Food & Function最新文献

{"title":"Diet, genetic factors, and the risk of gastroesophageal reflux disease, Barrett's esophagus and esophageal adenocarcinoma","authors":"Tongyu Zhang, Meiyou Lu, Zihan Li, Jianan Zheng, Jing Cao, Yichan Zhou, Weibing Wu, Liang Chen, Ting Wang and Jing Xu","doi":"10.1039/D5FO00369E","DOIUrl":"10.1039/D5FO00369E","url":null,"abstract":"<p > <em>Introduction</em>: Diet has been recognized as the most pivotal modifiable lifestyle factor in the development of Gastroesophageal Reflux Disease (GERD), Barrett's Esophagus (BE) and Esophageal Adenocarcinoma (EA). However, the associations between dietary ingredients, patterns, and diet–gene interactions with the risk of GERD, BE and EA remain unclear. <em>Methods</em>: The prospective cohort study included 502 412 participants from the UK Biobank. Dietary ingredients, patterns, and the associations with the incidence of GERD, BE and EA were investigated using Cox proportional hazard models. Additionally, we calculated a healthy dietary score based on eight primary dietary factors. Furthermore, polygenic risk scores were developed to explore potential diet–gene interactions. <em>Results</em>: Over an average follow-up of 12.5 years, we identified 29 564 incident cases of GERD, 4081 cases of BE and 539 cases of EA. Frequent tea intake was consistently associated with an increased risk of GERD (HR = 1.04, CI: 1.03, 1.05), BE (HR = 1.08, CI: 1.06, 1.11) and EA (HR = 1.07, CI: 1.01, 1.14), while higher dietary fiber consumption was inversely associated with the risks (HR = 0.92 for GERD, CI: 0.90, 0.94; HR = 0.78 for BE, CI: 0.73, 0.84; HR = 0.81 for EA, CI: 0.68, 0.97). In the dietary pattern analysis, the prudent pattern was linked to a lower risk of GERD, BE and EA (HR = 0.95 for GERD, CI: 0.91, 0.98; HR = 0.84 for BE, CI: 0.76, 0.92; HR = 0.70 for EA, CI: 0.53, 0.93). Significant additive and multiplicative interactions were observed between diet and genetic risk for BE (RERI = 0.32, CI: 0.11, 0.52; <em>P</em><small>_{multiplicative interaction}</small> = 0.039) and EA (RERI = 0.84, CI: 0.34, 1.33; <em>P</em><small>_{multiplicative interaction}</small> = 0.038). <em>Discussion</em>: Our study highlights the role of dietary exposure in the etiology of GERD, BE and EA. Healthy dietary interventions may be beneficial, especially for populations with high genetic risk.</p>","PeriodicalId":77,"journal":{"name":"Food & Function","volume":" 18","pages":" 7082-7093"},"PeriodicalIF":5.4,"publicationDate":"2025-08-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144936780","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corynebacterium glutamicum alleviated colitis by downregulating the TNF signaling pathway mediated by cIAP1/2 in mice","authors":"Ting Liu, Qiang Meng, Yijun Zhang, Mengxi Yu, Jianming Ye, Wei Song, Yane Luo and Tianli Yue","doi":"10.1039/D5FO01880C","DOIUrl":"10.1039/D5FO01880C","url":null,"abstract":"<p >The gut microbiota and its associated micro-ecosystem are closely related to the onset and development of ulcerative colitis (UC). It is known that <em>Corynebacterium glutamicum</em> (<em>C. glutamicum</em>) helps rebuild gut eubiosis from diabetes dysbiosis; however, its effects on UC remain unknown. This study aims to investigate the therapeutic effects and mechanisms of <em>C. glutamicum</em> on UC. In this study, <em>C. glutamicum</em> was encapsulated with thiolated hyaluronic acid (HA-SH) to form a hydrogel, termed as CG-HA-SH. The adhesion and distribution of CG-HA-SH in the intestine were evaluated, along with its therapeutic effects on UC mice, including its impact on the gut microbiota. Additionally, changes in short-chain fatty acids (SCFAs) in the intestines of UC mice were analyzed, and RNA sequencing (RNA-Seq) was employed to investigate the mechanisms by which <em>C. glutamicum</em> alleviated inflammation. HA-SH enhanced the resistance of <em>C. glutamicum</em> in gastric and intestinal fluids, providing approximately 12 hours of adhesion at colitis inflammation sites. <em>C. glutamicum</em> reduced the levels of pro-inflammatory factors such as IL-1β (by 97.31%) and TNF-α (by 90.10%) while increasing anti-inflammatory IL-10 levels (by 197.59%) in the colon. It also increased