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Antioxidants
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Oxidative Stress in Obesity
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Oxidative Stress 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 (31 January 2022) | Viewed by 71863

Special Issue Editors

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
Dr. Ernesto Martínez-Martínez

E-Mail Website
Guest Editor
Physiology Department, School of Medicine, Universidad Complutense, 28040 Madrid, Spain
Interests: cardiovascular disease; renal research; biomarkers; mitochondrial dysfunction
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

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 celular structures. Overexpression of oxidative stress together with under-production of antioxidant defence could explain the prooxidant enviroment 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, 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, as well as clinical studies relating to any of the following topics: the role of oxidative stress in the obesity complications, the interaction between mitochondrial oxidative stress and endoplasmic reticulum stress or autophagy in these complications, the regulation of antioxidant defense in the context of obesity, and the effects of antioxidants in the complications associated with obesity.

We look forward to receiving your contribution.

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

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Published Papers (20 papers)

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Editorial

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3 pages, 195 KiB  
Editorial
Oxidative Stress in Obesity
by Ernesto Martínez-Martínez and Victoria Cachofeiro
Antioxidants 2022, 11(4), 639; https://doi.org/10.3390/antiox11040639 - 26 Mar 2022
Cited by 7 | Viewed by 1847
Abstract
Obesity is defined by the World Health Organization (WHO) as abnormal or excessive fat accumulation that presents a health risk [...] Full article
(This article belongs to the Special Issue Oxidative Stress in Obesity)

