Food & Function最新文献

Inflammatory bowel diseases (IBDs), including Crohn's disease (CD) and ulcerative colitis (UC), are chronic conditions characterized by periods of intestinal inflammation and have become global diseases. Dietary pectins have shown protective effects on IBD models. However, the development of pectin-based diet intervention for IBD individuals requires knowledge of both the bioactive structural patterns and the mechanisms underlying diet–microbiota–host interactions. Here, dextran sulfate sodium (DSS) induced colitis mice were fed with different pectins with various domain compositions, including AG, P37, P55 and P85, in order to understand why different structural patterns function differently on colitis mouse models. The structural diversity of pectin manifests in the different percentages of the homogalacturonan (HG) backbone, Ara sidechains, and Gal sidechains. AG comprises only neutral sugar chains consisting of 14% Ara and 86% Gal, and P85 is a commercial HG pectin mainly composed of 85% HG. P37 and P55 were isolated from raspberry pulps with different domain ratios (P37 = 37% HG + 22% Ara + 32% Gal; P55 = 55% HG + 16% Ara + 18% Gal). Compared to the monotonous structure of AG and P85, the domain-diverse pectins P37 and P55 show superior protective effects against colitis through inhibiting the proliferation of the mucin-consuming bacteria and the pro-inflammatory microorganisms, potentiating the MUC2 expression and the mucus layer and regulating the gut–spleen axis. The HG structure promoted the proliferation of the mucin-degrading microbiota and potentiated mucus erosion. AG enhanced the mucus thickness but increased the growth of the pro-inflammatory microbiota. Our study revealed that the specific domain composition of pectic fibers was a key factor on which the diet-induced alterations in the gut microbiota and the intestinal barrier function highly depended.

Astaxanthin is a xanthophyll carotenoid which has been associated with a number of health-promoting effects, including anti-aging; however, the underlying mechanisms are not fully understood. In the present study, it was found that astaxanthin promoted the longevity of wild-type (N2) Caenorhabditis elegans (C. elegans). The lifespan-extending effect of astaxanthin was associated with a significant decrease of lipofuscin accumulation and the reduction of the age-related decline in spontaneous motility. Meanwhile, astaxanthin enhanced the oxidative stress resistance in C. elegans, preventing the elevation of the reactive oxygen species and alleviating juglone-induced toxicity. Further studies revealed that astaxanthin treatment induced the expression of the skn-1 gene; besides, the lifespan-extending effect of astaxanthin relied on SKN-1. Additionally, the expression of age-1, a PI3K homolog gene, and let-363, a target of the rapamycin (TOR) homolog gene, was decreased, while the expression of PHA-4, a transcription factor negatively regulated by TOR signaling, was increased by astaxanthin treatment. PHA-4 has been demonstrated to regulate the expression of genes playing critical roles in the autophagy-lysosome pathway (ALP). Consistently, several key genes related to ALP, including lgg-1, atg-5, vps-34, ncr-1 and asm-1 were upregulated in C. elegans treated with astaxanthin. Knockdown of pha-4 expression by siRNA prevented the elevation of the above ALP-related genes, while diminishing the lifespan-extension effect of astaxanthin. Overall, these results indicated that astaxanthin prolonged the lifespan of C. elegans via modulating the intracellular redox status and promoting PHA-4-mediated autophagy.

The purpose of this study was to compare the effects of quinoa versus multigrain supplementation on glycemia and lipid metabolism among individuals with impaired glucose tolerance (IGT). In total, 207 participants diagnosed with IGT were randomly assigned to the quinoa group (QG; 100 g day⁻¹, replacing about half of the total daily staple food), multiple whole grain group (WGG; 100 g day⁻¹), or control group (CG) and followed for one year. Biomarkers were measured before and after the intervention. At the efficacy endpoint, the quinoa group (QG) demonstrated significantly longer time in range (TIR) and normal glucose tolerance (NGT) conversion rate, along with lower rates of 2-hour postprandial glucose (2hPG), fasting insulin (FINS), homeostatic model assessment of insulin resistance (HOMA-IR), 14-day mean blood glucose (14dMBG), and diabetes mellitus development compared to those of the multigrain and control groups (P < 0.05). Significant improvements in glycated hemoglobin (HbA1c) were also found in both the quinoa and multigrain groups compared to the control group (P < 0.05). No significant difference in glycemic variability (CV) was observed between the quinoa and control groups, while a significant difference was observed between the quinoa and multigrain groups (P < 0.05). These results suggest that quinoa consumption is significantly more effective than a multiple whole-grain diet in controlling IGT by reducing postprandial glucose and HbA1c levels, improving insulin resistance, and enhancing lipid profiles, making it a superior dietary choice for managing IGT.

