Lei Wang, Na Qin, Liuliu Shi, Rujuan Liu, Ting Zhu
Scope: The intestinal flora is involved in the maintenance of human health and the development of diseases, and is closely related to the brain. As an essential amino acid, tryptophan (TRP) participates in a variety of physiological functions in the body and affects the growth and health of the human body. TRP catabolites produced by the gut microbiota are important signaling molecules for microbial communities and host-microbe interactions, and play an important role in maintaining health and disease pathogenesis.
Methods and results: The review first demonstrates the evidence of TRP metabolism in stroke and the relationship between gut microbiota and TRP metabolism. Furthermore, the review reveals that food homologous plants (FHP) bioactive compounds have been shown to regulate various metabolic pathways of the gut microbiota, including the biosynthesis of valine, leucine, isoleucine, and vitamin B6 metabolism. The most notable metabolic alteration is in TRP metabolism.
Conclusion: The interaction between gut microbiota and TRP metabolism offers a plausible explanation for the notable bioactivities of FHP in the treatment of ischemic stroke (IS). This review enhances the comprehension of the underlying mechanisms associated with the bioactivity of FHP on IS.
{"title":"Gut Microbiota and Tryptophan Metabolism in Pathogenesis of Ischemic Stroke: A Potential Role for Food Homologous Plants.","authors":"Lei Wang, Na Qin, Liuliu Shi, Rujuan Liu, Ting Zhu","doi":"10.1002/mnfr.202400639","DOIUrl":"https://doi.org/10.1002/mnfr.202400639","url":null,"abstract":"<p><strong>Scope: </strong>The intestinal flora is involved in the maintenance of human health and the development of diseases, and is closely related to the brain. As an essential amino acid, tryptophan (TRP) participates in a variety of physiological functions in the body and affects the growth and health of the human body. TRP catabolites produced by the gut microbiota are important signaling molecules for microbial communities and host-microbe interactions, and play an important role in maintaining health and disease pathogenesis.</p><p><strong>Methods and results: </strong>The review first demonstrates the evidence of TRP metabolism in stroke and the relationship between gut microbiota and TRP metabolism. Furthermore, the review reveals that food homologous plants (FHP) bioactive compounds have been shown to regulate various metabolic pathways of the gut microbiota, including the biosynthesis of valine, leucine, isoleucine, and vitamin B6 metabolism. The most notable metabolic alteration is in TRP metabolism.</p><p><strong>Conclusion: </strong>The interaction between gut microbiota and TRP metabolism offers a plausible explanation for the notable bioactivities of FHP in the treatment of ischemic stroke (IS). This review enhances the comprehension of the underlying mechanisms associated with the bioactivity of FHP on IS.</p>","PeriodicalId":212,"journal":{"name":"Molecular Nutrition & Food Research","volume":" ","pages":"e2400639"},"PeriodicalIF":4.5,"publicationDate":"2024-11-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142646397","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}
Sijia Liao, Lisa Börmel, Anke Katharina Müller, Luisa Gottschalk, Nadine Pritsch, Lara Zoé Preisner, Oleksandra Samokhina, Maria Schwarz, Anna P. Kipp, Wiebke Schlörmann, Michael Glei, Martin Schubert, Lisa Schmölz, Maria Wallert, Stefan Lorkowski
ScopeThe α‐tocopherol long‐chain metabolite α‐tocopherol‐13′‐hydroxy‐chromanol (α‐T‐13′‐COOH) is a proposed regulatory intermediate of endogenous vitamin E metabolism. Effects of α‐T‐13′‐COOH on cell viability and adaptive stress response are not well understood. The present study aims to investigate the concentration‐dependent effects of α‐T‐13′‐COOH on cellular redox homeostasis, genotoxicity, and cytotoxicity in murine RAW264.7 macrophages as a model system.Methods and resultsMurine RAW264.7 macrophages are exposed to various dosages of α‐T‐13′‐COOH to determine its regulatory effects on reactive oxygen species (ROS) production, DNA damage, expression of stress‐related markers, and the activity of ROS scavenging enzymes including superoxide dismutases, catalase, and glutathione‐S‐transferases. The impact on cell viability is assessed by analyzing cell proliferation, cell cycle arrest, and cell apoptosis.Conclusionα‐T‐13′‐COOH influences ROS production and induces DNA damage in a dose‐dependent manner. The metabolite modulates the activity of ROS‐scavenging enzymes, with significant changes observed in the activities of antioxidant enzymes. A biphasic response affecting cell viability is noted: sub‐micromolar doses of α‐T‐13′‐COOH promote cell proliferation and enhance DNA synthesis, whereas supraphysiological doses lead to DNA damage and cytotoxicity. It hypothesizes an adaptive stress response, characterized by upregulation of ROS detoxification mechanisms, enhanced cell cycle arrest, and increased apoptosis, indicating a correlation with oxidative stress and subsequent cellular damage.
