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Antioxidants
Special Issues
Oxidative Stress and Inflammation in Obesity
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Oxidative Stress and Inflammation in Obesity

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 (10 October 2023) | Viewed by 12680

Special Issue Editors

Prof. Dr. Maurizio Crestani

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Guest Editor
Dipartimento di Scienze Farmacologiche e Biomolecolari - DiSFeB, Università degli Studi di Milano, via Balzaretti 9, 20133 Milan, Italy
Interests: adipose tissue; obesity; type 2 diabetes; epigenetics; regulation of metabolism
Prof. Dr. Catherine Mounier

E-Mail Website
Guest Editor
Laboratoire du Métabolisme Moléculaire des Lipides, Centre de Recherches CERMO-FC, Département des Sciences Biologiques, Université du Québec à Montréal (UQAM), 141 av. du Président-Kennedy, Montreal, QC H2X 1Y4, Canada
Interests: lipogenesis; NAFLD; inflammation; neurodegenerative diseases
Prof. Dr. Christian Wolfrum

E-Mail Website
Guest Editor
Institute of Food, Nutrition and Health, ETH Zurich, 8603 Schwerzenbach, Switzerland
Interests: adipose tissue; oxidative stress; metabolism; obesity

Special Issue Information

Dear Colleagues,

The prevalence of obesity has been dramatically escalating across the globe over the last 40 years; nowadays, over 2 billion people worldwide, including children, are affected. It has been proposed that obesity may induce systemic oxidative stress and low-grade inflammation. Consequently, oxidative stress and inflammation in hypertrophic and hyperplastic adipose depots of obese subjects contribute to the dysregulation of adipose tissue and to the development of metabolic syndrome. However, obesity also affects other organs/tissues and increases the incidence of various diseases, including diabetes, hypertension, dyslipidemia, fatty liver disease, atherosclerosis, and cancer. Notably, the recent COVID-19 pandemic has highlighted that obesity represents a risk factor that makes obese patients more predisposed to a poor prognosis upon infection with the SARS-CoV-2 virus, most likely because of the global systemic low-grade inflammation already existing in obese patients, which is exacerbated by the viral infection.

The goal of this Special Issue is to gather updated knowledge on the topic of oxidative stress and inflammation in different organs, including, but not limited to, adipose tissues, the liver, skeletal muscles, the pancreas, and the brain. We aim to publish manuscripts in the form of both research and review articles. Authors are encouraged to submit the results of their recent investigations in basic science as well as clinical studies and to discuss original ideas and hypotheses in the field. We expect to stimulate discussion on fundamental questions that may translate to clinical settings.

Prof. Dr. Maurizio Crestani
Prof. Dr. Catherine Mounier
Prof. Dr. Christian Wolfrum
Guest Editors

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.

Keywords

  • redox stress
  • inflammation
  • adipose tissue
  • viral infection

Published Papers (6 papers)

