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Antioxidants
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Oxidative Stress in Metabolic Syndrome: The Role of Gut Microbiota
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Oxidative Stress in Metabolic Syndrome: The Role of Gut Microbiota

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: closed (20 August 2024) | Viewed by 21106

Special Issue Editor

Dr. Sunmin Park

E-Mail Website
Guest Editor
Department of Food and Nutrition, Obesity/Diabetes Research Center, Hoseo University, Asan 31499, Republic of Korea
Interests: Alzheimer’s disease; insulin resistance; nutritional epidemiology; nutrigenomics; gut microbiome; type 2 diabetes; bioinformatics
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Metabolic syndrome, characterized by a constellation of conditions including obesity, insulin resistance, dyslipidemia, and hypertension, presents a significant public health challenge worldwide. Emerging research suggests that oxidative stress, exacerbated by alterations in gut microbiota composition and function, plays a pivotal role in the pathogenesis and progression of metabolic syndrome. Oxidative stress arises from an imbalance between reactive oxygen species (ROS) production and antioxidant defense mechanisms, contributing to cellular damage, inflammation, and metabolic dysfunction.

This Special Issue aims to deepen our understanding of the intricate interplay between gut microbiota, oxidative stress, and metabolic syndrome. We invite original research articles, reviews, and meta-analyses exploring various aspects of oxidative stress in the context of metabolic syndrome, specifically focusing on the gut microbiota. Topics of interest include, but are not limited to:

  • Mechanisms linking gut dysbiosis to oxidative stress and the development of metabolic syndrome;
  • The role of gut microbiota-derived metabolites in modulating oxidative stress pathways and metabolic dysfunction;
  • The impact of gut-barrier integrity and intestinal permeability on oxidative stress and metabolic syndrome;
  • Interactions between gut microbiota, dietary factors, and host metabolism in shaping oxidative stress profiles in metabolic syndrome;
  • Therapeutic strategies targeting gut microbiota and oxidative stress for the prevention and management of metabolic syndrome complications.

Furthermore, we welcome studies investigating the efficacy of interventions to modulate gut microbiota composition and reduce oxidative stress burden in individuals with metabolic syndrome, including dietary modifications, prebiotics, probiotics, synbiotics, and fecal microbiota transplantation.

Researchers are encouraged to submit manuscripts that provide insights into the complex interactions between gut microbiota, oxidative stress, and metabolic syndrome and offer potential avenues for therapeutic intervention. Studies involving human subjects, animal models, and in vitro experimentation are all within the scope of this Special Issue.

We invite you to contribute to this important discussion by submitting your high-quality research to this Special Issue. Together, we can advance our understanding of gut microbiota-mediated oxidative stress in metabolic syndrome and pave the way for novel preventive and therapeutic strategies.

Prof. Dr. Sunmin Park
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Antioxidants is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

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Published Papers (4 papers)