范围α-生育酚长链代谢产物α-生育酚-13′-羟基色醇（α-T-13′-COOH）是一种拟议的内源性维生素 E 代谢调节中间产物。α-T-13′-COOH对细胞活力和适应性应激反应的影响尚不十分清楚。本研究旨在以小鼠 RAW264.7 巨噬细胞为模型系统，研究 α-T-13′-COOH 对细胞氧化还原平衡、基因毒性和细胞毒性的浓度依赖性影响。7巨噬细胞暴露于不同剂量的α-T-13′-COOH，以确定其对活性氧（ROS）产生、DNA损伤、应激相关标志物的表达以及ROS清除酶（包括超氧化物歧化酶、过氧化氢酶和谷胱甘肽-S-转移酶）活性的调节作用。结论α-T-13′-COOH 以剂量依赖的方式影响 ROS 的产生并诱导 DNA 损伤。这种代谢物会调节 ROS 清除酶的活性，抗氧化酶的活性也会发生显著变化。我们注意到影响细胞活力的双相反应：亚微摩尔剂量的 α-T-13′-COOH 可促进细胞增殖并增强 DNA 合成，而超生理剂量则会导致 DNA 损伤和细胞毒性。该研究假设了一种适应性应激反应，其特点是上调 ROS 解毒机制、加强细胞周期停滞和增加细胞凋亡，这表明与氧化应激和随后的细胞损伤有关。
{"title":"α‐Tocopherol Long‐Chain Metabolite α‐T‐13′‐COOH Exhibits Biphasic Effects on Cell Viability, Induces ROS‐Dependent DNA Damage, and Modulates Redox Status in Murine RAW264.7 Macrophages","authors":"Sijia Liao, Lisa Börmel, Anke Katharina Müller, Luisa Gottschalk, Nadine Pritsch, Lara Zoé Preisner, Oleksandra Samokhina, Maria Schwarz, Anna P. Kipp, Wiebke Schlörmann, Michael Glei, Martin Schubert, Lisa Schmölz, Maria Wallert, Stefan Lorkowski","doi":"10.1002/mnfr.202400455","DOIUrl":"https://doi.org/10.1002/mnfr.202400455","url":null,"abstract":"ScopeThe α‐tocopherol long‐chain metabolite α‐tocopherol‐13′‐hydroxy‐chromanol (α‐T‐13′‐COOH) is a proposed regulatory intermediate of endogenous vitamin E metabolism. Effects of α‐T‐13′‐COOH on cell viability and adaptive stress response are not well understood. The present study aims to investigate the concentration‐dependent effects of α‐T‐13′‐COOH on cellular redox homeostasis, genotoxicity, and cytotoxicity in murine RAW264.7 macrophages as a model system.Methods and resultsMurine RAW264.7 macrophages are exposed to various dosages of α‐T‐13′‐COOH to determine its regulatory effects on reactive oxygen species (ROS) production, DNA damage, expression of stress‐related markers, and the activity of ROS scavenging enzymes including superoxide dismutases, catalase, and glutathione‐S‐transferases. The impact on cell viability is assessed by analyzing cell proliferation, cell cycle arrest, and cell apoptosis.Conclusionα‐T‐13′‐COOH influences ROS production and induces DNA damage in a dose‐dependent manner. The metabolite modulates the activity of ROS‐scavenging enzymes, with significant changes observed in the activities of antioxidant enzymes. A biphasic response affecting cell viability is noted: sub‐micromolar doses of α‐T‐13′‐COOH promote cell proliferation and enhance DNA synthesis, whereas supraphysiological doses lead to DNA damage and cytotoxicity. It hypothesizes an adaptive stress response, characterized by upregulation of ROS detoxification mechanisms, enhanced cell cycle arrest, and increased apoptosis, indicating a correlation with oxidative stress and subsequent cellular damage.","PeriodicalId":212,"journal":{"name":"Molecular Nutrition & Food Research","volume":"166 1","pages":""},"PeriodicalIF":5.2,"publicationDate":"2024-11-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142642629","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}
This comprehensive review explores the intricate relationship between gut microbiota, diet, and insulin resistance, emphasizing the novel roles of diet-induced microbial changes in influencing metabolic health. It highlights how diet significantly influences gut microbiota composition, with different dietary patterns fostering diverse microbial communities. These diet-induced changes in the microbiome impact human metabolism by affecting inflammation, energy balance, and insulin sensitivity, particularly through microbial metabolites like short-chain fatty acids (SCFAs). Focusing the key mediators like endotoxemia and systemic inflammation, and introduces personalized microbiome-based therapeutic strategies, it also investigates the effects of dietary components—fiber, polyphenols, and lipids—on microbiota and insulin sensitivity, along with the roles of protein intake and amino acid metabolism. The study compares the effects of Western and Mediterranean diets on the microbiota-insulin resistance axis. Therapeutic implications, including probiotics, fecal microbiota transplantation (FMT), and personalized diets, are discussed. Key findings reveal that high-fat diets, especially those rich in saturated fats, contribute to dysbiosis and increased intestinal permeability, while high-fiber diets promote beneficial bacteria and SCFAs. The review underscores the future potential of food and microbiota interventions for preventing or managing insulin resistance.
