Food & Function最新文献

This study aimed to develop a novel astaxanthin nanoparticle using gum arabic (GA) and whey protein powder enriched with milk fat globule membranes (MFGM-WPI) as carriers and to investigate its effect and alleviation mechanism on colitis in mice. We demonstrated that MFGM–GA-astaxanthin could improve the bioaccessibility of astaxanthin and cope with oxidative stress more effectively in a Caco-2 cell model. In vivo studies demonstrated that MFGM–GA-astaxanthin alleviated colitis symptoms and repaired intestinal barrier function by increasing the expression of mucin 2, occludin, and zonula occludens-1. This was attributed to the alleviating effect of MFGM–GA-astaxanthin on oxidative stress. Moreover, MFGM–GA-astaxanthin restored the abnormalities of flora caused by dextran sulfate sodium, including Lactobacillus, Bacteroides, Ruminococcus, and Shigella. This study provides a basis for the therapeutic effect of astaxanthin nanoparticles on colon diseases.

This study investigated the potential benefits of black chokeberry polyphenol (BCP) supplementation on lipopolysaccharide (LPS)-stimulated inflammatory response in RAW264.7 cells and obesity-induced colonic inflammation in a high fat diet (HFD)-fed rat model. Our findings demonstrated that BCP treatment effectively reduced the production of nitric oxide (NO) and pro-inflammatory cytokines (TNF-α, IL-1β, IL-6, and MCP-1) in LPS-induced RAW264.7 cells and concurrently mitigated oxidative stress by modulating the levels of malondialdehyde (MDA), catalase (CAT), and glutathione peroxidase (GSH-Px) in a dose-dependent manner. Furthermore, BCP supplementation significantly ameliorated HFD-induced obesity, improved glucose tolerance, and reduced systemic inflammation in HFD-fed rats. Notably, BCP treatment suppressed the mRNA expression of pro-inflammatory cytokines and alleviated intestinal barrier dysfunction by regulating the mRNA and protein expression of key tight junction proteins (ZO-1, occludin, and claudin-1), thereby inhibiting colonic inflammation caused by the TLR4/NF-κB signaling pathway. Additionally, BCP treatment altered the composition and function of the gut microbiota, leading to an increase in the total content of short-chain fatty acids (SCFAs), particularly acetic acid, propionic acid, isobutyric acid, and butyric acid. Collectively, our results highlighted the potential of BCP supplementation as a promising prebiotic strategy for treating obesity-induced colonic inflammation.

Correction for ‘Probiotic and prebiotic supplementation ameliorates chronic restraint stress-induced male reproductive dysfunction’ by Mohd Akram et al., Food Funct., 2023, 14, 8558–8574, https://doi.org/10.1039/D3FO03153E.

Epidemiological and experimental studies suggest that there is a strong correlation between maternal high-fat diet and fetal–placental development. The current study aims to investigate the effects of maternal high-fat diet on fetal growth, placental nutrient transporters and circular RNA expression profiles in a mouse model. Forty C57BL/6 female mice were randomly assigned to two groups, fed either a control (10% fat for energy) diet (CON) or a high-fat (60% fat for energy) diet (HFD) for 4 weeks before mating and throughout pregnancy, and were killed on day 19.5 of pregnancy. The serum glucose, total cholesterol and low-density lipoprotein, the glucolipid metabolism-related hormones, and the insulin resistance index were significantly increased. High-throughput sequencing showed that differentially expressed circRNAs (DE circRNAs) in the placenta can regulate various biological processes, cellular components, and molecular functions through various energy metabolism pathways, and mmu-let-7g-5p was found to target and bind to multiple DE circRNAs. In addition, this study also predicted that various circRNAs with protein coding functions can regulate maternal placental nutrient transport. In general, the ceRNA (circRNAs–miRNAs–mRNAs) regulatory network of maternal placental nutrient transport constructed in this study is of great significance for further understanding the effect of maternal nutrition on fetal growth in the future.