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Research

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15 pages, 3037 KiB  
Article
Dietary Polyphenols Support Akkermansia muciniphila Growth via Mediation of the Gastrointestinal Redox Environment
by Charlene B. Van Buiten, Valerie A. Seitz, Jessica L. Metcalf and Ilya Raskin
Antioxidants 2024, 13(3), 304; https://doi.org/10.3390/antiox13030304 - 29 Feb 2024
Cited by 4 | Viewed by 3913
Abstract
Obesity and metabolic dysfunction have been shown to be associated with overproduction of reactive oxygen species (ROS) in the gastrointestinal (GI) tract, which contributes to dysbiosis or imbalances in the gut microbiota. Recently, the reversal of dysbiosis has been observed as a result [...] Read more.
Obesity and metabolic dysfunction have been shown to be associated with overproduction of reactive oxygen species (ROS) in the gastrointestinal (GI) tract, which contributes to dysbiosis or imbalances in the gut microbiota. Recently, the reversal of dysbiosis has been observed as a result of dietary supplementation with antioxidative compounds including polyphenols. Likewise, dietary polyphenols have been associated with scavenging of GI ROS, leading to the hypothesis that radical scavenging in the GI tract is a potential mechanism for the reversal of dysbiosis. The objective of this study was to investigate the relationship between GI ROS, dietary antioxidants and beneficial gut bacterium Akkermansia muciniphila. The results of this study demonstrated A. muciniphila to be a discriminant microorganism between lean (n = 7) and obese (n = 7) mice. The relative abundance of A. muciniphila was also found to have a significant negative correlation with extracellular ROS in the GI tract as measured using fluorescent probe hydroindocyanine green. The ability of the dietary antioxidants ascorbic acid, β-carotene and grape polyphenols to scavenge GI ROS was evaluated in tandem with their ability to support A. muciniphila bloom in lean mice (n = 20). While the relationship between GI ROS and relative abundance of A. muciniphila was conserved in lean mice, only grape polyphenols stimulated the bloom of A. muciniphila. Analysis of fecal antioxidant capacity and differences in the bioavailability of the antioxidants of interest suggested that the poor bioavailability of grape polyphenols contributes to their superior radical scavenging activity and support of A. muciniphila in comparison to the other compounds tested. These findings demonstrate the utility of the GI redox environment as a modifiable therapeutic target in the treatment of chronic inflammatory diseases like metabolic syndrome. Full article
(This article belongs to the Special Issue Oxidative Stress in Metabolic Syndrome: The Role of Gut Microbiota)
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Review

