The aldehyde acrolein has been associated with diabetes, cardiovascular, respiratory, and neurodegenerative diseases, and gut microbiota possesses the potential for acrolein release via the key enzyme glycerol/diol dehydratase (PduCDE). This study aimed at estimating the contribution of gut microbiota to endogenous acrolein production. To minimize confounding sources, we investigated the intestinal acrolein-producing potential of 20 volunteers housed under defined conditions. Glycerol was present in every meal and was detected in feces, suggesting availability to intestinal microbiota. Based on fecal metagenomics and pduC analysis, all volunteers showed potential for intestinal glycerol transformation to acrolein; the genus Anaerobutyricum was the major contributor across donors and time. Levels of urine biomarkers N-acetyl-S-(3-hydroxypropyl)-L-cysteine (3-HPMA) and N-acetyl-S-(carboxyethyl)-L-cysteine (CEMA) were higher after the consumption of meals with high glycerol levels, suggesting immediate microbial transformation to acrolein. Only a small proportion of acrolein metabolites was recovered in urine, possibly due to high compound reactivity. Donors could be separated into 3-HPMA or CEMA phenotypes based on the predominance of urine biomarkers, and phenotypes related to overall fecal microbiota and fermentation metabolite profiles. Our data show that oral fat/glycerol intake together with intestinal microbiota activity might temporarily increase endogenous acrolein formation and that urinary biomarkers link to the intestinal microbiome.
醛丙烯醛与糖尿病、心血管、呼吸和神经退行性疾病有关,肠道微生物群具有通过关键酶甘油/二醇脱水酶(PduCDE)释放丙烯醛的潜力。本研究旨在估计肠道菌群对内源性丙烯醛生产的贡献。为了尽量减少混杂源,我们调查了20名志愿者在规定条件下的肠道丙烯醛生成潜力。每顿饭中都有甘油,粪便中也检测到甘油,表明肠道微生物群可获得甘油。基于粪便宏基因组学和pduC分析,所有志愿者都显示出肠道甘油转化为丙烯醛的潜力;厌氧丁酸菌属是供体和时间上的主要供体。食用甘油含量高的食物后,尿液生物标志物n -乙酰基- s -(3-羟丙基)- l-半胱氨酸(3-HPMA)和n -乙酰基- s -(羧乙基)- l-半胱氨酸(CEMA)水平更高,表明微生物立即转化为丙烯醛。只有一小部分丙烯醛代谢物在尿液中被回收,可能是由于高的化合物反应性。根据尿液生物标志物的优势,供体可以分为3-HPMA或CEMA表型,以及与总体粪便微生物群和发酵代谢物谱相关的表型。我们的数据表明,口服脂肪/甘油摄入量与肠道微生物群活性可能会暂时增加内源性丙烯醛的形成,并且尿液生物标志物与肠道微生物群有关。
{"title":"Microbial Transformation of Dietary Glycerol Contributes to Intestinal Acrolein Formation and Urinary Excretion.","authors":"Clarissa Schwab,Hanna Lang,Simone Stegmüller,Jiri Hosek,Angeliki Marietou,Lucia Huertas-Díaz,Qing Li,Asta Petrine Smedgaard Krings,Andrea Zander,Ulrik Kræmer Sundekilde,Elke Richling","doi":"10.1002/mnfr.70289","DOIUrl":"https://doi.org/10.1002/mnfr.70289","url":null,"abstract":"The aldehyde acrolein has been associated with diabetes, cardiovascular, respiratory, and neurodegenerative diseases, and gut microbiota possesses the potential for acrolein release via the key enzyme glycerol/diol dehydratase (PduCDE). This study aimed at estimating the contribution of gut microbiota to endogenous acrolein production. To minimize confounding sources, we investigated the intestinal acrolein-producing potential of 20 volunteers housed under defined conditions. Glycerol was present in every meal and was detected in feces, suggesting availability to intestinal microbiota. Based on fecal metagenomics and pduC analysis, all volunteers showed potential for intestinal glycerol transformation to acrolein; the genus Anaerobutyricum was the major contributor across donors and time. Levels of urine biomarkers N-acetyl-S-(3-hydroxypropyl)-L-cysteine (3-HPMA) and N-acetyl-S-(carboxyethyl)-L-cysteine (CEMA) were higher after the consumption of meals with high glycerol levels, suggesting immediate microbial transformation to acrolein. Only a small proportion of acrolein metabolites was recovered in urine, possibly due to high compound reactivity. Donors could be separated into 3-HPMA or CEMA phenotypes based on the predominance of urine biomarkers, and phenotypes related to overall fecal microbiota and fermentation metabolite profiles. Our data show that oral fat/glycerol intake together with intestinal microbiota activity might temporarily increase endogenous acrolein formation and that urinary biomarkers link to the intestinal microbiome.","PeriodicalId":212,"journal":{"name":"Molecular Nutrition & Food Research","volume":"39 1","pages":"e70289"},"PeriodicalIF":5.2,"publicationDate":"2025-10-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145381054","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Felipe Miceli de Farias,David Hourigan,Paula M O'Connor,Colin Hill,Reynolds Paul Ross