Purpose: This study explores the impact of brown rice bran powder (BRBP), known for its beneficial components, such as dietary fiber and γ-oryzanol, on individuals suffering from metabolic syndrome (MetS). Subjects/Methods: In this eight-week open-label controlled trial, fifty participants with MetS were randomly assigned to either a control group, which received a standard diet (SDiet), or an intervention group, which incorporated 15 grams of BRBP daily into their diet. Demographic, anthropometric and clinical data were collected, and blood samples were taken to assess metabolic factors and antioxidant enzyme activities. Additionally, the participants completed the gastrointestinal symptom rating scale questionnaire. Results: Analysis of covariance controlled for the baseline levels and medication consumptions revealed that postthis trial, compared to the controls, patients who received BRBP showed significant reductions in BMI (P-value = 0.001; effect size (ES): −1.13), waist circumference (P-value < 0.001; ES: −1.28), total-cholesterol (P-value = 0.028; ES: −0.74), LDL-cholesterol (P-value = 0.002; ES: −0.86), blood sugar (P-value = 0.013; ES: −0.82), as well as triglyceride glucose (TyG)-BMI index (as a marker of insulin resistance) (P-value < 0.001; ES: −1.35). Further, BRBP resulted in significant improvements in antioxidant enzyme activities, including glutathione peroxidase (P-value = 0.010; ES: 0.86), superoxide dismutase serum activities (P-value = 0.021; ES: 0.78), and constipation rate (P-value = 0.018; ES: −0.85) compared to SDiet alone. However, no significant changes were found regarding levels of triglyceride, HDL-cholesterol, glutathione, catalase and blood pressure after the trial. Conclusion: The findings of this trial support the weight-reducing, hypocholestrolemic, anti-hyperglycemic, and antioxidative effects of adding BRBP to SDiet that is prescribed for MetS patients.

Obesity-related metabolic syndrome is intimately associated with infiltrated adipose tissue macrophages (ATMs), gut microbiota, and metabolic disorders. Pediococcus acidilactici holds the potential to mitigate obesity; however, there exist strain-specific functionalities and diverse mechanisms, which deserve extensive exploration. This study aims to explore the potential of P. acidilactici Y01, isolated from traditional sour whey, in alleviating HFD-induced metabolic syndrome in mice and elucidating its underlying mechanism. The results showed that P. acidilactici Y01 could inhibit the increase of body weight gain, the deposition of fat, lipid disorders and chronic low-grade inflammation, improve glucose tolerance and insulin resistance, and could reduce adipose tissue inflammation by decreasing M1-type ATMs and increasing M2-type ATMs. Meanwhile, P. acidilactici Y01 significantly increased the abundance of potentially beneficial intestinal bacteria, such as Akkermansia, Alistipes, Bifidobacterium, Lachnospiraceae_NK4A136_group, Lactobacillus, norank_f__Muribaculaceae, and Parabacteroides, and partially restored the levels of metabolites, such as phosphatidylcholines, glycerophosphocholines, sphingolipids and unsaturated fatty acids. The fecal microbiota transplantation experiment demonstrated that P. acidilactici Y01 ameliorated obesity-related metabolic syndrome by modulating the polarization of M1/M2 ATMs mediated by gut microbiota. Overall, as a dietary supplement, P. acidilactici Y01 has good potential in the prevention and treatment of obesity.

Whey protein (WP) contains two major allergenic proteins, α-lactalbumin and β-lactoglobulin, which significantly impact its incorporation and application in food products. Current research primarily focuses on the dynamic changes in allergenicity during the processing of individual protein components. To simulate realistic conditions in food processing, this study aims to investigate the effect of polyphenol oxidase cross-linking on the allergenicity of complex protein matrices. Our findings indicate that mice receiving polyphenol oxidase-crosslinked WP (CL-WP) exhibited more severe systemic food allergic reactions, characterized by decreased body temperature and significantly increased serum levels of specific IgE and mMCPT-1 compared to the WP group. Furthermore, mice in the CL-WP group displayed more pronounced intestinal injury. Flow cytometry results showed a significant decrease in CD103⁺MHC-II⁺CD11c⁺ cells and a significant increase in the proportion of Th2 cells in the CL-WP group. Simultaneously, the marked elevation of Th2 cytokine levels in spleen cell supernatants further indicated a significant Th2 bias in these mice. Lastly, miRNA sequencing of CD4⁺ T cells from the spleen revealed that among the differentially expressed miRNAs, miR-532-5p was significantly upregulated in both WP and CL-WP groups compared to controls, while miR-322-3p was downregulated in both groups. miR-27a-5p remained unchanged in the WP group but was significantly downregulated in the CL-WP group, and miR-92a-3p was upregulated in the WP group but unchanged in the CL-WP group. These results suggest that miRNAs may serve as potential biomarkers for the severity of milk allergy.