the abundance of <em>E. fissicatena</em>, <em>Muribaculum</em>, and butyrate and enhanced intestinal tight junctions (OCC, by 318.93%) and the mucus barrier (MUC2, by 515.93%). The mRNA levels of cIAP1/2 decreased by 4.33-fold, and their protein expression levels were reduced by 36.97% correspondingly. The enrichment of the TNF pathway was the most significant. Therefore, <em>C. glutamicum</em> exhibited remarkable efficacy in alleviating inflammation and reshaping dysbiotic gut microbiota by downregulating the cIAP1/2-mediated TNF signaling pathway and NF-κB signaling pathway. cIAP1 and cIAP2 might serve as effective therapeutic targets.</p>","PeriodicalId":77,"journal":{"name":"Food & Function","volume":" 18","pages":" 7238-7252"},"PeriodicalIF":5.4,"publicationDate":"2025-08-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144936557","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A non-pharmacological intervention for insomnia: tryptophan-fructooligosaccharides combination improves sleep in mice via anti-inflammation and gut microbiota modulation","authors":"Wing-Yan Wong, Brandon Dow Chan, Pak-Ting Cho and William Chi-Shing Tai","doi":"10.1039/D5FO01651G","DOIUrl":"10.1039/D5FO01651G","url":null,"abstract":"<p >Insomnia, a widespread condition affecting approximately 30% of the global population, is characterized by persistent sleep disturbances and leads to significant impairments in physical and psychological health. While current treatments can provide beneficial outcomes, limitations including accessibility, efficacy, side effects, and short-term usage hinder their use. Tryptophan, an essential amino acid, serves as the precursor for serotonin synthesis, a neurotransmitter critical for sleep regulation, and its dietary supplementation has been linked to improved sleep quality. Fructooligosaccharides (FOS) are a prebiotic able to promote the growth of beneficial bacteria such as <em>Lactobacillus</em> and <em>Bifidobacterium</em>, which are involved in serotonin production and anti-inflammatory processes. This study explores the potential of a novel combination of tryptophan and FOS (TF) as a non-pharmacological intervention for insomnia. C57BL/6J mice were treated with TF at low (10 mg kg<small>⁻¹</small> tryptophan, 500 mg kg<small>⁻¹</small> FOS; LD) or high (20 mg kg<small>⁻¹</small> tryptophan, 1000 mg kg<small>⁻¹</small> FOS; HD) doses in caffeine-induced sleep disturbance and <em>p</em>-chlorophenylalanine (PCPA)-induced insomnia mouse models for 14 and 7 days respectively. The efficacy of TF treatment on sleep duration, inflammation, and gut microbiota composition was evaluated. Sleep duration was improved by high dose TF in both caffeine-induced (81.0%, <em>p</em> &lt; 0.001) and PCPA-induced (50.8%, <em>p</em> &lt; 0.01) models. In the PCPA-induced model, TF-HD treatment significantly reduced plasma levels of TNFα in mice by 38% (<em>p</em> &lt; 0.05). Furthermore, TF-LD and -HD-treated mice exhibited a 26% (<em>p</em> &lt; 0.001) and 28% (<em>p</em> &lt; 0.001) respective reduction in plasma IL-6 levels. In PCPA-induced mice, TF-LD and -HD treatments increased the abundance of <em>Lactobacillus</em> by 5.04 (<em>p</em> &lt; 0.05) and 9.75 (<em>p</em> &lt; 0.05) -fold respectively and <em>Bifidobacterium</em> by 610-fold (<em>p</em> &lt; 0.05) and 979-fold (<em>p</em> &lt; 0.05) respectively. Our findings suggest that the sleep-promoting effects of TF are mediated through anti-inflammatory mechanisms and gut microbiota modulation. This study highlights the potential of TF as an effective non-pharmacological intervention for insomnia.