{"title":"Synergistic Interplay of Diet, Gut Microbiota, and Insulin Resistance: Unraveling the Molecular Nexus","authors":"Rajesh Kanna Gopal, Pitchaipillai Sankar Ganesh, Naji Naseef Pathoor","doi":"10.1002/mnfr.202400677","DOIUrl":"https://doi.org/10.1002/mnfr.202400677","url":null,"abstract":"This comprehensive review explores the intricate relationship between gut microbiota, diet, and insulin resistance, emphasizing the novel roles of diet-induced microbial changes in influencing metabolic health. It highlights how diet significantly influences gut microbiota composition, with different dietary patterns fostering diverse microbial communities. These diet-induced changes in the microbiome impact human metabolism by affecting inflammation, energy balance, and insulin sensitivity, particularly through microbial metabolites like short-chain fatty acids (SCFAs). Focusing the key mediators like endotoxemia and systemic inflammation, and introduces personalized microbiome-based therapeutic strategies, it also investigates the effects of dietary components—fiber, polyphenols, and lipids—on microbiota and insulin sensitivity, along with the roles of protein intake and amino acid metabolism. The study compares the effects of Western and Mediterranean diets on the microbiota-insulin resistance axis. Therapeutic implications, including probiotics, fecal microbiota transplantation (FMT), and personalized diets, are discussed. Key findings reveal that high-fat diets, especially those rich in saturated fats, contribute to dysbiosis and increased intestinal permeability, while high-fiber diets promote beneficial bacteria and SCFAs. The review underscores the future potential of food and microbiota interventions for preventing or managing insulin resistance.","PeriodicalId":212,"journal":{"name":"Molecular Nutrition & Food Research","volume":"12 1","pages":""},"PeriodicalIF":5.2,"publicationDate":"2024-11-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142642680","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}
ScopeThis study investigates whether vitamin E (VE) deficiency in subjects with obesity could, at least partly, be due to a defect in VE intestinal absorption.Methods and resultsMice follow either a high‐fat (HF) or a control (CTL) diet for 12 weeks. The study evaluates their VE status, the expression of genes encoding proteins involved in lipid and fat‐soluble vitamin intestinal absorption, and VE absorption using a γ‐tocopherol‐rich emulsion. HF mice have a weight (+23.0%) and an adiposity index (AI, +157.0) superior to CTL mice (p < 0.05). α‐Tocopherol concentrations are higher in both plasma (+45.0%) and liver (+116.9%) of HF mice compared to CTL mice (p < 0.05). α‐Tocopherol concentration in the adipose tissue of HF mice is higher than that of CTL mice after correction by the AI (+72.4%, p < 0.05). No difference is found in the expression of genes coding for proteins involved in intestinal lipid metabolism in fasting mice. After force‐feeding, γ‐tocopherol plasma concentration is higher in HF mice compared to CTL mice (+181.5% at 1.5 h after force‐feeding, p < 0.05).ConclusionHF mice display higher status and more efficient absorption of VE than CTL mice. VE absorption is thus likely not impaired in the early stages of obesity.