Members of the genus Streptococcus are gram-positive bacteria, commonly found in humans and animals. This group of microorganisms has been associated with severe infections and the development of resistance to antibiotics and production of bacteriocins. Many class I bacteriocins, especially lanthipeptides, have been described for streptococci; however, only one circular bacteriocin has been described for the group (uberolysin). The objective of this study was to characterize streptocyclin BTW, a 64 amino acid circular bacteriocin produced by Streptococcus devriesei DSM 19639, as well as to assess the diversity of circular bacteriocins within the genus. Streptocyclin BTW displayed a broad inhibitory spectrum with pronounced activity against strains of streptococci. A colony mass spectrum of the strain revealed a 6118.75 Da mass, which matches the predicted mass from sequencing. The gene cluster is composed of five genes: a core peptide (stpA), a membrane protein (stpB), a DUF95 family protein (stpC), an ATP-binding protein (stpD), and a putative immunity protein (stpE). Sequence Similarity Network (SSN) analysis revealed that streptocyclin BTW-like circular bacteriocins were found in Streptococcus orisasini, Streptococcus equi, Streptococcus pneumoniae, Streptococcus pseudopneumoniae, Streptococcus mitis, and Streptococcus bouchesdurhonensis species. This is the first report of a bacteriocin produced by S. devriesei.
{"title":"Streptocyclin BTW is a novel member of a diverse family of circular bacteriocins in the genus Streptococcus.","authors":"Felipe Miceli de Farias,David Hourigan,Paula M O'Connor,Colin Hill,Reynolds Paul Ross","doi":"10.1002/mnfr.70290","DOIUrl":"https://doi.org/10.1002/mnfr.70290","url":null,"abstract":"Members of the genus Streptococcus are gram-positive bacteria, commonly found in humans and animals. This group of microorganisms has been associated with severe infections and the development of resistance to antibiotics and production of bacteriocins. Many class I bacteriocins, especially lanthipeptides, have been described for streptococci; however, only one circular bacteriocin has been described for the group (uberolysin). The objective of this study was to characterize streptocyclin BTW, a 64 amino acid circular bacteriocin produced by Streptococcus devriesei DSM 19639, as well as to assess the diversity of circular bacteriocins within the genus. Streptocyclin BTW displayed a broad inhibitory spectrum with pronounced activity against strains of streptococci. A colony mass spectrum of the strain revealed a 6118.75 Da mass, which matches the predicted mass from sequencing. The gene cluster is composed of five genes: a core peptide (stpA), a membrane protein (stpB), a DUF95 family protein (stpC), an ATP-binding protein (stpD), and a putative immunity protein (stpE). Sequence Similarity Network (SSN) analysis revealed that streptocyclin BTW-like circular bacteriocins were found in Streptococcus orisasini, Streptococcus equi, Streptococcus pneumoniae, Streptococcus pseudopneumoniae, Streptococcus mitis, and Streptococcus bouchesdurhonensis species. This is the first report of a bacteriocin produced by S. devriesei.","PeriodicalId":212,"journal":{"name":"Molecular Nutrition & Food Research","volume":"150 1","pages":"e70290"},"PeriodicalIF":5.2,"publicationDate":"2025-10-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145381005","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Diego Aguirre-Ramírez,María Garrido,Lourdes Sánchez,Laura Grasa
