant dextrin or mulberry leaf extract alone. MR significantly upregulated hepatic mRNA expression involved in glycogen synthesis and glucose uptake while downregulating the genes related to gluconeogenesis and glycogenolysis. Meanwhile, MR markedly improved gut microbiota diversity and selectively enriched bacterial taxa associated with SCFAs, such as acetic and propionic acids. Collectively, MR enhances glycemic control by modulating hepatic glucose metabolism, enriching SCFA-producing bacterial taxa, increasing SCFA levels, and alleviating insulin resistance.

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.