Food frontiers最新文献

{"title":"Structural Characteristics and Immunoregulatory Effects of Colla Corii Asini Peptides with Iron-Chelating Capacity","authors":"Qing-Tao Zhan,&nbsp;Zi-Wei Zhao,&nbsp;Jian-Hang Cai,&nbsp;Xue-Mei Ge,&nbsp;Shuang-Di Chen,&nbsp;Xue Tang,&nbsp;Xue-Ying Ma,&nbsp;Liu-Ping Fan,&nbsp;Issoufou Amadou,&nbsp;Xiang-Rong Cheng","doi":"10.1002/fft2.70347","DOIUrl":"https://doi.org/10.1002/fft2.70347","url":null,"abstract":"<p>Iron homeostasis is closely related to immune function, yet the structural basis of food-derived peptides that modulate this iron-immune crosstalk remains unclear. This study investigated the structure-function relationship of <i>Colla Corii Asini</i> (Ejiao) peptides fractionated by immobilized metal affinity chromatography (IMAC-Fe²⁺). The strongly iron-chelating fraction (F2) exhibited a capacity of 34.57 ± 0.59 µg Fe²⁺/mg peptide, which was 10.7-fold higher than the weakly chelating fraction (F1). Sequence analysis revealed that F2 was characterized by a high abundance of acidic amino acids (42.87 ± 1.76%) and a recurrent E-Xn-P motif, which may represent an important structural feature associated with Fe²⁺ coordination. In cyclophosphamide-induced immunosuppressed mice, F2 significantly outperformed the weak-chelating fraction (F1) in restoring immune function, including increasing splenic CD3⁺ T cells and mucosal IgA levels. Mechanistically, F2 restored systemic iron homeostasis by normalizing hepatic transferrin and hepcidin levels. These findings characterize F2 as a structurally distinct peptide fraction with potential functional-food relevance for regulating the iron-immune axis.</p>","PeriodicalId":73042,"journal":{"name":"Food frontiers","volume":"7 5","pages":""},"PeriodicalIF":6.3,"publicationDate":"2026-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/fft2.70347","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148753721","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Conjugated Linoleic Acid-Enriched Fermented Dairy Modulates Microbiota and Metabolites to Alleviate MASLD: Insights From Multi-Omics and Causal Mediation Analysis","authors":"Fei Mi,&nbsp;Yanjiao Wang,&nbsp;Jia Xiong,&nbsp;Yiyuan Ma,&nbsp;Hongmei Pan,&nbsp;Jianzhong Yin,&nbsp;Yunmei Chai,&nbsp;Yao Wang,&nbsp;Xin Xu,&nbsp;Ai Zhang,&nbsp;Qingwen Ma,&nbsp;Hui Wang,&nbsp;Dongbai Liu,&nbsp;Shaoxiong Wu","doi":"10.1002/fft2.70349","DOIUrl":"https://doi.org/10.1002/fft2.70349","url":null,"abstract":"<p>Metabolic dysfunction-associated steatotic liver disease (MASLD) is a prevalent metabolic disorder linked to gut–liver axis dysregulation. Dietary interventions targeting gut microbiota and host metabolism are promising, yet the effects of specific bioactive components remain unclear. Conjugated linoleic acid (CLA), a functional fatty acid in dairy, may regulate lipid metabolism and inflammation, but its clinical efficacy and mechanisms in MASLD are not well defined. This study evaluated CLA-enriched fermented dairy using a multi-omics and causal modeling framework. In a 120-day randomized controlled trial, 60 MASLD patients consumed CLA-enriched fermented dairy or standard yogurt. Fecal samples underwent 16S rRNA sequencing, and serum samples were analyzed by untargeted liquid chromatography–mass spectrometry (LC–MS) metabolomics. Liver function and metabolic markers were assessed before and after the intervention. Causal mediation analyses explored mechanistic links among the intervention, microbiota, metabolites, and clinical outcomes. The intervention group showed significant reductions in serum alanine aminotransferase (ALT), total cholesterol (TC), creatinine, and high-sensitivity C-reactive protein (hs-CRP). Gut microbiota shifts included increased <i>Bacteroides</i>, <i>Blautia</i>, and <i>Fusicatenibacter</i> and decreased <i>Enterococcus</i> and <i>Sutterella</i>. Metabolomics revealed upregulated energy pathways and negative associations between liver enzymes, phosphatidylcholines, and acylcarnitines. Causal mediation identified key microbial (e.g., <i>Lachnospiraceae</i> UCG-008) and metabolic (e.g., 5-Benzylacyclouridine and vaccenic acid) mediators linking the intervention to clinical improvements. CLA-enriched fermented dairy beneficially modulates gut microbiota and host metabolism, improving liver and systemic metabolic health in MASLD patients. The study highlights CLA's therapeutic potential and demonstrates the value of multi-omics and causal inference to elucidate diet–host interactions.</p>","PeriodicalId":73042,"journal":{"name":"Food frontiers","volume":"7 5","pages":""},"PeriodicalIF":6.3,"publicationDate":"2026-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/fft2.70349","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148753723","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Structural Characteristics and Immunoregulatory Effects of Colla Corii Asini Peptides with Iron-Chelating Capacity","authors":"Qing-Tao Zhan,&nbsp;Zi-Wei Zhao,&nbsp;Jian-Hang Cai,&nbsp;Xue-Mei Ge,&nbsp;Shuang-Di Chen,&nbsp;Xue Tang,&nbsp;Xue-Ying Ma,&nbsp;Liu-Ping Fan,&nbsp;Issoufou Amadou,&nbsp;Xiang-Rong Cheng","doi":"10.1002/fft2.70347","DOIUrl":"https://doi.org/10.1002/fft2.70347","url":null,"abstract":"<p>Iron homeostasis is closely related to immune function, yet the structural basis of food-derived peptides that modulate this iron-immune crosstalk remains unclear. This study investigated the structure-function relationship of <i>Colla Corii Asini</i> (Ejiao) peptides fractionated by immobilized metal affinity chromatography (IMAC-Fe²⁺). The strongly iron-chelating fraction (F2) exhibited a capacity of 34.57 ± 0.59 µg Fe²⁺/mg peptide, which was 10.7-fold higher than the weakly chelating fraction (F1). Sequence analysis revealed that F2 was characterized by a high abundance of acidic amino acids (42.87 ± 1.76%) and a recurrent E-Xn-P motif, which may represent an important structural feature associated with Fe²⁺ coordination. In cyclophosphamide-induced immunosuppressed mice, F2 significantly outperformed the weak-chelating fraction (F1) in restoring immune function, including increasing splenic CD3⁺ T cells and mucosal IgA levels. Mechanistically, F2 restored systemic iron homeostasis by normalizing hepatic transferrin and hepcidin levels. These findings characterize F2 as a structurally distinct peptide fraction with potential functional-food relevance for regulating the iron-immune axis.</p>","PeriodicalId":73042,"journal":{"name":"Food frontiers","volume":"7 5","pages":""},"PeriodicalIF":6.3,"publicationDate":"2026-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/fft2.70347","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148753461","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Conjugated Linoleic Acid-Enriched Fermented Dairy Modulates Microbiota and Metabolites to Alleviate MASLD: Insights From Multi-Omics and Causal Mediation Analysis","authors":"Fei Mi,&nbsp;Yanjiao Wang,&nbsp;Jia Xiong,&nbsp;Yiyuan Ma,&nbsp;Hongmei Pan,&nbsp;Jianzhong Yin,&nbsp;Yunmei Chai,&nbsp;Yao Wang,&nbsp;Xin Xu,&nbsp;Ai Zhang,&nbsp;Qingwen Ma,&nbsp;Hui Wang,&nbsp;Dongbai Liu,&nbsp;Shaoxiong Wu","doi":"10.1002/fft2.70349","DOIUrl":"https://doi.org/10.1002/fft2.70349","url":null,"abstract":"<p>Metabolic dysfunction-associated steatotic liver disease (MASLD) is a prevalent metabolic disorder linked to gut–liver axis dysregulation. Dietary interventions targeting gut microbiota and host metabolism are promising, yet the effects of specific bioactive components remain unclear. Conjugated linoleic