范围本研究探讨肥胖症患者缺乏维生素 E（VE）是否至少部分是由于 VE 肠道吸收缺陷所致。研究使用富含γ-生育酚的乳液对小鼠的 VE 状态、编码参与脂质和脂溶性维生素肠道吸收的蛋白质的基因表达以及 VE 吸收情况进行了评估。HF 小鼠的体重（+23.0%）和脂肪指数（AI，+157.0）均优于 CTL 小鼠（p < 0.05）。与 CTL 小鼠相比，高频小鼠血浆（+45.0%）和肝脏（+116.9%）中的 α-生育酚浓度更高（p < 0.05）。经 AI 校正后，HF 小鼠脂肪组织中的α-生育酚浓度高于 CTL 小鼠（+72.4%，p <0.05）。空腹小鼠肠道脂质代谢蛋白编码基因的表达没有差异。与 CTL 小鼠相比，强制喂食后，HF 小鼠血浆中的γ-生育酚浓度更高（强制喂食后 1.5 小时时为 +181.5%，p < 0.05）。因此，在肥胖的早期阶段，VE的吸收可能不会受到影响。
{"title":"Overweight Leads to an Increase in Vitamin E Absorption and Status in Mice","authors":"Katherine Alvarado‐Ramos, Ángela Bravo‐Núñez, Donato Vairo, Charlotte Sabran, Jean‐François Landrier, Emmanuelle Reboul","doi":"10.1002/mnfr.202400509","DOIUrl":"https://doi.org/10.1002/mnfr.202400509","url":null,"abstract":"ScopeThis study investigates whether vitamin E (VE) deficiency in subjects with obesity could, at least partly, be due to a defect in VE intestinal absorption.Methods and resultsMice follow either a high‐fat (HF) or a control (CTL) diet for 12 weeks. The study evaluates their VE status, the expression of genes encoding proteins involved in lipid and fat‐soluble vitamin intestinal absorption, and VE absorption using a γ‐tocopherol‐rich emulsion. HF mice have a weight (+23.0%) and an adiposity index (AI, +157.0) superior to CTL mice (<jats:italic>p</jats:italic> < 0.05). α‐Tocopherol concentrations are higher in both plasma (+45.0%) and liver (+116.9%) of HF mice compared to CTL mice (<jats:italic>p</jats:italic> < 0.05). α‐Tocopherol concentration in the adipose tissue of HF mice is higher than that of CTL mice after correction by the AI (+72.4%, <jats:italic>p</jats:italic> < 0.05). No difference is found in the expression of genes coding for proteins involved in intestinal lipid metabolism in fasting mice. After force‐feeding, γ‐tocopherol plasma concentration is higher in HF mice compared to CTL mice (+181.5% at 1.5 h after force‐feeding, <jats:italic>p</jats:italic> < 0.05).ConclusionHF mice display higher status and more efficient absorption of VE than CTL mice. VE absorption is thus likely not impaired in the early stages of obesity.","PeriodicalId":212,"journal":{"name":"Molecular Nutrition & Food Research","volume":"21 1","pages":""},"PeriodicalIF":5.2,"publicationDate":"2024-11-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142642631","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}
Fen Wu, Meilin Wang, Xiaoyue Chen, Dongchen Zhang, Wei Peng, Xinyi Hu, Haoran Xu, WenNa Zhang, Chao Yan, Yongming Lu, Min Sun, Yan Chen, Lei Chen
Scope: Cordyceps cicadae polysaccharides have received attention due to their potential in treating hyperglycemia and enhancing renal function. The beneficial effect of the purified C. cicadae polysaccharides fraction (CCP-1) on the reproductive impairments and spermatogenesis dysfunction of immunocompromised mice is unavailable and is studied herein.
Methods and results: The study establishes a GC-1 spg cell apoptosis model induced by TNF-α+SM-164 (TS) and male mouse reproductive injury model induced by cyclophosphamide (CTX), and then intervened by CCP-1. CCP-1 improves the viability of GC-1 spg cell and inhibits cells apoptosis induced by TS in vitro. CCP-1 enhances sperm quality and spermatogenesis function, as well as ameliorating the histological lesions in the hypothalamus, testicular, and kidney. CCP-1 elevates gonadotropin-releasing hormone (GnRH) level that secreted by the hypothalamus, and increases the levels of follicle stimulating hormone (FSH) and luteizing hormone (LH) in the anterior pituitary stimulated by GnRH, and promotes the secretion of testosterone (T) by testis. Moreover, CCP-1 could protect the reproductive system by activating reproductive regulatory pathway such as SCF/C-kit pathway and inhibiting apoptotic signaling pathway such as Bax/Caspase-3 pathway.
Conclusion: These results manifest that CCP-1 could serve as a natural promising reproductive system protective supplement for ameliorating CTX biotoxicity.