Acute pancreatitis (AP) severely disrupts gut microbiota, leading to dysbiosis. This study investigated whether kefir derived from pasteurized whole milk (PMK) or whey (WK) could mitigate AP-induced gut microbiota alterations and promote gut health in a murine model. Male BALB/cJRj mice were assigned to CONTROL, AP-induced (PAN), PMK, WK, PMKPAN, or WKPAN groups. Fecal bacterial DNA was analyzed via 16S rRNA sequencing. AP induction caused characteristic dysbiosis, increasing Marinifilaceae, Tannerellaceae, Odoribacter, and Parabacteroides. In AP mice, PMK treatment significantly reduced Tannerellaceae and Parabacteroides, while increasing potentially anti-inflammatory Marinifilaceae and butyrate-producing Odoribacter. In healthy mice, PMK reduced pro inflammatory Desulfovibrionaceae and Bilophila, enriching short-chain fatty acid (SCFA) producers like Acetatifactor and Roseburia, with pathway analysis showing increased acetate kinase activity. WK treatment in healthy animals also promoted SCFA-producers (Acetatifactor, Odoribacter) and Muribaculaceae. In the AP model, WK upregulated bacteria involved in fatty acid biosynthesis pathways. Dairy-based kefir, particularly PMK, demonstrates a significant capacity to counteract AP-induced gut microbiota imbalances. These findings highlight kefir's nutritional relevance as a functional food with potential preventive and therapeutic applications for supporting gut health in the context of AP.
{"title":"Modulation of Intestinal Microbiota Through Kefir-Based Beverages in a Murine Model of Acute Pancreatitis.","authors":"Diego Aguirre-Ramírez,María Garrido,Lourdes Sánchez,Laura Grasa","doi":"10.1002/mnfr.70304","DOIUrl":"https://doi.org/10.1002/mnfr.70304","url":null,"abstract":"Acute pancreatitis (AP) severely disrupts gut microbiota, leading to dysbiosis. This study investigated whether kefir derived from pasteurized whole milk (PMK) or whey (WK) could mitigate AP-induced gut microbiota alterations and promote gut health in a murine model. Male BALB/cJRj mice were assigned to CONTROL, AP-induced (PAN), PMK, WK, PMKPAN, or WKPAN groups. Fecal bacterial DNA was analyzed via 16S rRNA sequencing. AP induction caused characteristic dysbiosis, increasing Marinifilaceae, Tannerellaceae, Odoribacter, and Parabacteroides. In AP mice, PMK treatment significantly reduced Tannerellaceae and Parabacteroides, while increasing potentially anti-inflammatory Marinifilaceae and butyrate-producing Odoribacter. In healthy mice, PMK reduced pro inflammatory Desulfovibrionaceae and Bilophila, enriching short-chain fatty acid (SCFA) producers like Acetatifactor and Roseburia, with pathway analysis showing increased acetate kinase activity. WK treatment in healthy animals also promoted SCFA-producers (Acetatifactor, Odoribacter) and Muribaculaceae. In the AP model, WK upregulated bacteria involved in fatty acid biosynthesis pathways. Dairy-based kefir, particularly PMK, demonstrates a significant capacity to counteract AP-induced gut microbiota imbalances. These findings highlight kefir's nutritional relevance as a functional food with potential preventive and therapeutic applications for supporting gut health in the context of AP.","PeriodicalId":212,"journal":{"name":"Molecular Nutrition & Food Research","volume":"43 1","pages":"e70304"},"PeriodicalIF":5.2,"publicationDate":"2025-10-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145381043","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Platelets play a central role in hemostasis and thrombosis, but their hyperactivity is closely associated with an increased risk of cardiovascular diseases (CVDs). Appearing evidence emphasizes the importance of plant-based diets, especially those rich in nuts and legumes, which are associated with modulating platelet function and reducing CVD risks. Nuts and legumes are abundant sources of nutrients, including mono/polyunsaturated fatty acids, fiber, vitamins, minerals, and bioactive compounds, such as polyphenols, flavonoids, and phenolic acids. These components, both nutrients and bioactive compounds, were reported to have antiplatelet aggregation properties. Furthermore, epigenetic mechanisms, particularly DNA methylation, regulate gene expression, including genes involved in platelet activation pathways, such as platelet endothelial aggregation receptor 1 (PEAR1), which are related to nutrients such as folate and methionine, contribute to one-carbon metabolism, and bioactive compounds promote methylation patterns related to DNA methylation enzymes and reduced platelet hyperactivity. So, this review summarizes current findings and explores the potential association between nuts and legumes consumption and platelet aggregation (PA) through DNA methylation, emphasizing their role in cardiovascular health and the potential for targeted dietary interventions.