acid (CLA), a functional fatty acid in dairy, may regulate lipid metabolism and inflammation, but its clinical efficacy and mechanisms in MASLD are not well defined. This study evaluated CLA-enriched fermented dairy using a multi-omics and causal modeling framework. In a 120-day randomized controlled trial, 60 MASLD patients consumed CLA-enriched fermented dairy or standard yogurt. Fecal samples underwent 16S rRNA sequencing, and serum samples were analyzed by untargeted liquid chromatography–mass spectrometry (LC–MS) metabolomics. Liver function and metabolic markers were assessed before and after the intervention. Causal mediation analyses explored mechanistic links among the intervention, microbiota, metabolites, and clinical outcomes. The intervention group showed significant reductions in serum alanine aminotransferase (ALT), total cholesterol (TC), creatinine, and high-sensitivity C-reactive protein (hs-CRP). Gut microbiota shifts included increased <i>Bacteroides</i>, <i>Blautia</i>, and <i>Fusicatenibacter</i> and decreased <i>Enterococcus</i> and <i>Sutterella</i>. Metabolomics revealed upregulated energy pathways and negative associations between liver enzymes, phosphatidylcholines, and acylcarnitines. Causal mediation identified key microbial (e.g., <i>Lachnospiraceae</i> UCG-008) and metabolic (e.g., 5-Benzylacyclouridine and vaccenic acid) mediators linking the intervention to clinical improvements. CLA-enriched fermented dairy beneficially modulates gut microbiota and host metabolism, improving liver and systemic metabolic health in MASLD patients. The study highlights CLA's therapeutic potential and demonstrates the value of multi-omics and causal inference to elucidate diet–host interactions.</p>","PeriodicalId":73042,"journal":{"name":"Food frontiers","volume":"7 5","pages":""},"PeriodicalIF":6.3,"publicationDate":"2026-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/fft2.70349","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148753650","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting Microglial HDAC3 Enhances Aβ Clearance and Neuroprotection in APP/PS1 Mice: A Ketogenic Diet-Driven Strategy","authors":"Mingxiao Zheng,&nbsp;Gabriele Loers,&nbsp;Shengnan Lin,&nbsp;Hans-Christian Siebert,&nbsp;Qingpeng Wang,&nbsp;Ruiyan Zhang,&nbsp;Xuexing Zheng,&nbsp;Ning Zhang","doi":"10.1002/fft2.70346","DOIUrl":"https://doi.org/10.1002/fft2.70346","url":null,"abstract":"<p>Growing evidence suggests that impaired phagocytosis/autophagy and histone deacetylase 3 (HDAC3)-mediated microglial activation contribute significantly to Alzheimer's disease (AD) pathogenesis by promoting pathological protein aggregation. The ketogenic diet (KD) has demonstrated neuroprotective effects in AD, potentially through modulation of phagocytosis, autophagy, and inflammation. However, the underlying mechanisms remain unclear. Here, we report that a 12-week KD treatment ameliorated cognitive deficits, reduced amyloid-β (Aβ) deposition and tau hyperphosphorylation, and attenuated neuroinflammation in male APP/PS1 mice. Mechanistic studies revealed that these effects were associated with the modulation of microglial HDAC3. Specifically, KD downregulated microglial HDAC3, thereby enhancing Aβ phagocytosis, activating AMPK–ULK1-dependent autophagy, and restraining NLRP3 inflammasome activation, thereby promoting pathologic protein clearance. Given that β-hydroxybutyrate (BHB) is a major circulating ketone body produced during KD, we tested whether BHB recapitulates these effects in vitro. In Aβ-induced BV2 microglia, BHB mimicked the neuroprotective effects by downregulating HDAC3, which markedly enhanced Aβ clearance and suppressed inflammatory responses; these neuroprotective effects were largely abrogated by HDAC3 