Casein (CN) represents many proline residues that may bind polyphenols. Some evidence exists of CN-polyphenols interaction in model systems. The formation of such interactions upon digestion and the effects on CN digestibility and potential functionality due to the release of bioactive peptides are obscure. This study aimed to explore the interactions of CN with different phenol compounds under digestive conditions and monitor how they affect the bioaccessibility of phenol compounds and bioactive peptides. CN or CN hydrolysate and phenol compounds such as chlorogenic acid, ellagic acid, catechin, green tea extract, and tea extract, singularly or in combination with CN were digested in vitro. Total antioxidant capacity (TAC), degree of hydrolysis, and bioactive peptide formation were assessed in the samples collected through the digestion. The results showed that bioaccessible TAC was 1.17 to 1.93-fold higher in CN co-digested with phenol compounds than initially due to a higher release of antioxidant peptides in the presence of phenolic compounds. However, TAC values in the intestinal insoluble part of CN–phenol digests were higher than the initial, indicating that such interactions may be functional to transport phenols to the colon. Bioactive peptide release was affected by the phenol type (catechins were the most effective) as well as phenol concentration. As an opioid peptide released from β-CN, β-casomorphin formation was significantly influenced by the co-digestion of CN with phenol compounds. This study confirmed the possible CN–phenol interaction during digestion, affecting bioactive peptide release.

We previously found greater reduction of colon cancer (CC) biomarkers for red wheat compared to white wheat regardless of refinement state. In the present study we examined whether the phenolic-rich aleurone and testa layers are drivers of chemoprevention by red wheat and their influence on gut microbiota composition using a 1,2-dimethylhydrazine-induced CC rat model. Rats were fed a low-fat diet (16% of energy as fat), high-fat diet (50% of energy as fat), or high-fat diet containing whole red wheat, refined red wheat, refined white wheat, or aleurone- or testa-enriched fractions for 12 weeks. Morphological markers (aberrant crypt foci, ACF) were assessed after methylene blue staining and biochemical markers (3-nitrotyrosine [3-NT], Dclk1) by immunohistochemical determination of staining positivity within aberrant crypts. Gut microbiota composition was evaluated from 16S rRNA gene sequencing of DNA extracted from cecal contents. Relative to the high-fat diet, the whole and refined red wheat, refined white wheat, and testa-enriched fraction decreased ACF, while only the refined red wheat and aleurone-enriched fraction decreased 3-NT. No significant differences were observed for Dclk1. An increase in microbial diversity was observed for the aleurone-enriched fraction (ACE index) and whole red wheat (Inverse Simpson Index). The diet groups significantly modified overall microbiome composition, including altered abundances of Lactobacillus, Mucispirillum, Phascolarctobacterium, and Blautia coccoides. These results suggest that red wheat may reduce CC risk through modifications to the gut microbiota and nitrosative stress, which may be due, in part, to the influence of dietary fiber and the phenolic-rich aleurone layer.

Vasoactive intrinsic peptide receptor (VIPR2), a circadian gene, is involved in metabolic homeostasis and metabolic syndrome (MetS). Seaweeds contain polysaccharides that regulate metabolic homeostasis, possibly by altering the effects of VIPR2 variants. We examined the relationship between VIPR2 expression and the incidence of MetS based on seaweed consumption. This study included 4979 Koreans aged ≥40 years using data from the Ansan–Ansung cohort of the Korean Genome and Epidemiology Study. The total seaweeds included were laver, kelp, and sea mustard. A multivariable Cox proportional hazards model was used to analyze the interactions between the VIPR2 rs6950857 genotype associated with MetS incidence and seaweed intake after adjusting for covariates such as region. A total of 2134 patients with MetS were followed for an average of 8.9 years. In men with the GG genotype of rs6950857, the highest quintile of seaweed consumption was associated with a decreased incidence of MetS compared with that of the lowest quintile (hazard ratio, 0.78; 95% confidence interval, 0.62–0.98). We identified a unique association between the rs6950857 genotype, seaweed intake, and MetS. These findings highlight the importance of VIPR2 and the regulatory role of seaweed consumption in MetS incidence.