Research

Jump to: Editorial, Review

18 pages, 3242 KiB  
Article
Exosomes from Human Placenta Choriodecidual Membrane-Derived Mesenchymal Stem Cells Mitigate Endoplasmic Reticulum Stress, Inflammation, and Lung Injury in Lipopolysaccharide-Treated Obese Mice
by Milton D. Chiang, Chao-Yuan Chang, Hung-Jen Shih, Van Long Le, Yen-Hua Huang and Chun-Jen Huang
Antioxidants 2022, 11(4), 615; https://doi.org/10.3390/antiox11040615 - 23 Mar 2022
Cited by 7 | Viewed by 3004
Abstract
Endoplasmic reticulum (ER) stress mediates the effects of obesity on aggravating sepsis-induced lung injury. We investigated whether exosomes from human placenta choriodecidual membrane-derived mesenchymal stem cells (pcMSCs) can mitigate pulmonary ER stress, lung injury, and the mechanisms of inflammation, oxidation, and apoptosis in [...] Read more.
Endoplasmic reticulum (ER) stress mediates the effects of obesity on aggravating sepsis-induced lung injury. We investigated whether exosomes from human placenta choriodecidual membrane-derived mesenchymal stem cells (pcMSCs) can mitigate pulmonary ER stress, lung injury, and the mechanisms of inflammation, oxidation, and apoptosis in lipopolysaccharide-treated obese mice. Diet-induced obese (DIO) mice (adult male C57BL/6J mice fed with a 12-week high-fat diet) received lipopolysaccharide (10 mg/kg, i.p.; DIOLPS group) or lipopolysaccharide plus exosomes (1 × 108 particles/mouse, i.p.; DIOLPSExo group). Our data demonstrated lower levels of ER stress (upregulation of glucose-regulated protein 78, phosphorylated eukaryotic initiation factor 2α, and C/EBP homologous protein; p = 0.038, <0.001, and <0.001, respectively), inflammation (activation of nuclear factor-kB, hypoxia-inducible factor-1α, macrophages, and NLR family pyrin domain containing 3; upregulation of tumor necrosis factor-α, interleukin-1β, and interleukin-6; p = 0.03, <0.001, <0.001, <0.001, <0.001, <0.001, and <0.001, respectively), lipid peroxidation (p < 0.001), and apoptosis (DNA fragmentation, p = 0.003) in lung tissues, as well as lower lung injury level (decreases in tidal volume, peak inspiratory flow, and end expiratory volume; increases in resistance, injury score, and tissue water content; p < 0.001, <0.001, <0.001, <0.001, <0.001, and =0.002, respectively) in the DIOLPSExo group than in the DIOLPS group. In conclusion, exosomes from human pcMSCs mitigate pulmonary ER stress, inflammation, oxidation, apoptosis, and lung injury in lipopolysaccharide-treated obese mice. Full article
(This article belongs to the Special Issue Oxidative Stress in Obesity)
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24 pages, 5355 KiB  
Article
Anti-Obesity Effects of Ecklonia cava Extract in High-Fat Diet-Induced Obese Rats
by Muhammad Aleem Abbas, Naila Boby, Eon-Bee Lee, Joo-Heon Hong and Seung-Chun Park
Antioxidants 2022, 11(2), 310; https://doi.org/10.3390/antiox11020310 - 3 Feb 2022
Cited by 16 | Viewed by 3308
Abstract
Obesity is becoming a global epidemic as a result of high-calorie food intake and unhealthy lifestyles. Different marine plants, especially brown algae (Ecklonia cava), are traditionally used to treat different health-related issues. The study was carried out to investigate the anti-obesity [...] Read more.
Obesity is becoming a global epidemic as a result of high-calorie food intake and unhealthy lifestyles. Different marine plants, especially brown algae (Ecklonia cava), are traditionally used to treat different health-related issues. The study was carried out to investigate the anti-obesity properties of E. cava 70% ethanol extract. To evaluate the anti-obesity effect of E. cava, both in vitro and in vivo tests were performed. E. cava suppresses pre-adipocyte 3T3-L1 differentiation in a dose-dependent manner. In HFD-induced obese rats’ models, administration of E. cava 125, 250, and 500 mg/kg significantly decreases total body weight and organs, especially liver weight, in all treatment groups. Adipose tissue weight, including subcutaneous, epididymal, peritoneal, and mesenteric adipose tissue, was markedly reduced in E. cava-treated HFD rats in dose-dependent manners. In addition, liver-related biomarkers AST, ALP, ALT, and GGT were evaluated; the lower level of liver-related biomarkers indicates no liver injury or fatty liver issue in E. cava HFD treatment groups. In addition, E. cava treatment has significant effects on the expression of adipogenic and lipogenic (PPAR-γ, FAS, LPL, and SREBP-1c) genes. Altogether, these results show the anti-obesity effect of E. cava. We concluded that E. cava could be a potential candidate for the prevention of obesity-induced by a high-fat diet. Full article
(This article belongs to the Special Issue Oxidative Stress in Obesity)
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15 pages, 2178 KiB  
Article