overexpression. To further confirm the causal role of microglial HDAC3 in mediating KD effects, we performed microglia-specific HDAC3 knockdown via AAV11-Iba1-shHDAC3. Notably, this manipulation enhanced both Aβ phagocytosis and autophagic degradation while inhibiting NLRP3 activation and contributed to neuroprotection. Overall, our findings suggest a novel mechanism by which KD exerts neuroprotective effects through modulation of the microglial HDAC3–AMPK–ULK1 axis and highlight microglia-specific HDAC3 inhibition as a promising therapeutic strategy for AD that simultaneously enhances Aβ clearance and attenuates neuroinflammation.</p>","PeriodicalId":73042,"journal":{"name":"Food frontiers","volume":"7 5","pages":""},"PeriodicalIF":6.3,"publicationDate":"2026-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/fft2.70346","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148753720","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Kiwifruit Seed Polyphenols Ameliorate High-Fat-Induced Obese Mice via Inhibition of Inflammation and Regulation of Gut Microbiota Balance","authors":"Qingqing Liu,&nbsp;Jianxin Huang,&nbsp;Jinyue Xu,&nbsp;Qi Zhang,&nbsp;Ying Zhang,&nbsp;Haixia Yang,&nbsp;Wei Cao,&nbsp;Jianjun Deng","doi":"10.1002/fft2.70342","DOIUrl":"https://doi.org/10.1002/fft2.70342","url":null,"abstract":"<p>Kiwifruit seeds are a polyphenol‑rich by‑product of kiwifruit processing. This study evaluated the anti‑obesity effects of kiwifruit seed polyphenols (KSP) in C57BL/6 obese mice induced by high-fat diet (HFD). The results demonstrated that KSP attenuated body weight gain and adiposity in mice, improved glucose tolerance and insulin sensitivity, and reduced serum and hepatic triglycerides, total cholesterol, low-density lipoprotein cholesterol (LDL-C), and alanine aminotransferase (ALT)/aspartate aminotransferase (AST). Histology results confirmed KSP alleviated hepatic steatosis and adipocyte hypertrophy. In addition, KSP decreased interleukin-6 (IL-6), interleukin-1β (IL-1β), and tumor necrosis factor-α (TNF-α) in serum, liver, and colon; up-regulated UCP2 and PPAR-γ; and down-regulated SREBP-1c, FAS, and CPT-1a/b. KSP also reshaped gut microbiota by correcting the <i>Firmicutes/Bacteroidetes</i> imbalance, suppressing <i>Proteobacteria</i>, and enriching <i>Bacteroides</i>, <i>Parabacteroides</i>, <i>Alistipes</i>, and <i>Alloprevotella</i>, accompanied by the restoration of short-chain fatty acids, especially propionate. This study provides new evidence supporting KSP as a promising adjunct strategy for mitigating obesity and associated metabolic disorders through the gut-liver axis.</p>","PeriodicalId":73042,"journal":{"name":"Food frontiers","volume":"7 5","pages":""},"PeriodicalIF":6.3,"publicationDate":"2026-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/fft2.70342","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148752878","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Kiwifruit Seed Polyphenols Ameliorate High-Fat-Induced Obese Mice via Inhibition of Inflammation and Regulation of Gut Microbiota Balance","authors":"Qingqing Liu,&nbsp;Jianxin Huang,&nbsp;Jinyue Xu,&nbsp;Qi Zhang,&nbsp;Ying Zhang,&nbsp;Haixia Yang,&nbsp;Wei Cao,&nbsp;Jianjun Deng","doi":"10.1002/fft2.70342","DOIUrl":"https://doi.org/10.1002/fft2.70342","url":null,"abstract":"<p>Kiwifruit seeds are a polyphenol‑rich by‑product of kiwifruit processing. This study evaluated the anti‑obesity effects of kiwifruit seed polyphenols (KSP) in C57BL/6 obese mice induced by high-fat diet (HFD). The results demonstrated that KSP attenuated body weight gain and adiposity in mice, improved glucose tolerance and insulin sensitivity, and reduced serum and hepatic triglycerides, total cholesterol, low-density lipoprotein