The green tea polyphenol, (−)-epigallocatechin-3-gallate (EGCG), has been studied for its potential positive health effects, but human and animal model studies have reported potential toxicity at high oral bolus doses. This study used liquid chromatography-mass spectrometry-based metabolomics to compare the urinary EGCG metabolite profile after administration of a single non-toxic (100 mg kg⁻¹) or toxic (750 mg kg⁻¹) oral bolus dose to male C57BL6/J mice to better understand how EGCG metabolism varies with dose. EGCG metabolites, including methyl, glucuronide, sulfate, and glucoside conjugates, were tentatively identified based on their mass to charge (m/z) ratio and fragment ion patterns. Partial least squares discriminant analysis (PLS-DA) results showed clear separation of the urine metabolite profiles between treatment groups. The most differentiating metabolites in the negative and positive ion modes were provisionally identified as di-glucuronidated EGCG quinone and di-glucuronidated EGCG, respectively. The presence of EGCG oxidation products at toxic dose is consistent with studies showing that EGCG toxicity is associated with oxidative stress. Relative amounts of methylated metabolites increased with dose to a lesser extent than glucuronide and sulfate metabolites, indicating that methylation is more prominent at low doses, whereas glucuronidation and sulfation may be more important at higher doses. One limitation of the current work is that the lack of commercially-available EGCG metabolite standards prevented absolute metabolite quantification and identification. Despite this limitation, these findings provide a basis for better understanding the dose-dependent changes in EGCG metabolism and advance studies on how these differences may contribute to the toxicity of high doses of EGCG.

Background: Hypertension is closely associated with excessive sodium intake, and low-sodium salt has been shown to lower blood pressure. However, whether low-sodium salt interacts with genetic variation related to salt sensitivity of blood pressure is unclear. Methods: A total of 259 hypertensive patients who completed the previous 3 years of a low-sodium salt vs. normal salt intervention were included in our study. Genetic risk scores (GRSs) of systolic blood pressure (SBP) and diastolic blood pressure (DBP) were respectively built for each participant. A general linear regression model and a generalized mixed model were applied to identify the interaction effects between low-sodium salt intervention and ENaC genetic variation on SBP/DBP changes and trajectories over 3 years. Findings: during the 3-year intervention, both SBP and DBP levels showed a significant decline in the low-sodium salt intervention group than those in the normal salt intervention group over 3 years (P_{salt intervention group} = 0.001 for SBP and P_{salt intervention group} = 0.006 for DBP). Furthermore, a gene–diet interaction was found for the SBP change trajectory over 3 years (P_{SBP-GRS×salt intervention group} = 0.011); specifically, significant SBP reductions were found between salt intervention groups in the high SBP-GRS group (−18.77 vs. −9.58 mmHg, P_{salt intervention group} = 0.001), but not in the low SBP-GRS group (−15.71 vs. −14.62 mmHg, P_{salt intervention group} = 0.791). No interaction effect between low-sodium salt intervention and genetic variation of ENaC was found for changes in DBP. Conclusions: Higher ENaC genetic variation is associated with a greater reduction in SBP in response to a low-sodium salt intervention. Hypertensive patients with higher ENaC genetic variation may experience a greater benefit in SBP reductions by consuming low-sodium salt. (Trial registration: chiCTR-TRC-09000538, https://www.chictr.org.cn).

Diet is an important source of perfluoroalkyl and polyfluoroalkyl substance (PFAS) exposure, and the dietary inflammatory index (DII) is a tool used to assess the inflammatory potential of an individual's diet. However, limited research has explored the association between the DII and PFAS exposure in humans. This study is the first to analyze the association between the five PFASs and DII using the National Health and Nutrition Examination Survey (NHANES) 2007–2018 database. Additionally, we assessed the interaction between the DII and PFASs regarding oxidative stress and inflammatory markers, including alkaline phosphatase, albumin, neutrophil count, lymphocyte count, total bilirubin, and serum iron based on a previous study. A series of covariates were included in the analysis to reduce the confounding bias. The study included 7773 and 5933 participants based on the different models. The DII was significantly associated with serum perfluorooctanoic acid, perfluorononanoic acid, perfluorooctane sulfonic acid, and sum-PFAS. Some of the food parameters used to calculate the DII also showed associations with special PFAS serum concentrations. Specifically, dietary fiber, n-3 polyunsaturated fatty acids, energy intake, and vitamin D were associated with more than three PFASs. Higher DII levels in participants were linked to a more significant association between bilirubin (the interaction P-value is not significant), alkaline phosphatase, serum iron, neutrophil counts, and some PFASs. In conclusion, this study clarified the association between the three PFASs and DII, highlighting the diverse effects of PFASs on oxidative stress and inflammatory markers across different DII levels.