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Research

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23 pages, 3095 KiB  
Article
Melatonin Alleviates the Impairment of Muscle Bioenergetics and Protein Quality Control Systems in Leptin-Deficiency-Induced Obesity
by Yaiza Potes, Andrea Díaz-Luis, Juan C. Bermejo-Millo, Zulema Pérez-Martínez, Beatriz de Luxán-Delgado, Adrian Rubio-González, Iván Menéndez-Valle, José Gutiérrez-Rodríguez, Juan J. Solano, Beatriz Caballero, Ignacio Vega-Naredo and Ana Coto-Montes
Antioxidants 2023, 12(11), 1962; https://doi.org/10.3390/antiox12111962 - 03 Nov 2023
Viewed by 1076
Abstract
Leptin is critically compromised in the major common forms of obesity. Skeletal muscle is the main effector tissue for energy modification that occurs as a result of the effect of endocrine axes, such as leptin signaling. Our study was carried out using skeletal [...] Read more.
Leptin is critically compromised in the major common forms of obesity. Skeletal muscle is the main effector tissue for energy modification that occurs as a result of the effect of endocrine axes, such as leptin signaling. Our study was carried out using skeletal muscle from a leptin-deficient animal model, in order to ascertain the importance of this hormone and to identify the major skeletal muscle mechanisms affected. We also examined the therapeutic role of melatonin against leptin-induced muscle wasting. Here, we report that leptin deficiency stimulates fatty acid β-oxidation, which results in mitochondrial uncoupling and the suppression of mitochondrial oxidative damage; however, it increases cytosolic oxidative damage. Thus, different nutrient-sensing pathways are disrupted, impairing proteostasis and promoting lipid anabolism, which induces myofiber degeneration and drives oxidative type I fiber conversion. Melatonin treatment plays a significant role in reducing cellular oxidative damage and regulating energy homeostasis and fuel utilization. Melatonin is able to improve both glucose and mitochondrial metabolism and partially restore proteostasis. Taken together, our study demonstrates melatonin to be a decisive mitochondrial function-fate regulator in skeletal muscle, with implications for resembling physiological energy requirements and targeting glycolytic type II fiber recovery. Full article
(This article belongs to the Special Issue Oxidative Stress and Inflammation in Obesity)
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18 pages, 3415 KiB  
Article
Do Intestinal Unicellular Parasites Have a Role in the Inflammatory and Redox Status among the Severely Obese?
by Jana Caudet, María Trelis, Susana Cifre, Gabriela Tapia, José M. Soriano, Regina Rodrigo and Juan F. Merino-Torres
Antioxidants 2022, 11(11), 2090; https://doi.org/10.3390/antiox11112090 - 23 Oct 2022
Viewed by 1855
Abstract
The diagnosis of obesity comprises subjects with totally different phenotypes and metabolic profiles. Systemic inflammation and oxidative stress derived from the white adipose tissue are suggested as the link between this disease and the development of insulin resistance and metabolic comorbidities. The presence [...] Read more.
The diagnosis of obesity comprises subjects with totally different phenotypes and metabolic profiles. Systemic inflammation and oxidative stress derived from the white adipose tissue are suggested as the link between this disease and the development of insulin resistance and metabolic comorbidities. The presence of unicellular eukaryotic parasites colonizing the human gut ecosystem is a common circumstance, and yet their influence on the inflammatory and redox status of the obese host has not been assessed. Herein, a set of inflammatory and redox biomarkers were assessed together with a parasitological analysis of 97 severely obese subjects. Information was also collected on insulin resistance and on the antioxidant composition of the diet. The global prevalence of intestinal unicellular parasites was 49.5%, with Blastocystis sp. the most prevalent protozoan found (42.3%). Colonized subjects displayed a higher total antioxidant capacity and a trend towards higher extracellular superoxide dismutase activity, regardless of their insulin resistance status, along with lower reduced glutathione/oxidized glutathione (GSH/GSSG) ratios in plasma in the insulin-resistant subgroup. No changes in malondialdehyde levels, or in inflammatory cytokines in plasma, were found in regard to the colonization status. In conclusion, enteric eukaryotic unicellular parasites may play an important role in modulating the antioxidant defenses of an obese host, thus could have beneficial effects with respect to the development of systemic metabolic disorders. Full article
(This article belongs to the Special Issue Oxidative Stress and Inflammation in Obesity)
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Review