cholesterol (LDL-C), and alanine aminotransferase (ALT)/aspartate aminotransferase (AST). Histology results confirmed KSP alleviated hepatic steatosis and adipocyte hypertrophy. In addition, KSP decreased interleukin-6 (IL-6), interleukin-1β (IL-1β), and tumor necrosis factor-α (TNF-α) in serum, liver, and colon; up-regulated UCP2 and PPAR-γ; and down-regulated SREBP-1c, FAS, and CPT-1a/b. KSP also reshaped gut microbiota by correcting the <i>Firmicutes/Bacteroidetes</i> imbalance, suppressing <i>Proteobacteria</i>, and enriching <i>Bacteroides</i>, <i>Parabacteroides</i>, <i>Alistipes</i>, and <i>Alloprevotella</i>, accompanied by the restoration of short-chain fatty acids, especially propionate. This study provides new evidence supporting KSP as a promising adjunct strategy for mitigating obesity and associated metabolic disorders through the gut-liver axis.</p>","PeriodicalId":73042,"journal":{"name":"Food frontiers","volume":"7 5","pages":""},"PeriodicalIF":6.3,"publicationDate":"2026-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/fft2.70342","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148752879","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"3D Food Printing for Dysphagia: Navigating Safety, Nutrition, and Technological Challenges","authors":"Deepa Agarwal,&nbsp;Annie-Claude M. Lassemillante,&nbsp;Sahiti Peddisetti,&nbsp;Rebecca Smith,&nbsp;Roman Buckow","doi":"10.1002/fft2.70341","DOIUrl":"https://doi.org/10.1002/fft2.70341","url":null,"abstract":"<p>Dysphagia, or difficulty in swallowing, affects a significant proportion of the aging population and individuals with neurological or physiological impairments, necessitating the development of safe, nutritious, and appealing texture-modified foods. The International Dysphagia Diet Standardisation Initiative (IDDSI) provides a globally recognized framework to ensure consistent food texture and fluid thickness; however, delivering meals that are both compliant and sensory-acceptable remains a challenge. This narrative review explores current research on 3D food printing for dysphagia, encompassing nutrition, food science, engineering, and clinical practice. Particular attention is given to the practicality of printing a complete, safe, and nutritionally adequate meal using 3D printing. Key challenges include formulation variability, printability of IDDSI-compliant foods, equipment limitations, and practical issues in meal preparation and service. This review highlights the technological challenge of 3D food printing in dysphagia care, emphasizing that coordinated, multidisciplinary research is essential to translate this technology into routine clinical use.</p>","PeriodicalId":73042,"journal":{"name":"Food frontiers","volume":"7 5","pages":""},"PeriodicalIF":6.3,"publicationDate":"2026-08-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/fft2.70341","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148662113","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"3D Food Printing for Dysphagia: Navigating Safety, Nutrition, and Technological Challenges","authors":"Deepa Agarwal,&nbsp;Annie-Claude M. Lassemillante,&nbsp;Sahiti Peddisetti,&nbsp;Rebecca Smith,&nbsp;Roman Buckow","doi":"10.1002/fft2.70341","DOIUrl":"https://doi.org/10.1002/fft2.70341","url":null,"abstract":"<p>Dysphagia, or difficulty in swallowing, affects a significant proportion of the aging population and individuals with neurological or physiological impairments, necessitating the development of safe, nutritious, and appealing texture-modified foods. The International Dysphagia Diet Standardisation Initiative (IDDSI) provides a globally recognized framework to ensure consistent food texture and fluid thickness; however, delivering meals that are both compliant and