{"title":"Polysaccharides from Cordyceps cicadae Ameliorate Reproductive Impairments in Male Mouse through the Hypothalamic-Pituitary-Testicular Axis.","authors":"Fen Wu, Meilin Wang, Xiaoyue Chen, Dongchen Zhang, Wei Peng, Xinyi Hu, Haoran Xu, WenNa Zhang, Chao Yan, Yongming Lu, Min Sun, Yan Chen, Lei Chen","doi":"10.1002/mnfr.202400446","DOIUrl":"https://doi.org/10.1002/mnfr.202400446","url":null,"abstract":"<p><strong>Scope: </strong>Cordyceps cicadae polysaccharides have received attention due to their potential in treating hyperglycemia and enhancing renal function. The beneficial effect of the purified C. cicadae polysaccharides fraction (CCP-1) on the reproductive impairments and spermatogenesis dysfunction of immunocompromised mice is unavailable and is studied herein.</p><p><strong>Methods and results: </strong>The study establishes a GC-1 spg cell apoptosis model induced by TNF-α+SM-164 (TS) and male mouse reproductive injury model induced by cyclophosphamide (CTX), and then intervened by CCP-1. CCP-1 improves the viability of GC-1 spg cell and inhibits cells apoptosis induced by TS in vitro. CCP-1 enhances sperm quality and spermatogenesis function, as well as ameliorating the histological lesions in the hypothalamus, testicular, and kidney. CCP-1 elevates gonadotropin-releasing hormone (GnRH) level that secreted by the hypothalamus, and increases the levels of follicle stimulating hormone (FSH) and luteizing hormone (LH) in the anterior pituitary stimulated by GnRH, and promotes the secretion of testosterone (T) by testis. Moreover, CCP-1 could protect the reproductive system by activating reproductive regulatory pathway such as SCF/C-kit pathway and inhibiting apoptotic signaling pathway such as Bax/Caspase-3 pathway.</p><p><strong>Conclusion: </strong>These results manifest that CCP-1 could serve as a natural promising reproductive system protective supplement for ameliorating CTX biotoxicity.</p>","PeriodicalId":212,"journal":{"name":"Molecular Nutrition & Food Research","volume":" ","pages":"e2400446"},"PeriodicalIF":4.5,"publicationDate":"2024-11-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142613285","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}
Zebin Zou, Nan Xiao, Zhixian Chen, Xucong Lin, Yaqi Li, Pan Li, Qian Cheng, Bing Du
Scope
Depression as a global neurological disorder, and hippocampal neuronal apoptosis and disorders of the gut microbiota are closely related to it. This study aims to expose the ameliorative effect of enzyme peptides (AP) from brewer's yeast on depressive behavior caused by chronic restraint stress (CRS) in rats.
Methods and results
After 4 weeks of AP intervention, a significant alleviation of depressive behavior in the sucrose preference test (SPT), forced swim test (FST), and light-dark test (LDT) is observed in depressed rats. AP ameliorates neuronal damage with increased the expression of the key CREB/BDNF/TrkB/Akt signaling pathway, which increases the levels of the monoamine neurotransmitters 5-hydroxytryptamine (5-HT) and norepinephrine (NE) in the hippocampus, buffering hyperactivity of the hypothalamo-pituitary-adrenal axis (HPA), and decreasing the serum cortisol (CORT) and adrenocorticotropic hormone (ACTH) levels in rats. In addition, AP modulates the disruption of the rat gut microbiota by chronic restraint stress (CRS), and the changes in the abundance of Lactobacillus animalis and Lactobacillus johnsonii are probably the key for AP performing antidepressant benefits. A strong correlation is found between gut microbiota and biochemical markers of depression.
Conclusion
AP, as a natural and safe active substance, has a positive effect in the treatment of depression.
{"title":"Yeast Extract Peptides Alleviate Depression in Chronic Restraint Stress Rats by Alleviating Hippocampal Neuronal Apoptosis and Dysbiosis of the Gut Microbiota","authors":"Zebin Zou, Nan Xiao, Zhixian Chen, Xucong Lin, Yaqi Li, Pan Li, Qian Cheng, Bing Du","doi":"10.1002/mnfr.202300467","DOIUrl":"10.1002/mnfr.202300467","url":null,"abstract":"<div>\u0000 \u0000 <section>\u0000 \u0000 <h3> Scope</h3>\u0000 \u0000 <p>Depression as a global neurological disorder, and hippocampal neuronal apoptosis and disorders of the gut microbiota are closely related to it. This study aims to expose the ameliorative effect of enzyme peptides (AP) from brewer's yeast on depressive behavior caused by chronic restraint stress (CRS) in rats.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods and results</h3>\u0000 \u0000 <p>After 4 weeks of AP intervention, a significant alleviation of depressive behavior in the sucrose preference test (SPT), forced swim test (FST), and light-dark test (LDT) is observed in depressed rats. AP ameliorates neuronal damage with increased the expression of the key CREB/BDNF/TrkB/Akt signaling pathway, which increases the levels of the monoamine neurotransmitters 5-hydroxytryptamine (5-HT) and norepinephrine (NE) in the hippocampus, buffering hyperactivity of the hypothalamo-pituitary-adrenal axis (HPA), and decreasing the serum cortisol (CORT) and adrenocorticotropic hormone (ACTH) levels in rats. In addition, AP modulates the disruption of the rat gut microbiota by chronic restraint stress (CRS), and the changes in the abundance of <i>Lactobacillus animalis</i> and <i>Lactobacillus johnsonii</i> are probably the key for AP performing antidepressant benefits. A strong correlation is found between gut microbiota and biochemical markers of depression.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>AP, as a natural and safe active substance, has a positive effect in the treatment of depression.</p>\u0000 </section>\u0000 </div>","PeriodicalId":212,"journal":{"name":"Molecular Nutrition & Food Research","volume":"68 21","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-10-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142451947","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}
Chenglin Guo, Shengduo He, Mélanie Le Barz, Sylvie Binda, Huahong Wang
Scope
The gut microbiota plays a role in fat accumulation and energy homeostasis. Therefore, probiotic supplementation may improve metabolic parameters and control body weight.