</p>","PeriodicalId":77,"journal":{"name":"Food & Function","volume":" 17","pages":" 6848-6860"},"PeriodicalIF":5.4,"publicationDate":"2025-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144792989","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genetic influence of coffee intake on bladder cancer risk: a two-sample Mendelian randomization analysis","authors":"Qi Zeng, Yu Cheng, Chenlong Wang, Haichao Chao, Chen Tao and Guanghao Zheng","doi":"10.1039/D4FO05538A","DOIUrl":"10.1039/D4FO05538A","url":null,"abstract":"<p > <em>Background</em>. Bladder cancer (BLCA) is one of the most common malignancies of the urinary system, presenting significant public health challenges due to its rising incidence and associated healthcare costs. Despite known risk factors such as genetic predisposition and environmental exposures, the relationship between coffee consumption and the risk of BLCA remains contentious and inadequately understood. <em>Method</em>. This study employed univariable Mendelian randomization (UVMR) to assess the causal relationship between genetically predicted coffee intake and BLCA risk. Genetic variants associated with coffee intake were used as instrumental variables to estimate this potential causal relationship. We also used multivariable Mendelian Randomization (MVMR) to adjust for smoking status to determine the independent impact of coffee on BLCA. Potential mechanisms were explored through two-step MR and bioinformatics analyses. <em>Result</em>. UVMR revealed a significant positive association between genetically driven coffee intake and BLCA risk (OR = 2.074, 95% CI 1.014–4.244, <em>P</em> = 0.046). MVMR showed that there was a significant positive correlation between coffee intake and BLCA (OR = 2.019, 95% CI 1.043–3.910, <em>P</em> = 0.037) after adjustment for smoking. These findings indicate that coffee intake may be an independent risk factor for BLCA. <em>Conclusion</em>. Our study provides genetic evidence supporting a potential association between coffee intake and BLCA risk. While these findings suggest a possible link, moderation in coffee intake may be advisable. Additionally, the study highlights potential mechanisms that warrant further exploration in future research.</p>","PeriodicalId":77,"journal":{"name":"Food & Function","volume":" 17","pages":" 6861-6869"},"PeriodicalIF":5.4,"publicationDate":"2025-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144792990","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"In vitro colon fermentation of a traditional fermented food using stool from consumers and non-consumers","authors":"Murambiwa Nyati, Oscar van Mastrigt, Sibbe Bakker, John Shindano, Elise F. Talsma, Bas J. Zwaan and Sijmen E. Schoustra","doi":"10.1039/D5FO01627D","DOIUrl":"10.1039/D5FO01627D","url":null,"abstract":"<p >Traditional fermented foods (TFFs) spark debates about their potential health benefits as much is still unclear. Mostly conjectured as functional or living foods, TFFs are produced by live organisms through spontaneous or controlled fermentation processes. Here, we assessed the effect of exposure to Mabisi, a traditional Zambian fermented dairy food product, on the gut microbiota and production of short-chain fatty acids (SCFAs) in stool samples of consumers and non-consumers of Mabisi. We hypothesize that non-consumers of Mabisi will exhibit greater shifts in the gut microbiota composition and a more pronounced increase in SCFA production compared to Mabisi consumers. Stool samples of consumers and non-consumers of Mabisi were exposed to three treatments: (1) Mabisi, (2) fructooligosaccharides (FOSs) as a positive control, and (3) sterile water as a negative control. Treatments were digested using the <em>in vitro</em> INFOGEST static digestion model protocol 2.0 before anaerobic incubation for 24 h with the stool of consumers and non-consumers of Mabisi. We sequenced the hypervariable region (V3–V4) of the 16S rRNA gene to determine the microbial communities. We measured SCFA production as a proxy for gut microbiota functionality. Mabisi supplementation increased <em>Pediococcus</em> in both consumers and non-consumers of Mabisi compared to sterile water. After treatment with Mabisi, the gut microbiota of consumers showed greater resilience, with limited changes in community composition compared to non-consumers, as indicated by beta diversity (Mabisi consumers: <em>R</em><small>²</small> = 0.07, <em>p</em>-adjusted = 0.375; Mabisi non-consumers: <em>R</em><small>²</small> = 0.08, <em>p</em>-adjusted = 0.05) relative to their respective negative controls. Non-consumers were associated with higher production of SCFAs, including acetate, butyrate, formate and succinate, compared to Mabisi consumers. In conclusion, Mabisi has the potential to modulate <em>in vitro</em> gut microbiota by increasing beneficial bacteria and the production of SCFAs, with a particularly strong effect in non-consumers.