sensory-acceptable remains a challenge. This narrative review explores current research on 3D food printing for dysphagia, encompassing nutrition, food science, engineering, and clinical practice. Particular attention is given to the practicality of printing a complete, safe, and nutritionally adequate meal using 3D printing. Key challenges include formulation variability, printability of IDDSI-compliant foods, equipment limitations, and practical issues in meal preparation and service. This review highlights the technological challenge of 3D food printing in dysphagia care, emphasizing that coordinated, multidisciplinary research is essential to translate this technology into routine clinical use.</p>","PeriodicalId":73042,"journal":{"name":"Food frontiers","volume":"7 5","pages":""},"PeriodicalIF":6.3,"publicationDate":"2026-08-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/fft2.70341","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148662422","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Acrylamide Exposure, Biological Aging Acceleration, With Ankle-Brachial Index and Peripheral Artery Disease: Exploring Association, Interaction, and Underlying Mechanism","authors":"Feifei Wang,&nbsp;Zhiying Huo,&nbsp;Jiahao Song,&nbsp;Shuhui Wan,&nbsp;Yongfang Zhang,&nbsp;Le Hong,&nbsp;Qing Liu,&nbsp;Yani Xiong,&nbsp;Pengfei Chen,&nbsp;Yanjun Guo,&nbsp;Weihong Chen,&nbsp;Bin Wang","doi":"10.1002/fft2.70317","DOIUrl":"https://doi.org/10.1002/fft2.70317","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <p>Health risks from acrylamide (ACR) exposure have attracted global attention. We sought to investigate the relationships of ACR exposure with ankle-brachial index (ABI) and peripheral arterial disease (PAD) and explore the underlying mechanism. We included 890 adults from National Health and Nutrition Examination Survey 2003–2004. Hemoglobin adducts of acrylamide (HbAA) and glycidamide (HbGA) as authentic ACR exposure biomarkers were detected to examine their associations with ABI and prevalent PAD. Role of phenotypic age acceleration (PhenoAgeAccel; biological aging acceleration marker) and underlying mechanism in these associations were explored by mediation analysis and network pharmacology, respectively. Each doubling in the concentration of HbAA, HbGA, or HbAA + HbGA was linearly associated with ABI decrement by 0.022 (95% confidence interval [CI]: −0.035 to −0.009), 0.011 (−0.021 to −0.0005), or 0.020 (−0.034 to −0.006), respectively, and PAD odds increment by 83.6% (odds ratio [OR] = 1.836; 95% CI: 1.206–2.797), 56.7% (1.567; 1.007–2.438), or 82.7% (1.827; 1.173–2.846), respectively. HbAA (<i>β</i> = 0.907; 95% CI: 0.421–1.393), HbGA (0.354; 0.043–0.666), and HbAA + HbGA (0.789; 0.344–1.234) were positively related to PhenoAgeAccel, which was related to decreased ABI (−0.003; −0.006 to −0.0003) and increased PAD odds (1.078; 1.024–1.135). PhenoAgeAccel mediated 7.33%–13.11% of the ACR exposure biomarkers-ABI/-PAD relationships and intensified (<i>P</i>_interaction &lt; 0.05) the relationships of HbAA and HbGA/HbAA with ABI. Lipid and atherosclerosis pathways were enriched in ACR-ABI/-PAD association. Exposure of general adults to ACR was related to ABI decrement and PAD odds increment, which might be partly associated with accelerated biological aging. Lipid and atherosclerosis pathway may be suggestively implicated in the mechanism underlying these associations.</p>\u0000 </section>\u0000 </div>","PeriodicalId":73042,"journal":{"name":"Food frontiers","volume":"7 4","pages":""},"PeriodicalIF":6.3,"publicationDate":"2026-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/fft2.70317","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148466953","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}