Methods and results
In this study, mice are fed either a high-fat diet (HFD) or an HFD supplemented with oral gavage of a mixture of three probiotic strains, Bifidobacterium lactis Lafti B94, Lactobacillus plantarum HA-119, and Lactobacillus helveticus Lafti L10 for 7 weeks. It finds that probiotic supplementation modulates body weight gain, food energy efficiency, and fat accumulation caused by the HFD. This probiotic mix prevents liver damage and lipid metabolic disorders in HFD-fed obese mice. The probiotic supplementation significantly downregulates the expression of the proinflammatory cytokines interleukin-1β, tumor necrosis factor-α, and malondialdehyde (MDA) in the liver and upregulated catalase (CAT), superoxide dismutase (SOD), and nuclear respiratory factor 1 (Nrf1) expression. Mice supplemented with the probiotic mix also show different microbiota compositions, with an increase in Clostridia_UCG-014 and Lachnospiraceae_nk4a136_group and a decrease in the Dubosiella genus compared with those in mice fed only an HFD. Finally, the amounts of fecal pentanoic acid and the three bile acid species increase in mice with probiotic supplementation.
Conclusion
Treatment with a combination of a mixture of three probiotic strains, B. lactis Lafti B94, L. plantarum HA-119, and L. helveticus Lafti L10 for 7 weeks, ameliorates the effects of HFD induced obesity in mice.
摘要肠道微生物群在脂肪积累和能量平衡中发挥作用。因此，补充益生菌可改善代谢参数并控制体重。方法和结果在本研究中，小鼠被喂食高脂饮食（HFD）或口服三种益生菌菌株混合物（乳双歧杆菌 Lafti B94、植物乳杆菌 HA-119 和螺旋乳杆菌 Lafti L10）7 周。研究发现，补充益生菌可调节体重增加、食物能量效率以及高密度脂蛋白食物引起的脂肪积累。这种益生菌混合物可预防高纤维食物喂养肥胖小鼠的肝损伤和脂质代谢紊乱。补充益生菌后，白细胞介素-1β、肿瘤坏死因子-α和丙二醛（MDA）等促炎细胞因子在肝脏中的表达明显下调，过氧化氢酶（CAT）、超氧化物歧化酶（SOD）和核呼吸因子1（Nrf1）的表达上调。与只摄入高纤维食物的小鼠相比，补充益生菌混合物的小鼠也表现出不同的微生物群组成，梭菌_UCG-014 和 Lachnospiraceae_nk4a136_group 增加，而杜博斯菌属减少。最后，补充益生菌后，小鼠粪便中戊酸和三种胆汁酸的含量增加。结论连续 7 周服用三种益生菌菌株（B. lactis Lafti B94、L. plantarum HA-119 和 L. helveticus Lafti L10）的混合物可改善高纤维食物诱发小鼠肥胖的影响。
{"title":"A Mix of Probiotic Strains Prevents Hepatic Steatosis, and Improves Oxidative Stress Status and Gut Microbiota Composition in Obese Mice","authors":"Chenglin Guo, Shengduo He, Mélanie Le Barz, Sylvie Binda, Huahong Wang","doi":"10.1002/mnfr.202300672","DOIUrl":"10.1002/mnfr.202300672","url":null,"abstract":"<div>\u0000 \u0000 <section>\u0000 \u0000 <h3> Scope</h3>\u0000 \u0000 <p>The gut microbiota plays a role in fat accumulation and energy homeostasis. Therefore, probiotic supplementation may improve metabolic parameters and control body weight.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods and results</h3>\u0000 \u0000 <p>In this study, mice are fed either a high-fat diet (HFD) or an HFD supplemented with oral gavage of a mixture of three probiotic strains, <i>Bifidobacterium lactis</i> Lafti B94, <i>Lactobacillus plantarum</i> HA-119, and <i>Lactobacillus helveticus</i> Lafti L10 for 7 weeks. It finds that probiotic supplementation modulates body weight gain, food energy efficiency, and fat accumulation caused by the HFD. This probiotic mix prevents liver damage and lipid metabolic disorders in HFD-fed obese mice. The probiotic supplementation significantly downregulates the expression of the proinflammatory cytokines interleukin-1β, tumor necrosis factor-α, and malondialdehyde (MDA) in the liver and upregulated catalase (CAT), superoxide dismutase (SOD), and nuclear respiratory factor 1 (Nrf1) expression. Mice supplemented with the probiotic mix also show different microbiota compositions, with an increase in <i>Clostridia_UCG-014</i> and <i>Lachnospiraceae_nk4a136_group</i> and a decrease in the <i>Dubosiella</i> genus compared with those in mice fed only an HFD. Finally, the amounts of fecal pentanoic acid and the three bile acid species increase in mice with probiotic supplementation.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Treatment with a combination of a mixture of three probiotic strains, <i>B. lactis</i> Lafti B94, <i>L. plantarum</i> HA-119, and <i>L. helveticus</i> Lafti L10 for 7 weeks, ameliorates the effects of HFD induced obesity in mice.</p>\u0000 </section>\u0000 </div>","PeriodicalId":212,"journal":{"name":"Molecular Nutrition & Food Research","volume":"68 21","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142449398","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}
