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Antioxidants
Special Issues
Oxidative Stress in Obesity—3rd Edition
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Oxidative Stress in Obesity—3rd Edition

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: 1 May 2024 | Viewed by 2421

Special Issue Editors

Dr. Ernesto Martínez-Martínez

E-Mail Website
Guest Editor
Physiology Department, School of Medicine, Universidad Complutense, Madrid, Spain
Interests: biomarmarkers; cardiovascular fibrosis; obesity; metabolic disorders; cardiovascular disease
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Victoria Cachofeiro

E-Mail Website
Guest Editor
Physiology Department, School of Medicine, Universidad Complutense, Madrid, Spain
Interests: cardiovascular fibrosis; mitochondrial function; endoplasmic reticulum stress; cardiolipotoxicity; obesity; adipose tissue dysfunction
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Our previous Special Issue on "Oxidative Stress in Obesity" received an overwhelming number of submissions and was a successful compilation of research and review articles. As this is a rapidly evolving topic, we would like to further explore the role of oxidative stress in obesity with a follow-up Special Issue for the year 2024.

Obesity is a serious public health challenge of the 21st century. The risk of a plethora of major diseases, including type 2 diabetes mellitus, cardiovascular disease, and several common cancers is dramatically increased in obese patients. In recent years, it has been recognized that oxidative stress may be the mechanistic link between obesity and related complications since oxidative stress causes tissue damage through alterations of cellular structures. The overexpression of oxidative stress together with the underproduction of the antioxidant defence could explain the pro-oxidant environment observed in obese subjects. In physiological conditions, mitochondria are the major source of intracellular reactive oxygen species production due to electron leakage along the respiratory chain; however, other sources could include plasma membrane systems, the endoplasmic reticulum, and cytosolic enzymes.

We invite you to submit your latest research findings or review article to this Special Issue, which will bring together current research concerning oxidative stress in the context of obesity for acquiring a deeper understanding of the underlying pathophysiological mechanisms that could provide novel therapeutic targets. This research can include both experimental and clinical studies relating to any of the following topics: the role of oxidative stress in obesity complications, the interaction between mitochondrial oxidative stress and endoplasmic reticulum stress or autophagy in these complications, the regulation of antioxidant defence in the context of obesity, and the effects of antioxidants in the complications associated with obesity.

We look forward to receiving your contributions.

Dr. Ernesto Martínez-Martínez
Prof. Dr. Victoria Cachofeiro
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

  • obesity
  • oxidative stress
  • antioxidant defence
  • mitochondria
  • autophagy
  • endoplasmic reticulum stress

Published Papers (3 papers)