A Mixture of Pure, Isolated Polyphenols Worsens the Insulin Resistance and Induces Kidney and Liver Fibrosis Markers in Diet-Induced Obese Mice
by Hèctor Sanz-Lamora, Pedro F. Marrero, Diego Haro and Joana Relat
Antioxidants 2022, 11(1), 120; https://doi.org/10.3390/antiox11010120 - 5 Jan 2022
Cited by 3 | Viewed by 2569
Abstract
Obesity is a worldwide epidemic with severe metabolic consequences. Polyphenols are secondary metabolites in plants and the most abundant dietary antioxidants, which possess a wide range of health effects. The most relevant food sources are fruit and vegetables, red wine, black and green [...] Read more.
Obesity is a worldwide epidemic with severe metabolic consequences. Polyphenols are secondary metabolites in plants and the most abundant dietary antioxidants, which possess a wide range of health effects. The most relevant food sources are fruit and vegetables, red wine, black and green tea, coffee, virgin olive oil, and chocolate, as well as nuts, seeds, herbs, and spices. The aim of this work was to evaluate the ability of a pure, isolated polyphenol supplementation to counteract the pernicious metabolic effects of a high-fat diet (HFD). Our results indicated that the administration of pure, isolated polyphenols under HFD conditions for 26 weeks worsened the glucose metabolism in diet-induced obese mice. The data showed that the main target organ for these undesirable effects were the kidneys, where we observed fibrotic, oxidative, and kidney-disease markers. This work led us to conclude that the administration of pure polyphenols as a food supplement would not be advisable. Instead, the ingestion of complete “whole” foods would be the best way to get the health effects of bioactive compounds such as polyphenols. Full article
(This article belongs to the Special Issue Oxidative Stress in Obesity)
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16 pages, 1369 KiB  
Article
“Obesity and Insulin Resistance” Is the Component of the Metabolic Syndrome Most Strongly Associated with Oxidative Stress
by Grzegorz K. Jakubiak, Kamila Osadnik, Mateusz Lejawa, Tadeusz Osadnik, Marcin Goławski, Piotr Lewandowski and Natalia Pawlas
Antioxidants 2022, 11(1), 79; https://doi.org/10.3390/antiox11010079 - 29 Dec 2021
Cited by 49 | Viewed by 4706
Abstract
Metabolic syndrome (MS) is not a homogeneous entity, but this term refers to the coexistence of factors that increase the risk for the development of type 2 diabetes and cardiovascular disease. There are different versions of the criteria for the diagnosis of MS, [...] Read more.
Metabolic syndrome (MS) is not a homogeneous entity, but this term refers to the coexistence of factors that increase the risk for the development of type 2 diabetes and cardiovascular disease. There are different versions of the criteria for the diagnosis of MS, which makes the population of patients diagnosed with MS heterogeneous. Research to date shows that MS is associated with oxidative stress (OS), but it is unclear which MS component is most strongly associated with OS. The purpose of the study was to investigate the relationship between the parameters of OS and the presence of individual elements of MS in young adults, as well as to identify the components of MS by means of principal components analysis (PCA) and to investigate how the parameters of OS correlate with the presence of individual components. The study included 724 young adults with or without a family history of coronary heart disease (population of the MAGNETIC study). Blood samples were taken from the participants of the study to determine peripheral blood counts, biochemical parameters, and selected parameters of OS. In addition, blood pressure and anthropometric parameters were measured. In subjects with MS, significantly lower activity of superoxide dismutase (SOD), copper- and zinc-containing SOD (CuZnSOD), and manganese-containing SOD (MnSOD) were found, along with significantly higher total antioxidant capacity (TAC) and significantly lower concentration of thiol groups per gram of protein (PSH). We identified three components of MS by means of PCA: “Obesity and insulin resistance”, “Dyslipidemia”, and “Blood pressure”, and showed the component “Obesity and insulin resistance” to have the strongest relationship with OS. In conclusion, we documented significant differences in some parameters of OS between young adults with and without MS. We showed that “Obesity and insulin resistance” is the most important component of MS in terms of relationship with OS. Full article
(This article belongs to the Special Issue Oxidative Stress in Obesity)
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16 pages, 2442 KiB  
Article
The Interplay of Mitochondrial Oxidative Stress and Endoplasmic Reticulum Stress in Cardiovascular Fibrosis in Obese Rats