Wenhui Zhang, Jiaming Zhang, Haoxuan Xue, Xi Chen, Meixiang Li, Shenghua Chen, Zhiling Li, Leonardo Antonio Sechi, Qian Wang, Giampiero Capobianco, Xiaocan Lei
Scope
Polycystic ovary syndrome (PCOS) is a common endocrine disorder that can lead to insulin resistance (IR) and dysregulation of glucose metabolism, resulting in an imbalance in the endometrial environment, which is unfavorable for embryo implantation of PCOS. This study aims to investigate whether nicotinamide mononucleotide (NMN) improves the stability of the endometrium in a rat model of PCOS and identifies whether it is related to reduce IR and increase glycolysis levels and its potential signaling pathway.
Methods and results
Female Sprague-Dawley (SD) rats are fed letrozole and a high-fat diet (HFD) to form the PCOS model, then the model rats are treated with or without NMN. It randomly divided into control, PCOS, and PCOS-NMN groups according to the feeding and treating method. Compared with the PCOS group, the regular estrous cycles are restored, the serum androgen (p<0.01) and fasting insulin levels (p<0.05) are reduced, and endometrial morphology (p<0.05) is improved in NMN-PCOS group. Furthermore, NMN inhibits endometrial cell apoptosis, improves endometrial decidualization transition, reduces IR, restores the expression of glycolysis rate-limiting enzymes, and activates the PI3K/AKT pathway in the uterus.
Conclusions
These results suggest that NMN enhances endometrial tissue homeostasis by decreasing uterine IR and regulating the glycolysis through the PI3K/AKT pathway.
{"title":"Nicotinamide Mononucleotide Improves Endometrial Homeostasis in a Rat Model of Polycystic Ovary Syndrome by Decreasing Insulin Resistance and Regulating the Glylytic Pathway","authors":"Wenhui Zhang, Jiaming Zhang, Haoxuan Xue, Xi Chen, Meixiang Li, Shenghua Chen, Zhiling Li, Leonardo Antonio Sechi, Qian Wang, Giampiero Capobianco, Xiaocan Lei","doi":"10.1002/mnfr.202400340","DOIUrl":"10.1002/mnfr.202400340","url":null,"abstract":"<div>\u0000 \u0000 <section>\u0000 \u0000 <h3> Scope</h3>\u0000 \u0000 <p>Polycystic ovary syndrome (PCOS) is a common endocrine disorder that can lead to insulin resistance (IR) and dysregulation of glucose metabolism, resulting in an imbalance in the endometrial environment, which is unfavorable for embryo implantation of PCOS. This study aims to investigate whether nicotinamide mononucleotide (NMN) improves the stability of the endometrium in a rat model of PCOS and identifies whether it is related to reduce IR and increase glycolysis levels and its potential signaling pathway.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods and results</h3>\u0000 \u0000 <p>Female Sprague-Dawley (SD) rats are fed letrozole and a high-fat diet (HFD) to form the PCOS model, then the model rats are treated with or without NMN. It randomly divided into control, PCOS, and PCOS-NMN groups according to the feeding and treating method. Compared with the PCOS group, the regular estrous cycles are restored, the serum androgen (<i>p</i><0.01) and fasting insulin levels (<i>p</i><0.05) are reduced, and endometrial morphology (<i>p</i><0.05) is improved in NMN-PCOS group. Furthermore, NMN inhibits endometrial cell apoptosis, improves endometrial decidualization transition, reduces IR, restores the expression of glycolysis rate-limiting enzymes, and activates the PI3K/AKT pathway in the uterus.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>These results suggest that NMN enhances endometrial tissue homeostasis by decreasing uterine IR and regulating the glycolysis through the PI3K/AKT pathway.</p>\u0000 </section>\u0000 </div>","PeriodicalId":212,"journal":{"name":"Molecular Nutrition & Food Research","volume":"68 21","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142449397","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}
Farzad Mohammadi, Charles Joly Beauparlant, Stéphanie Bianco, Arnaud Droit, Nicolas Bertrand, Iwona Rudkowska
Scope
The study aims to analyze transcriptomic profiles in adipose tissues postconsumption of elaidic acid (EA; trans-18:1n-9) and trans-palmitoleic acid (TPA; trans-16:1n-7), elucidating their different effects on inflammation and glucose metabolism.