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Research

13 pages, 833 KiB  
Article
Obesity Is Associated with Oxidative Stress Markers and Antioxidant Enzyme Activity in Mexican Children
by Ana Isabel Cota-Magaña, Miguel Vazquez-Moreno, Andrés Rocha-Aguado, Selene Ángeles-Mejía, Adán Valladares-Salgado, Margarita Díaz-Flores, Norma Edith López-Díazguerrero and Miguel Cruz
Antioxidants 2024, 13(4), 457; https://doi.org/10.3390/antiox13040457 - 12 Apr 2024
Viewed by 386
Abstract
The relationship between metabolic disorders and oxidative stress is still controversial in the child population. The present cross-sectional study aimed to analyze the associations between obesity, cardiometabolic traits, serum level of carbonylated proteins (CPs), malondialdehyde (MDA), and the enzyme activity of catalase (CAT), [...] Read more.
The relationship between metabolic disorders and oxidative stress is still controversial in the child population. The present cross-sectional study aimed to analyze the associations between obesity, cardiometabolic traits, serum level of carbonylated proteins (CPs), malondialdehyde (MDA), and the enzyme activity of catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPx) in children from Mexico City (normal weight: 120; obesity: 81). Obesity resulted in being positively associated with CAT (β = 0.05 ± 0.01, p = 5.0 × 10−3) and GPx (β = 0.13 ± 0.01, p = 3.7 × 10−19) enzyme activity. A significant interaction between obesity and sex was observed in MDA and SOD enzymatic activity (PMDA = 0.03; PSOD = 0.04). The associations between obesity, MDA level, and SOD enzyme activity were only significant in boys (boys: PMDA = 3.0 × 10−3; PSOD = 7.0 × 10−3; girls: p ≥ 0.79). In both children with normal weight and those with obesity, CP levels were positively associated with SOD enzyme activity (PNormal-weight = 2.2 × 10−3; PObesity = 0.03). In conclusion, in Mexican children, obesity is positively associated with CAT and GPx enzyme activity, and its associations with MDA levels and SOD enzyme activity are sex-specific. Therefore, CP level is positively related to SOD enzyme activity independently of body weight. Full article
(This article belongs to the Special Issue Oxidative Stress in Obesity—3rd Edition)
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19 pages, 3200 KiB  
Article
PGC-1α-Coordinated Hypothalamic Antioxidant Defense Is Linked to SP1-LanCL1 Axis during High-Fat-Diet-Induced Obesity in Male Mice
by Shuai Shi, Jichen Wang, Huan Gong, Xiaohua Huang, Bin Mu, Xiangyu Cheng, Bin Feng, Lanlan Jia, Qihui Luo, Wentao Liu, Zhengli Chen and Chao Huang
Antioxidants 2024, 13(2), 252; https://doi.org/10.3390/antiox13020252 - 19 Feb 2024
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Abstract
High-fat-diet (HFD)-induced obesity parallels hypothalamic inflammation and oxidative stress, but the correlations between them are not well-defined. Here, with mouse models targeting the antioxidant gene LanCL1 in the hypothalamus, we demonstrate that impaired hypothalamic antioxidant defense aggravates HFD-induced hypothalamic inflammation and obesity progress, [...] Read more.
High-fat-diet (HFD)-induced obesity parallels hypothalamic inflammation and oxidative stress, but the correlations between them are not well-defined. Here, with mouse models targeting the antioxidant gene LanCL1 in the hypothalamus, we demonstrate that impaired hypothalamic antioxidant defense aggravates HFD-induced hypothalamic inflammation and obesity progress, and these could be improved in mice with elevated hypothalamic antioxidant defense. We also show that peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α), a critical transcriptional coactivator, is implicated in regulating hypothalamic LanCL1 transcription, in collaboration with SP1 through a direct interaction, in response to HFD-induced palmitic acid (PA) accumulation. According to our results, when exposed to HFD, mice undergo a process of overwhelming hypothalamic antioxidant defense; short-time HFD exposure induces ROS production to activate PGC-1α and elevate LanCL1-mediated antioxidant defense, while long-time exposure promotes ubiquitin-mediated PGC-1α degradation and suppresses LanCL1 expression. Our findings show the critical importance of the hypothalamic PGC-1α-SP1-LanCL1 axis in regulating HFD-induced obesity, and provide new insights describing the correlations of hypothalamic inflammation and oxidative stress during this process. Full article
(This article belongs to the Special Issue Oxidative Stress in Obesity—3rd Edition)
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20 pages, 1765 KiB  
Article
Dietary Marine Oils Selectively Decrease Obesogenic Diet-Derived Carbonylation in Proteins Involved in ATP Homeostasis and Glutamate Metabolism in the Rat Cerebellum
by Francisco Moreno, Lucía Méndez, Ana Raner, Bernat Miralles-Pérez, Marta Romeu, Sara Ramos-Romero, Josep Lluís Torres and Isabel Medina
Antioxidants 2024, 13(1), 103; https://doi.org/10.3390/antiox13010103 - 15 Jan 2024
Viewed by 870
Abstract
The regular intake of diets high in saturated fat and sugars increases oxidative stress and has been linked to cognitive decline and premature brain aging. The cerebellum is highly vulnerable to oxidative stress and thus, obesogenic diets might be particularly detrimental to this [...] Read more.
The regular intake of diets high in saturated fat and sugars increases oxidative stress and has been linked to cognitive decline and premature brain aging. The cerebellum is highly vulnerable to oxidative stress and thus, obesogenic diets might be particularly detrimental to this tissue. However, the precise molecular mechanisms behind obesity-related brain damage are still not clear. Since protein carbonylation, a biomarker of oxidative stress, influences protein functions and is involved in metabolic control, the current investigation addressed the effect of long-term high-fat and high-sucrose diet intake on the cerebellum of Sprague-Dawley rats by deciphering the changes caused in the carbonylated proteome. The antioxidant effects of fish oil supplementation on cerebellar carbonylated proteins were also investigated. Lipid peroxidation products and carbonylated proteins were identified and quantified using immunoassays and 2D-LC-MS/MS in the cerebellum. After 21 weeks of nutritional intervention, the obesogenic diet selectively increased carbonylation of the proteins that participate in ATP homeostasis and glutamate metabolism in the cerebellum. Moreover, the data demonstrated that fish oil supplementation restrained carbonylation of the main protein targets oxidatively damaged by the obesogenic diet, and additionally protected against carbonylation of several other proteins involved in amino acid biosynthesis and neurotransmission. Therefore, dietary interventions with fish oils could help the cerebellum to be more resilient to oxidative damage. The results could shed some light on the effect of high-fat and high-sucrose diets on redox homeostasis in the cerebellum and boost the development of antioxidant-based nutritional interventions to improve cerebellum health. Full article
(This article belongs to the Special Issue Oxidative Stress in Obesity—3rd Edition)
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