</p>","PeriodicalId":77,"journal":{"name":"Food & Function","volume":" 18","pages":" 7422-7433"},"PeriodicalIF":5.4,"publicationDate":"2025-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://pubs.rsc.org/en/content/articlepdf/2025/fo/d5fo01627d?page=search","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144936531","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Curcumin and its novel formulations for diabetes mellitus and its complications: a review","authors":"Xiaoqin Liu, Qingzhi Liang, Wei Jiang, Jianlong Zhou, Chun Liu, Ling Deng, Haoyue Feng and Rensong Yue","doi":"10.1039/D5FO00988J","DOIUrl":"10.1039/D5FO00988J","url":null,"abstract":"<p >Diabetes mellitus (DM), a growing global health crisis, drives demand for safe, effective therapies. Curcumin (CUR), a turmeric-derived polyphenol, shows promise in combating DM and its complications (such as diabetic wound healing (DWH), diabetic atherosclerosis (DA), and diabetic encephalopathy (DE)) <em>via</em> multi-target mechanisms. Despite its efficacy and low toxicity, CUR's clinical application is hindered by poor solubility and bioavailability. Recent advances in novel formulations (such as nanoparticles and liposomes) aim to overcome these limitations. This review summarizes CUR's therapeutic mechanisms, highlights cutting-edge delivery systems developed over 20 years, and identifies key challenges in translation. By bridging preclinical insights with formulation innovations, we provide a roadmap for optimizing CUR-based therapies, accelerating their clinical adoption for DM management.</p>","PeriodicalId":77,"journal":{"name":"Food & Function","volume":" 18","pages":" 6965-6999"},"PeriodicalIF":5.4,"publicationDate":"2025-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144936735","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integrating population-based metabolomics with computational microbiome modelling identifies methanol as a urinary biomarker for protective diet–microbiome–host interactions","authors":"Kristin Klier, Ameneh Mehrjerd, Daniel Fässler, Maximilien Franck, Antoine Weihs, Kathrin Budde, Martin Bahls, Fabian Frost, Ann-Kristin Henning, Almut Heinken, Henry Völzke, Marcus Dörr, Matthias Nauck, Hans Jörgen Grabe, Nele Friedrich and Johannes Hertel","doi":"10.1039/D5FO00761E","DOIUrl":"10.1039/D5FO00761E","url":null,"abstract":"<p > <em>Background</em>: Diet–microbiome interactions are core to human health, in particular through bacterial fibre degradation pathways. However, biomarkers reflective of these interactions are not well described. <em>Methods</em>: Using the population-based SHIP-START-0 cohort (<em>n</em> = 4017), we combined metabolome-wide screenings with elastic net machine learning models on 33 food items captured using a food frequency questionnaire (FFQ) and 43 targeted urine nuclear magnetic resonance (NMR) metabolites, identifying methanol as a marker of plant-derived food items. We utilised the independent SHIP-START-0 cohort for the replication of food–metabolite associations. Moreover, constraint-based microbiome community modelling using the Human Microbiome data (<em>n</em> = 149) was performed to predict and analyse the contribution of the microbiome to the human methanol pools through bacterial fibre degradation. Finally, we employed prospective survival analysis in the SHIP-START-0 cohort, testing urinary methanol on its predictive value for mortality. <em>Results</em>: Among 21 metabolites associated with 17 dietary FFQ variables after correction for multiple testing, urinary methanol emerged as the top hit for a range of plant-derived food items. In line with this, constraint-based community modelling demonstrated that gut microbiomes can produce methanol <em>via</em> pectin degradation with the genera <em>Bacteroides</em> (68.9%) and <em>Faecalibacterium</em> (20.6%) being primarily responsible. Moreover, microbial methanol production capacity was a marker of high microbiome diversity. Finally, prospective survival analysis in SHIP-START-0 revealed that higher urinary methanol is associated with lower all-cause mortality in fully adjusted Cox regressions. <em>Conclusion</em>: Integrating population-based metabolomics and computational microbiome modelling identified urinary methanol as a promising biomarker for protective diet–microbiome interactions linked to microbial pectin degradation.