Methods and results
Twenty C57BL/6 mice are divided into four groups. Each group receives one of the following formulations in drinking water: lecithin nanovesicles, nanovesicles containing either lecithin with EA or TPA (86:14 w/w), or water (control) for 28 days with a regular fat diet (18% calories from fat). Total RNA is extracted, and paired-end sequencing is performed. TPA intake alters the expression of 351 genes compared to EA intake, including 11 downregulated and 340 upregulated genes (fold change [FC] >1.5, p < 0.05). TPA compares to EA upregulated: Slc5a8, Lcn2, Csf3, Scube1, Mapk13, Bdkrb2, Ctla2a, Slc2a1, Oas3, Cx3cl1, Oas2, Nlrp6, Pycard, Cyba, Ddr1, and Prkab1 and downregulated Fas gene. These genes are related to the NOD-like receptor, lipid and atherosclerosis, IL-17 signaling, TNF, nonalcoholic fatty liver disease, cytokine–cytokine receptor interaction, adipocytokine, glucagon, insulin resistance, and inflammatory mediator regulation of TRP channels signaling.
Conclusion
TPA intake has a distinct impact on the regulation of inflammation and diabetes-related pathways in adipose tissue compared to EA.
{"title":"Ruminant Trans Fatty Acid Intake Modulates Inflammation Pathways in the Adipose Tissue Transcriptome of C57BL/6 Mice","authors":"Farzad Mohammadi, Charles Joly Beauparlant, Stéphanie Bianco, Arnaud Droit, Nicolas Bertrand, Iwona Rudkowska","doi":"10.1002/mnfr.202400290","DOIUrl":"10.1002/mnfr.202400290","url":null,"abstract":"<div>\u0000 \u0000 <section>\u0000 \u0000 <h3> Scope</h3>\u0000 \u0000 <p>The study aims to analyze transcriptomic profiles in adipose tissues postconsumption of elaidic acid (EA; <i>trans</i>-18:1<i>n</i>-9) and <i>trans</i>-palmitoleic acid (TPA; <i>trans</i>-16:1<i>n</i>-7), elucidating their different effects on inflammation and glucose metabolism.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods and results</h3>\u0000 \u0000 <p>Twenty C57BL/6 mice are divided into four groups. Each group receives one of the following formulations in drinking water: lecithin nanovesicles, nanovesicles containing either lecithin with EA or TPA (86:14 w/w), or water (control) for 28 days with a regular fat diet (18% calories from fat). Total RNA is extracted, and paired-end sequencing is performed. TPA intake alters the expression of 351 genes compared to EA intake, including 11 downregulated and 340 upregulated genes (fold change [FC] >1.5, <i>p</i> < 0.05). TPA compares to EA upregulated: Slc5a8, Lcn2, Csf3, Scube1, Mapk13, Bdkrb2, Ctla2a, Slc2a1, Oas3, Cx3cl1, Oas2, Nlrp6, Pycard, Cyba, Ddr1, and Prkab1 and downregulated Fas gene. These genes are related to the NOD-like receptor, lipid and atherosclerosis, IL-17 signaling, TNF, nonalcoholic fatty liver disease, cytokine–cytokine receptor interaction, adipocytokine, glucagon, insulin resistance, and inflammatory mediator regulation of TRP channels signaling.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>TPA intake has a distinct impact on the regulation of inflammation and diabetes-related pathways in adipose tissue compared to EA.</p>\u0000 </section>\u0000 </div>","PeriodicalId":212,"journal":{"name":"Molecular Nutrition & Food Research","volume":"68 21","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mnfr.202400290","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142431471","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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