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14 pages, 5033 KiB  
Review
Obese Adipocytes Have Altered Redox Homeostasis with Metabolic Consequences
by Saverio Cinti
Antioxidants 2023, 12(7), 1449; https://doi.org/10.3390/antiox12071449 - 19 Jul 2023
Cited by 2 | Viewed by 1206
Abstract
White and brown adipose tissues are organized to form a real organ, the adipose organ, in mice and humans. White adipocytes of obese animals and humans are hypertrophic. This condition is accompanied by a series of organelle alterations and stress of the endoplasmic [...] Read more.
White and brown adipose tissues are organized to form a real organ, the adipose organ, in mice and humans. White adipocytes of obese animals and humans are hypertrophic. This condition is accompanied by a series of organelle alterations and stress of the endoplasmic reticulum. This stress is mainly due to reactive oxygen species activity and accumulation, lending to NLRP3 inflammasome activation. This last causes death of adipocytes by pyroptosis and the formation of large cellular debris that must be removed by macrophages. During their chronic scavenging activity, macrophages produce several secretory products that have collateral consequences, including interference with insulin receptor activity, causing insulin resistance. The latter is accompanied by an increased noradrenergic inhibitory innervation of Langerhans islets with de-differentiation of beta cells and type 2 diabetes. The whitening of brown adipocytes could explain the different critical death size of visceral adipocytes and offer an explanation for the worse clinical consequence of visceral fat accumulation. White to brown transdifferentiation has been proven in mice and humans. Considering the energy-dispersing activity of brown adipose tissue, transdifferentiation opens new therapeutic perspectives for obesity and related disorders. Full article
(This article belongs to the Special Issue Oxidative Stress and Inflammation in Obesity)
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30 pages, 1569 KiB  
Review
The Preventive Mechanisms of Bioactive Food Compounds against Obesity-Induced Inflammation
by Marta Pelczyńska, Małgorzata Moszak, Agnieszka Wesołek and Paweł Bogdański
Antioxidants 2023, 12(6), 1232; https://doi.org/10.3390/antiox12061232 - 07 Jun 2023
Cited by 4 | Viewed by 1704
Abstract
Dietary patterns are promising strategies for preventing and treating obesity and its coexisting inflammatory processes. Bioactive food compounds have received considerable attention due to their actions against obesity-induced inflammation, with limited harmful side effects. They are perceived as food ingredients or dietary supplements [...] Read more.
Dietary patterns are promising strategies for preventing and treating obesity and its coexisting inflammatory processes. Bioactive food compounds have received considerable attention due to their actions against obesity-induced inflammation, with limited harmful side effects. They are perceived as food ingredients or dietary supplements other than those necessary to meet basic human nutritional needs and are responsible for positive changes in the state of health. These include polyphenols, unsaturated fatty acids, and probiotics. Although the exact mechanisms of bioactive food compounds’ action are still poorly understood, studies have indicated that they involve the modulation of the secretion of proinflammatory cytokines, adipokines, and hormones; regulate gene expression in adipose tissue; and modify the signaling pathways responsible for the inflammatory response. Targeting the consumption and/or supplementation of foods with anti-inflammatory potential may represent a new approach to obesity-induced inflammation treatment. Nevertheless, more studies are needed to evaluate strategies for bioactive food compound intake, especially times and doses. Moreover, worldwide education about the advantages of bioactive food compound consumption is warranted to limit the consequences of unhealthy dietary patterns. This work presents a review and synthesis of recent data on the preventive mechanisms of bioactive food compounds in the context of obesity-induced inflammation. Full article
(This article belongs to the Special Issue Oxidative Stress and Inflammation in Obesity)
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20 pages, 689 KiB  
Review
The Role of Oxidative Stress and Inflammation in Obesity and Its Impact on Cognitive Impairments—A Narrative Review
by Ruth Naomi, Soo Huat Teoh, Hashim Embong, Santhra Segaran Balan, Fezah Othman, Hasnah Bahari and Muhammad Dain Yazid
Antioxidants 2023, 12(5), 1071; https://doi.org/10.3390/antiox12051071 - 10 May 2023
Cited by 6 | Viewed by 3541
Abstract
Obesity is a chronic low-grade inflammatory condition that induces the generation of oxidative stress and inflammation. This oxidative stress and inflammation stimulate brain atrophy and some morphological changes in the brain that eventually result in cognitive impairments. However, there is no exact study [...] Read more.
Obesity is a chronic low-grade inflammatory condition that induces the generation of oxidative stress and inflammation. This oxidative stress and inflammation stimulate brain atrophy and some morphological changes in the brain that eventually result in cognitive impairments. However, there is no exact study that has summarized the role of oxidative stress and inflammation in obesity and its impact on cognitive impairments. Thus, the objective of this review is to recapitulate the current role of oxidative stress and inflammation in cognitive decline based on in vivo evidence. A comprehensive search was performed in Nature, Medline and Ovid, ScienceDirect, and PubMed, and the search was limited to the past 10 years of publication. From the search, we identified 27 articles to be further reviewed. The outcome of this study indicates that a greater amount of fat stored in individual adipocytes in obesity induces the formation of reactive oxygen species and inflammation. This will lead to the generation of oxidative stress, which may cause morphological changes in the brain, suppress the endogenous antioxidant system, and promote neuroinflammation and, eventually, neuronal apoptosis. This will impair the normal function of the brain and specific regions that are involved in learning, as well as memory. This shows that obesity has a strong positive correlation with cognitive impairments. Hence, this review summarizes the mechanism of oxidative stress and inflammation that induce memory loss based on animal model evidence. In conclusion, this review may serve as an insight into therapeutic development focusing on oxidative stress and inflammatory pathways to manage an obesity-induced cognitive decline in the future. Full article
(This article belongs to the Special Issue Oxidative Stress and Inflammation in Obesity)
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23 pages, 1379 KiB  
Review
Apolipoprotein D in Oxidative Stress and Inflammation
by Guillaume Fyfe-Desmarais, Fréderik Desmarais, Éric Rassart and Catherine Mounier
Antioxidants 2023, 12(5), 1027; https://doi.org/10.3390/antiox12051027 - 28 Apr 2023
Cited by 8 | Viewed by 2307
Abstract
Apolipoprotein D (ApoD) is lipocalin able to bind hydrophobic ligands. The APOD gene is upregulated in a number of pathologies, including Alzheimer’s disease, Parkinson’s disease, cancer, and hypothyroidism. Upregulation of ApoD is linked to decreased oxidative stress and inflammation in several models, including [...] Read more.
Apolipoprotein D (ApoD) is lipocalin able to bind hydrophobic ligands. The APOD gene is upregulated in a number of pathologies, including Alzheimer’s disease, Parkinson’s disease, cancer, and hypothyroidism. Upregulation of ApoD is linked to decreased oxidative stress and inflammation in several models, including humans, mice, Drosophila melanogaster and plants. Studies suggest that the mechanism through which ApoD modulates oxidative stress and regulate inflammation is via its capacity to bind arachidonic acid (ARA). This polyunsaturated omega-6 fatty acid can be metabolised to generate large variety of pro-inflammatory mediators. ApoD serves as a sequester, blocking and/or altering arachidonic metabolism. In recent studies of diet-induced obesity, ApoD has been shown to modulate lipid mediators derived from ARA, but also from eicosapentaenoic acid and docosahexaenoic acid in an anti-inflammatory way. High levels of ApoD have also been linked to better metabolic health and inflammatory state in the round ligament of morbidly obese women. Since ApoD expression is upregulated in numerous diseases, it might serve as a therapeutic agent against pathologies aggravated by OS and inflammation such as many obesity comorbidities. This review will present the most recent findings underlying the central role of ApoD in the modulation of both OS and inflammation. Full article
(This article belongs to the Special Issue Oxidative Stress and Inflammation in Obesity)
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