</p>","PeriodicalId":77,"journal":{"name":"Food & Function","volume":" 18","pages":" 7067-7081"},"PeriodicalIF":5.4,"publicationDate":"2025-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://pubs.rsc.org/en/content/articlepdf/2025/fo/d5fo00761e?page=search","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144936195","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Urate-lowering and renal-protective effects of sugarcane polyphenols in hyperuricemia: mechanisms and key components","authors":"Kexin Li, Yu Han, Yumei Wang, Chengfeng Zhang, Wanlu Liu, Yu Xi, Yanv Zhou, Lu Li and He Li","doi":"10.1039/D5FO00508F","DOIUrl":"10.1039/D5FO00508F","url":null,"abstract":"<p >Hyperuricemia (HUA) is a metabolic disorder characterized by abnormally elevated levels of uric acid (UA) in the blood, often accompanied by renal damage. The continuous rise in HUA incidence necessitates the development of safe, efficient natural urate-lowering pathways. This study combined network pharmacology prediction with rat model experiments to systematically evaluate the urate-lowering potential of sugarcane polyphenols (SP), a byproduct of the sugarcane sugar industry. The results showed that the intake of low, medium, and high doses of SP significantly reduced the serum UA levels in HUA rats to 19.77%, 27.42%, and 45.54%, respectively. Moreover, SP significantly improved liver and kidney function damage, as evidenced by reduced levels of blood urea nitrogen (BUN), creatinine (CRE), alanine aminotransferase (ALT), and aspartate aminotransferase (AST). Mechanistic studies revealed that SP regulates UA metabolism through two distinct mechanisms: reducing production and promoting excretion. Specifically, SP inhibited hepatic xanthine oxidase (XOR) activity, thereby reducing UA synthesis. Concurrently, SP enhanced UA excretion by upregulating the expression of ATP-binding cassette subfamily G member 2(ABCG2) and downregulating the expression of urate transporter 1(URAT1) and glucose transporter 9(GLUT9). When the total phenolic content was equivalent to SP, the chlorogenic acid (CGA) group showed urate-lowering activity similar to that of SP. This suggests that CGA may play an essential role in the ability of SP to reduce UA. Additionally, SP inhibited inflammation-related molecule expression and improved histopathological changes in the kidneys of HUA rats by affecting the PI3K/AKT/NF-κB signaling pathway, further substantiating the renal protective effects of SP in HUA conditions. The results of this study provide a theoretical basis for the <em>in vivo</em> urate-lowering activity of SP rich in CGA and its alleviation of renal damage. This may offer theoretical references for the comprehensive utilization of SP, a byproduct of the sugarcane sugar industry, laying the foundation for the high-value utilization of sugarcane byproducts and the development of polyphenol functional activity products.</p>","PeriodicalId":77,"journal":{"name":"Food & Function","volume":" 17","pages":" 6760-6772"},"PeriodicalIF":5.4,"publicationDate":"2025-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144783060","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Adherence to the EAT-Lancet reference diet and risk of type 2 diabetes, metabolic dysfunction-associated steatotic liver disease, and their co-occurrence","authors":"Shunming Zhang, Xu-Fen Zeng, Yan Borné, Zhenyu Huo, Yan Yan, Yeqing Gu, Hongmei Wu, Xiaoqin Luo, Rui Zhang, Anna Stubbendorff, Emily Sonestedt, Lu Qi, Tao Huang, Ming-Hua Zheng, Kaijun Niu and Le Ma","doi":"10.1039/D4FO05852F","DOIUrl":"10.1039/D4FO05852F","url":null,"abstract":"<p > <em>Background and aims</em>: The EAT-Lancet Commission proposed a healthy dietary pattern to prevent diet-related diseases while promoting planetary sustainability, but little is known regarding its associations with type 2 diabetes (T2D) and metabolic dysfunction-associated steatotic liver disease (MASLD), both of which are highly prevalent and frequently co-exist. We aimed to assess