Systemic lupus erythematosus (SLE) is a chronic autoimmune disease often treated with glucocorticoids, which can lead to complications such as osteoporosis and an increased infection risk. Hence, identifying safe and effective treatment strategies is crucial. Lactobacillus has shown promise in improving immune disorders. We investigated Lactobacillus rhamnosus LC-STH-13 for its probiotic properties. Female MRL/lpr mice, prone to lupus, were used to assess its impact on SLE development. The results showed that the intervention with L. rhamnosus LC-STH-13 significantly reduced the level of circulating anti-autoantibodies (p < 0.05) and rebalanced Th17/Treg cells (p < 0.05). Kidney tissue analysis revealed reduced immune cell infiltration and immune complex deposition in glomeruli. L. rhamnosus LC-STH-13 mitigated kidney inflammation via the TLR9/NF-κB pathway (p < 0.05) and attenuated complement-induced renal damage (p < 0.05). Furthermore, 16S rRNA sequencing data analysis indicated that L. rhamnosus LC-STH-13 can restore intestinal microecological imbalance caused by the development of SLE. These findings suggested that L. rhamnosus LC-STH-13 improves the development of SLE by regulating the TLR9/NF-κB pathway and intestinal microbiota, offering a foundation for exploring safe and effective treatments.

Food allergies are pathological adverse reactions against harmless dietary proteins. While studies have shown the involvement of host metabolic changes (e.g., lipid metabolism and amino acid metabolism) in the development of food allergy (FA), the adaptive changes in glucose metabolism induced by food allergen exposure remain largely unclear. In this study, BALB/c mice were sensitized intraperitoneally with an ovalbumin (OVA)/aluminum adjuvant, followed by oral OVA challenges to induce anaphylaxis. Increased levels of serum OVA-specific IgE and MCPT-1, and Th2 response bias were also presented in FA mice. Subsequently, the intestinal untargeted metabolomic analysis revealed the signature enrichment of glycolysis, manifested by increases in glycolytic metabolites including glucose-6-phosphate, fructose-6-phosphate, 2-phosphoglycerate, and lactate in FA mice. Consistently, the serum lactate level was found to be significantly elevated in allergic mice. Oral administration of OVA also upregulated the expression of critical metabolic enzymes in glycolysis, namely hexokinase 2, phosphoglycerate mutase 1, and lactate dehydrogenase. Moreover, the hypoxia inducible factor-1 (HIF-1) signaling pathway was activated in FA mice, and the expression of HIF-1α, known as the upstream regulator of glycolysis, was increased after oral OVA challenges. In vitro inhibition of HIF-1α was found to impede mast cell inflammatory responses to allergens. In summary, this study demonstrated that OVA-induced FA exhibited a glucose metabolic feature of HIF-1α-mediated glycolysis upregulation, suggesting the potential of HIF-1α/glycolysis targeted strategies in the alleviation of FA.

This study utilized in vitro colonic fermentation to examine the impact of astaxanthin on the microbial catabolism of tryptophan. Astaxanthin significantly altered the gut microbiota and raised the tryptophan catabolism metabolite levels in an in vitro human colonic fermentation system. To eliminate the influence of substrate availability, we conducted in vitro colonic fermentation of the gut microbiota of astaxanthin-domesticated mice. We observed that the capacity of astaxanthin-domesticated gut microbiota to catalyze the conversion of tryptophan to indole and derivatives was considerably augmented. Astaxanthin significantly increased the relative abundance of Akkermansia, Ruminococcus, Bacteroides and Lactobacillus and elevated the levels of indole-3-lactic acid and indole-3-propionic acid. These results demonstrated that astaxanthin regulates tryptophan metabolism by modifying gut microbiota and increasing the levels of indole metabolites, such as indole-3-lactic acid and indole-3-propionic acid. This study provides insights into the physiological activity of astaxanthin and sheds light on the potential for enhancing tryptophan metabolism through dietary manipulation of the gut microbiota.

Objective: The aim of the current study was to study the therapeutic potential of chrysin against repeated intranasal amyloid-beta (Aβ)-induced interleukin-17 (IL-17) signaling in a mouse model of AD. Methods: Male BALB/c mice were daily exposed to intranasal Aβ_1–42 (10 μg/10 μL) for seven consecutive days. Chrysin was orally administered at doses of 25, 50 and 100 mg kg⁻¹ in 0.5% sodium carboxy methyl cellulose suspension from day 5 of Aβ_1–42 administration for seven days. Following the treatment, the memory of the animals was appraised using Morris water maze, novel object recognition and passive avoidance tests. Further, the effects of chrysin on Aβ_1–42-induced IL-17 signaling and redox levels were evaluated in the cortex and hippocampus regions of the mouse brain through western blot and immunohistochemistry. Results: The exposure to Aβ_1–42 through the intranasal route induced a significant decline in the spatial, learning and cognitive memory of the animals, and most interestingly, exposure to Aβ_1–42 triggered IL-17-mediated signaling, which resulted in a significant increase in the expression of IL-17RA, Act1 and TRAF6. Furthermore, Aβ_1–42 impaired the tissue redox level and inflammatory cytokines in the mouse brain. Alternatively, treatment with chrysin at 25, 50 and 100 mg kg⁻¹ oral doses alleviated Aβ_1–42-mediated memory decline, impaired redox levels and inflammation. Specifically, chrysin downregulated the expression of IL-17 and mediated signaling in the brain regions of the mice. Conclusion: Chrysin was evidenced to be a potent antioxidant and anti-inflammatory agent, clearly showing a protective role against Aβ_1–42-induced IL-17-mediated inflammation in the brain of the mice