by Francisco V. Souza-Neto, Sara Jiménez-González, Beatriz Delgado-Valero, Raquel Jurado-López, Marie Genty, Ana Romero-Miranda, Cristina Rodríguez, María Luisa Nieto, Ernesto Martínez-Martínez and Victoria Cachofeiro
Antioxidants 2021, 10(8), 1274; https://doi.org/10.3390/antiox10081274 - 11 Aug 2021
Cited by 21 | Viewed by 3951
Abstract
We have evaluated the role of mitochondrial oxidative stress and its association with endoplasmic reticulum (ER) stress activation in the progression of obesity-related cardiovascular fibrosis. MitoQ (200 µM) was orally administered for 7 weeks to male Wistar rats that were fed a high-fat [...] Read more.
We have evaluated the role of mitochondrial oxidative stress and its association with endoplasmic reticulum (ER) stress activation in the progression of obesity-related cardiovascular fibrosis. MitoQ (200 µM) was orally administered for 7 weeks to male Wistar rats that were fed a high-fat diet (HFD, 35% fat) or a control diet (CT, 3.5% fat). Obese animals presented cardiovascular fibrosis accompanied by increased levels of extracellular matrix proteins and profibrotic mediators. These alterations were associated with ER stress activation characterized by enhanced levels (in heart and aorta vs. CT group, respectively) of immunoglobulin binding protein (BiP; 2.1-and 2.6-fold, respectively), protein disulfide-isomerase A6 (PDIA6; 1.9-fold) and CCAAT-enhancer-binding homologous protein (CHOP; 1.5- and 1.8-fold, respectively). MitoQ treatment was able to prevent (p < 0.05) these modifications at cardiac and aortic levels. MitoQ (5 nM) and the ER stress inhibitor, 4-phenyl butyric acid (4 µM), were able to block the prooxidant and profibrotic effects of angiotensin II (Ang II, 10−6 M) in cardiac and vascular cells. Therefore, the data show a crosstalk between mitochondrial oxidative stress and ER stress activation, which mediates the development of cardiovascular fibrosis in the context of obesity and in which Ang II can play a relevant role. Full article
(This article belongs to the Special Issue Oxidative Stress in Obesity)
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12 pages, 1897 KiB  
Article
Moderate Caloric Restriction Partially Improved Oxidative Stress Markers in Obese Humans
by Dominika Kanikowska, Alina Kanikowska, Ewelina Swora-Cwynar, Marian Grzymisławski, Maki Sato, Andrzej Bręborowicz, Janusz Witowski and Katarzyna Korybalska
Antioxidants 2021, 10(7), 1018; https://doi.org/10.3390/antiox10071018 - 24 Jun 2021
Cited by 20 | Viewed by 2409
Abstract
Oxidative stress and inflammation are implicated in obesity. Therefore, we investigated whether moderate and short-term calorie restriction (CR) reflects a real-life situation, mediates weight loss, and improves oxidative stress markers. We analyzed oxidative stress markers in patients with obesity undergoing moderate CR. Serum [...] Read more.
Oxidative stress and inflammation are implicated in obesity. Therefore, we investigated whether moderate and short-term calorie restriction (CR) reflects a real-life situation, mediates weight loss, and improves oxidative stress markers. We analyzed oxidative stress markers in patients with obesity undergoing moderate CR. Serum oxidative stress markers (myeloperoxidase (MPO), superoxide dismutase (SOD), catalase, total antioxidant status (TAS), and reactive oxygen species (ROS) (generation by endothelial cells in vitro)) were measured in 53 subjects (mean BMI 37.8 ± 5.9 kg/m2) who underwent 8 weeks of CR, which included a reduction of 300–500 kcal/day. MPO was the most CR-sensitive parameter. The mean level of serum MPO in patients with obesity was 20% higher than that in post CR intervention (p < 0.001). SOD increased by 12% after CR (p < 0.05), which was largely due to the improvement in glucose tolerance and the reduction in insulin resistance after CR. Other tested parameters were not modified during the treatment. CR resulted in an expected decrease in body weight (by 5.9 ± 4.6 kg, p < 0.0001) and other anthropometric parameters. Additionally, it was accompanied by a significant change in hsCRP, hsTNF alpha, hsIL-6, leptin (all p < 0.0001), and HOMA-IR (p < 0.05). Cardiovascular and metabolic parameters were also partially improved. Short-term, moderate CR partially improves antioxidant capacity but is enough to substantially change anthropometric parameters in obese patients. Our observations indicate that mimicking real-life situations and low-cost dietary intervention can be successfully implemented in obesity treatment with a simultaneous moderate effect on antioxidant status. Full article
(This article belongs to the Special Issue Oxidative Stress in Obesity)
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13 pages, 3103 KiB  
Article
Enhancement of the Antiobesity and Antioxidant Effect of Purple Sweet Potato Extracts and Enhancement of the Effects by Fermentation