{"title":"Benefits of Nutrients and Phytonutrients in Nuts and Legumes on Platelet Aggregation Through DNA Methylation.","authors":"Siwaphorn Chaimati,Jintana Sirivarasai,Nareerat Sutjarit","doi":"10.1002/mnfr.70297","DOIUrl":"https://doi.org/10.1002/mnfr.70297","url":null,"abstract":"Platelets play a central role in hemostasis and thrombosis, but their hyperactivity is closely associated with an increased risk of cardiovascular diseases (CVDs). Appearing evidence emphasizes the importance of plant-based diets, especially those rich in nuts and legumes, which are associated with modulating platelet function and reducing CVD risks. Nuts and legumes are abundant sources of nutrients, including mono/polyunsaturated fatty acids, fiber, vitamins, minerals, and bioactive compounds, such as polyphenols, flavonoids, and phenolic acids. These components, both nutrients and bioactive compounds, were reported to have antiplatelet aggregation properties. Furthermore, epigenetic mechanisms, particularly DNA methylation, regulate gene expression, including genes involved in platelet activation pathways, such as platelet endothelial aggregation receptor 1 (PEAR1), which are related to nutrients such as folate and methionine, contribute to one-carbon metabolism, and bioactive compounds promote methylation patterns related to DNA methylation enzymes and reduced platelet hyperactivity. So, this review summarizes current findings and explores the potential association between nuts and legumes consumption and platelet aggregation (PA) through DNA methylation, emphasizing their role in cardiovascular health and the potential for targeted dietary interventions.","PeriodicalId":212,"journal":{"name":"Molecular Nutrition & Food Research","volume":"144 1","pages":"e70297"},"PeriodicalIF":5.2,"publicationDate":"2025-10-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145373652","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Yu Wang,Juan Sun,Lamei Xue,Yujie Sun,Kuiliang Zhang,Mingcong Fan,Haifeng Qian,Yan Li,Li Wang
Hypercholesterolemia is a major risk factor for cardiovascular diseases. While gallic acid, a natural phenolic compound, shows hypolipidemic effects, its mechanisms remain elusive. This study investigated gallic acid's modulation of cholesterol and bile acid metabolism in high-fat diet (HFD)-induced hypercholesterolemia. Mice on an HFD were supplemented with gallic acid for 12 weeks. This study systematically examined gallic acid's modulation of cholesterol metabolism (synthesis, uptake, efflux) and enterohepatic bile acid circulation. The results indicated that gallic acid protected mice against diet-induced hypercholesterolemia and hepatic steatosis. Notably, gallic acid intervention favorably altered the dyslipidemic profile by increasing HDL-C while decreasing atherogenic lipids (TG, TC, and LDL-C) in HFD-fed mice. Mechanistically, gallic acid reduced cholesterol accumulation by modulating FXR-mediated liver-gut crosstalk of bile acids, significantly suppressing both ileal and hepatic FXR expression in HFD-fed mice. This inhibition downregulated key FXR target genes (ileal FGF15/SHP/I-BABP/ASBT and hepatic SHP/MAFG), reducing bile acid reabsorption while enhancing hepatic synthesis. Moreover, gallic acid activated Nrf2/HO-1 signaling and promoted antioxidant capacity in HFD-fed mice. Dietary gallic acid alleviates diet-induced hypercholesterolemia and hepatic steatosis, highlighting its potential as a safe and effective dietary supplement for managing hyperlipidemia and preventing metabolic liver disease.