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18 pages, 1215 KiB  
Review
Interplay of Oxidative Stress, Gut Microbiota, and Nicotine in Metabolic-Associated Steatotic Liver Disease (MASLD)
by Irene Mignini, Linda Galasso, Giulia Piccirilli, Valentin Calvez, Fabrizio Termite, Giorgio Esposto, Raffaele Borriello, Luca Miele, Maria Elena Ainora, Antonio Gasbarrini and Maria Assunta Zocco
Antioxidants 2024, 13(12), 1532; https://doi.org/10.3390/antiox13121532 - 14 Dec 2024
Cited by 1 | Viewed by 1733
Abstract
Oxidative stress has been described as one of the main drivers of intracellular damage and metabolic disorders leading to metabolic syndrome, a major health problem worldwide. In particular, free radicals alter lipid metabolism and promote lipid accumulation in the liver, existing in the [...] Read more.
Oxidative stress has been described as one of the main drivers of intracellular damage and metabolic disorders leading to metabolic syndrome, a major health problem worldwide. In particular, free radicals alter lipid metabolism and promote lipid accumulation in the liver, existing in the hepatic facet of metabolic syndrome, the metabolic dysfunction-associated steatotic liver disease (MASLD). Recent literature has highlighted how nicotine, especially if associated with a high-fat diet, exerts a negative effect on the induction and progression of MASLD by upregulating inflammation and increasing oxidative stress, abdominal fat lipolysis, and hepatic lipogenesis. Moreover, considerable evidence shows the central role of intestinal dysbiosis in the pathogenesis of MASLD and the impact of nicotine-induced oxidative stress on the gut microbiome. This results in an intricate network in which oxidative stress stands at the intersection point between gut microbiome, nicotine, and MASLD. The aim of this review is to delve into the molecular mechanisms linking tobacco smoking and MASLD, focusing on nicotine-induced microbiota modifications and their impact on MASLD development. Full article
(This article belongs to the Special Issue Oxidative Stress in Metabolic Syndrome: The Role of Gut Microbiota)
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23 pages, 763 KiB  
Review
Gut Microbiota and Metabolic Dysfunction-Associated Steatotic Liver Disease
by Emidio Scarpellini, Marialaura Scarcella, Jan F. Tack, Giuseppe Guido Maria Scarlata, Michela Zanetti and Ludovico Abenavoli
Antioxidants 2024, 13(11), 1386; https://doi.org/10.3390/antiox13111386 - 14 Nov 2024
Cited by 4 | Viewed by 2489
Abstract
Background: The gut microbiota constitutes a complex microorganism community that harbors bacteria, viruses, fungi, protozoa, and archaea. The human gut bacterial microbiota has been extensively proven to participate in human metabolism, immunity, and nutrient absorption. Its imbalance, namely “dysbiosis”, has been linked to [...] Read more.
Background: The gut microbiota constitutes a complex microorganism community that harbors bacteria, viruses, fungi, protozoa, and archaea. The human gut bacterial microbiota has been extensively proven to participate in human metabolism, immunity, and nutrient absorption. Its imbalance, namely “dysbiosis”, has been linked to disordered metabolism. Metabolic dysfunction-associated steatotic liver disease (MASLD) is one of the features of deranged human metabolism and is the leading cause of liver cirrhosis and hepatocellular carcinoma. Thus, there is a pathophysiological link between gut dysbiosis and MASLD. Aims and Methods: We aimed to review the literature data on the composition of the human bacterial gut microbiota and its dysbiosis in MASLD and describe the concept of the “gut–liver axis”. Moreover, we reviewed the approaches for gut microbiota modulation in MASLD treatment. Results: There is consolidated evidence of particular gut dysbiosis associated with MASLD and its stages. The model explaining the relationship between gut microbiota and the liver has a bidirectional organization, explaining the physiopathology of MASLD. Oxidative stress is one of the keystones in the pathophysiology of MASLD and fibrosis generation. There is promising and consolidated evidence for the efficacy of pre- and probiotics in reversing gut dysbiosis in MASLD patients, with therapeutic effects. Few yet encouraging data on fecal microbiota transplantation (FMT) in MASLD are available in the literature. Conclusions: The gut dysbiosis characteristic of MASLD is a key target in its reversal and treatment via diet, pre/probiotics, and FMT treatment. Oxidative stress modulation remains a promising target for MASLD treatment, prevention, and reversal. Full article
(This article belongs to the Special Issue Oxidative Stress in Metabolic Syndrome: The Role of Gut Microbiota)
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20 pages, 779 KiB  
Review
Gut Microbiota Dysbiosis, Oxidative Stress, Inflammation, and Epigenetic Alterations in Metabolic Diseases
by Hamid Mostafavi Abdolmaleky and Jin-Rong Zhou
Antioxidants 2024, 13(8), 985; https://doi.org/10.3390/antiox13080985 - 14 Aug 2024
Cited by 42 | Viewed by 11835
Abstract
Gut dysbiosis, resulting from an imbalance in the gut microbiome, can induce excessive production of reactive oxygen species (ROS), leading to inflammation, DNA damage, activation of the immune system, and epigenetic alterations of critical genes involved in the metabolic pathways. Gut dysbiosis-induced inflammation [...] Read more.
Gut dysbiosis, resulting from an imbalance in the gut microbiome, can induce excessive production of reactive oxygen species (ROS), leading to inflammation, DNA damage, activation of the immune system, and epigenetic alterations of critical genes involved in the metabolic pathways. Gut dysbiosis-induced inflammation can also disrupt the gut barrier integrity and increase intestinal permeability, which allows gut-derived toxic products to enter the liver and systemic circulation, further triggering oxidative stress, inflammation, and epigenetic alterations associated with metabolic diseases. However, specific gut-derived metabolites, such as short-chain fatty acids (SCFAs), lactate, and vitamins, can modulate oxidative stress and the immune system through epigenetic mechanisms, thereby improving metabolic function. Gut microbiota and diet-induced metabolic diseases, such as obesity, insulin resistance, dyslipidemia, and hypertension, can transfer to the next generation, involving epigenetic mechanisms. In this review, we will introduce the key epigenetic alterations that, along with gut dysbiosis and ROS, are engaged in developing metabolic diseases. Finally, we will discuss potential therapeutic interventions such as dietary modifications, prebiotics, probiotics, postbiotics, and fecal microbiota transplantation, which may reduce oxidative stress and inflammation associated with metabolic syndrome by altering gut microbiota and epigenetic alterations. In summary, this review highlights the crucial role of gut microbiota dysbiosis, oxidative stress, and inflammation in the pathogenesis of metabolic diseases, with a particular focus on epigenetic alterations (including histone modifications, DNA methylomics, and RNA interference) and potential interventions that may prevent or improve metabolic diseases. Full article
(This article belongs to the Special Issue Oxidative Stress in Metabolic Syndrome: The Role of Gut Microbiota)
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