association of this diet with risk of T2D, MASLD, and their co-occurrence. <em>Methods</em>: This study included 170 811 UK Biobank participants (prospective design) and 212 Chinese biopsy-proven MASLD patients (cross-sectional design). Adherence to the EAT-Lancet reference diet was quantified using three different diet indices. Cox and logistic models were applied to estimate the corresponding effect size. <em>Results</em>: During follow-up in the UK Biobank, we identified 4240 T2D cases, 1164 MASLD cases, and 215 co-incidents of the two diseases. The multivariable hazard ratios (95% confidence intervals) per standard deviation (SD) increase in the Planetary Health Diet Index were 0.85 (0.82, 0.87) for T2D, 0.80 (0.75, 0.85) for MASLD, and 0.84 (0.74, 0.97) for the co-occurrence of the two conditions. The associations were attenuated after additional adjustment for body mass index. In addition, 96 (45.3%) patients with biopsy-proven MASLD had prevalent T2D; adjusted odds ratios (95% confidence intervals) per SD of T2D were 0.72 (0.51, 1.00) for the Planetary Health Diet Index. Similar association patterns were observed in the other two indices. <em>Conclusions</em>: Greater adherence to the EAT-Lancet reference diet was not only associated with lower risks of incident T2D, MASLD, and the co-occurrence of the two conditions in the general adult population but was also associated with lower prevalence of T2D among biopsy-proven MASLD patients.</p>","PeriodicalId":77,"journal":{"name":"Food & Function","volume":" 17","pages":" 6773-6785"},"PeriodicalIF":5.4,"publicationDate":"2025-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144820102","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dietary hispidulin ameliorated chemically-induced colitis by inhibiting epithelial cell ferroptosis via the ACAT2-GPX4 axis and remodeling the gut microbiota","authors":"Dapeng Chen, Jiayi Li, Xinyu Li, Kexin Zhang, Shujie Zeng, Shenjun Zhang, Longyun Li and Yongjian Xiong","doi":"10.1039/D5FO02648B","DOIUrl":"10.1039/D5FO02648B","url":null,"abstract":"<p >Hispidulin, a dietary flavonoid occurring naturally in brown algae, has attracted considerable interest owing to its functions in modulating inflammatory responses and neutralizing reactive oxygen species. This study examined the consequences of hispidulin in a chemically induced acute colitis model. RNA sequencing (RNA_seq), 16s rRNA_seq, and non-targeted metabolomics were conducted to determine the mechanisms underlying hispidulin-induced effects on colitis. The findings revealed that hispidulin exhibited significant therapeutic benefits against colitis. In addition, treatment with hispidulin led to a decrease in pro-inflammatory cytokine levels as well as serum FITC-dextran concentrations. RNA_seq analysis demonstrated a notable increase in colonic ACAT2 expression in mice with colitis following hispidulin treatment. Furthermore, hispidulin administration resulted in the upregulation of GPX4, a reduction in ROS levels, and inhibition of epithelial ferroptosis in mice with colitis. Both genetic inhibition of ACAT2 <em>in vitro</em> and AAV-mediated knockdown of ACAT2 <em>in vivo</em> substantially negated the effects of hispidulin on GPX4/GSH levels, ROS levels, and lipid hydroperoxide accumulation in both NCM460 cells and epithelial cells derived from DSS exposed murine models. 16s rRNA_seq results showed that hispidulin increased the abundance of <em>Lactobacillus</em>, <em>NK4A136_group</em>, <em>Oscillibacter</em>, <em>Peptococcus</em>, and <em>Adlercreutzia</em> and decreased the abundance of <em>Turicimonas</em> in colitic mice. Non-targeted metabolomics results showed that hispidulin facilitated the metabolism of galactose and promoted unsaturated fatty acid biosynthesis in colitic mice. In summary, hispidulin reduced the advancement of acute colitis in mice by reducing ACAT2-mediated ferroptosis in epithelial cells, as well as altering the composition of the gut microbiota.</p>","PeriodicalId":77,"journal":{"name":"Food & Function","volume":" 18","pages":" 7036-7052"},"PeriodicalIF":5.4,"publicationDate":"2025-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144936706","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}