{"title":"Dietary Gallic Acid Alleviates Hypercholesterolemia in High-Fat-Diet-Fed Mice by Modulating Cholesterol and Bile Acid Metabolism.","authors":"Yu Wang,Juan Sun,Lamei Xue,Yujie Sun,Kuiliang Zhang,Mingcong Fan,Haifeng Qian,Yan Li,Li Wang","doi":"10.1002/mnfr.70291","DOIUrl":"https://doi.org/10.1002/mnfr.70291","url":null,"abstract":"Hypercholesterolemia is a major risk factor for cardiovascular diseases. While gallic acid, a natural phenolic compound, shows hypolipidemic effects, its mechanisms remain elusive. This study investigated gallic acid's modulation of cholesterol and bile acid metabolism in high-fat diet (HFD)-induced hypercholesterolemia. Mice on an HFD were supplemented with gallic acid for 12 weeks. This study systematically examined gallic acid's modulation of cholesterol metabolism (synthesis, uptake, efflux) and enterohepatic bile acid circulation. The results indicated that gallic acid protected mice against diet-induced hypercholesterolemia and hepatic steatosis. Notably, gallic acid intervention favorably altered the dyslipidemic profile by increasing HDL-C while decreasing atherogenic lipids (TG, TC, and LDL-C) in HFD-fed mice. Mechanistically, gallic acid reduced cholesterol accumulation by modulating FXR-mediated liver-gut crosstalk of bile acids, significantly suppressing both ileal and hepatic FXR expression in HFD-fed mice. This inhibition downregulated key FXR target genes (ileal FGF15/SHP/I-BABP/ASBT and hepatic SHP/MAFG), reducing bile acid reabsorption while enhancing hepatic synthesis. Moreover, gallic acid activated Nrf2/HO-1 signaling and promoted antioxidant capacity in HFD-fed mice. Dietary gallic acid alleviates diet-induced hypercholesterolemia and hepatic steatosis, highlighting its potential as a safe and effective dietary supplement for managing hyperlipidemia and preventing metabolic liver disease.","PeriodicalId":212,"journal":{"name":"Molecular Nutrition & Food Research","volume":"13 1","pages":"e70291"},"PeriodicalIF":5.2,"publicationDate":"2025-10-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145351477","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Eva Kranenburg, Ruslan Kubant, Clara E. Cho, Zeyu Yang, Mahaylia Datars, Jianzhang Dong, G. Harvey Anderson
The cover image is based on the article Folic Acid Reduces Insulin Resistance in Mice With Diet-Induced Obesity by Altering One-Carbon Metabolism and DNA Methylation Patterns of Hypothalamic and Hepatic Insulin Receptor Gene by Harvey Anderson et al., https://doi.org/10.1002/mnfr.70181