by Seul Gi Lee, Jongbeom Chae, Dong Se Kim, Jung-Bok Lee, Gi-Seok Kwon, Taeg Kyu Kwon and Ju-Ock Nam
Antioxidants 2021, 10(6), 888; https://doi.org/10.3390/antiox10060888 - 31 May 2021
Cited by 7 | Viewed by 3071
Abstract
The browning of white adipocytes, which transforms energy-storing white adipocytes to heat-producing beige adipocytes, is considered a strategy against metabolic diseases. Several dietary compounds, such as anthocyanins, flavonoids, and phenolic acids, induce a brown adipocyte-like phenotype in white adipocytes. In this study, we [...] Read more.
The browning of white adipocytes, which transforms energy-storing white adipocytes to heat-producing beige adipocytes, is considered a strategy against metabolic diseases. Several dietary compounds, such as anthocyanins, flavonoids, and phenolic acids, induce a brown adipocyte-like phenotype in white adipocytes. In this study, we demonstrated that purple sweet potato (Ipomoea batatas) extract (PSP) exhibited potent radical scavenging activity. In addition, PSP was found to contain large amounts of phenolic, flavonoid, and anthocyanin compounds; the amount of these compounds was affected by fermentation. Functionally, PSP-induced adipose browning in high-fat-diet (HFD)-induced obese mice. The administration of PSP significantly suppressed the body weight gain and abnormal expansion of white adipose tissues in the obese mice. The expression of adipose browning-related genes was higher in the inguinal white adipose tissues from the PSP-treated mice than those in the HFD-fed mice. Moreover, PSP-treated 3T3-L1 adipocytes formed multilocular lipid droplets, similar to those formed in the 3T3-L1 adipocytes treated with a browning induction cocktail. The PSP-treated cells had an increased expression level of mitochondria and lipolysis-related genes. The browning effects of PSP were enhanced by fermentation with Lactobacillus. This study, to our knowledge, is the first to identify a new mechanism to increase the antiobesity effects of PSP by inducing adipocyte browning of adipocytes. Full article
(This article belongs to the Special Issue Oxidative Stress in Obesity)
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16 pages, 838 KiB  
Article
Association of Metabolically Healthy and Unhealthy Obesity Phenotypes with Oxidative Stress Parameters and Telomere Length in Healthy Young Adult Men. Analysis of the MAGNETIC Study
by Mateusz Lejawa, Kamila Osadnik, Tadeusz Osadnik and Natalia Pawlas
Antioxidants 2021, 10(1), 93; https://doi.org/10.3390/antiox10010093 - 11 Jan 2021
Cited by 18 | Viewed by 2828
Abstract
Obesity is a significant factor related to metabolic disturbances that can lead to metabolic syndrome (MetS). Metabolic dysregulation causes oxidative stress, which affects telomere structure. The current study aimed to evaluate the relationships between telomere length, oxidative stress and the metabolically healthy and [...] Read more.
Obesity is a significant factor related to metabolic disturbances that can lead to metabolic syndrome (MetS). Metabolic dysregulation causes oxidative stress, which affects telomere structure. The current study aimed to evaluate the relationships between telomere length, oxidative stress and the metabolically healthy and unhealthy phenotypes in healthy young men. Ninety-eight participants were included in the study (49 healthy slim and 49 obese patients). Study participants were divided into three subgroups according to body mass index and metabolic health. Selected oxidative stress markers were measured in serum. Relative telomere length (rTL) was measured using quantitative polymerase chain reaction. The analysis showed associations between laboratory markers, oxidative stress markers and rTL in metabolically healthy and unhealthy participants. Total oxidation status (TOS), total antioxidant capacity (TAC) and rTL were significantly connected with metabolically unhealthy obesity. TAC was associated with metabolically healthy obesity. Telomeres shorten in patients with metabolic dysregulation related to oxidative stress and obesity linked to MetS. Further studies among young metabolically healthy and unhealthy individuals are needed to determine the pathways related to metabolic disturbances that cause oxidative stress that leads to MetS. Full article
(This article belongs to the Special Issue Oxidative Stress in Obesity)
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23 pages, 3717 KiB  
Article
Western Diet Causes Obesity-Induced Nonalcoholic Fatty Liver Disease Development by Differentially Compromising the Autophagic Response
by Ines C. M. Simoes, Agnieszka Karkucinska-Wieckowska, Justyna Janikiewicz, Sylwia Szymanska, Maciej Pronicki, Pawel Dobrzyn, Michal Dabrowski, Agnieszka Dobrzyn, Paulo J. Oliveira, Hans Zischka, Yaiza Potes and Mariusz R. Wieckowski
Antioxidants 2020, 9(10), 995; https://doi.org/10.3390/antiox9100995 - 15 Oct 2020
Cited by 28 | Viewed by 3912
Abstract
Nonalcoholic fatty liver disease (NAFLD) is characterized by the development of steatosis, which can ultimately compromise liver function. Mitochondria are key players in obesity-induced metabolic disorders; however, the distinct role of hypercaloric diet constituents in hepatic cellular oxidative stress and metabolism is unknown. [...] Read more.
Nonalcoholic fatty liver disease (NAFLD) is characterized by the development of steatosis, which can ultimately compromise liver function. Mitochondria are key players in obesity-induced metabolic disorders; however, the distinct role of hypercaloric diet constituents in hepatic cellular oxidative stress and metabolism is unknown. Male mice were fed either a high-fat (HF) diet, a high-sucrose (HS) diet or a combined HF plus HS (HFHS) diet for 16 weeks. This study shows that hypercaloric diets caused steatosis; however, the HFHS diet induced severe fibrotic phenotype. At the mitochondrial level, lipidomic analysis showed an increased cardiolipin content for all tested diets. Despite this, no alterations were found in the coupling efficiency of oxidative phosphorylation and neither in mitochondrial fatty acid oxidation (FAO). Consistent with unchanged mitochondrial function, no alterations in mitochondrial-induced reactive oxygen species (ROS) and antioxidant capacity were found. In contrast, the HF and HS diets caused lipid peroxidation and provoked altered antioxidant enzyme levels/activities in liver tissue. Our work provides evidence that hepatic oxidative damage may be caused by augmented levels of peroxisomes and consequently higher peroxisomal FAO-induced ROS in the early NAFLD stage. Hepatic damage is also associated with autophagic flux impairment, which was demonstrated to be diet-type dependent. The HS diet induced a reduction in autophagosomal formation, while the HF diet reduced levels of cathepsins. The accumulation of damaged organelles could instigate hepatocyte injuries and NAFLD progression. Full article
(This article belongs to the Special Issue Oxidative Stress in Obesity)
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17 pages, 2732 KiB  
Article
Myeloid GRK2 Regulates Obesity-Induced Endothelial Dysfunction by Modulating Inflammatory Responses in Perivascular Adipose Tissue
by María González-Amor, Rocío Vila-Bedmar, Raquel Rodrigues-Díez, Rosa Moreno-Carriles, Alba C. Arcones, Marta Cruces-Sande, Mercedes Salaices, Federico Mayor, Jr., Ana M. Briones and Cristina Murga
Antioxidants 2020, 9(10), 953; https://doi.org/10.3390/antiox9100953 - 4 Oct 2020
Cited by 4 | Viewed by 2826
Abstract
Perivascular adipose tissue (PVAT) is increasingly being regarded as an important endocrine organ that directly impacts vessel function, structure, and contractility in obesity-associated diseases. We uncover here a role for myeloid G protein-coupled receptor kinase 2 (GRK2) in the modulation of PVAT-dependent vasodilation [...] Read more.
Perivascular adipose tissue (PVAT) is increasingly being regarded as an important endocrine organ that directly impacts vessel function, structure, and contractility in obesity-associated diseases. We uncover here a role for myeloid G protein-coupled receptor kinase 2 (GRK2) in the modulation of PVAT-dependent vasodilation responses. GRK2 expression positively correlates with myeloid- (CD68) and lymphoid-specific (CD3, CD4, and CD8) markers and with leptin in PVAT from patients with abdominal aortic aneurysms. Using mice hemizygous for GRK2 in the myeloid lineage (LysM-GRK2+/−), we found that GRK2 deficiency in myeloid cells allows animals to preserve the endothelium-dependent acetylcholine or insulin-induced relaxation, which is otherwise impaired by PVAT, in arteries of animals fed a high fat diet (HFD). Downregulation of GRK2 in myeloid cells attenuates HFD-dependent infiltration of macrophages and T lymphocytes in PVAT, as well as the induction of tumor necrosis factor-α (TNFα) and NADPH oxidase (Nox)1 expression, whereas blocking TNFα or Nox pathways by pharmacological means can rescue the impaired vasodilator responses to insulin in arteries with PVAT from HFD-fed animals. Our results suggest that myeloid GRK2 could be a potential therapeutic target in the development of endothelial dysfunction induced by PVAT in the context of obesity. Full article
(This article belongs to the Special Issue Oxidative Stress in Obesity)
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14 pages, 407 KiB  
Article
Systemic Oxidative Stress and Visceral Adipose Tissue Mediators of NLRP3 Inflammasome and Autophagy Are Reduced in Obese Type 2 Diabetic Patients Treated with Metformin
by Zaida Abad-Jiménez, Sandra López-Domènech, Rubén Díaz-Rúa, Francesca Iannantuoni, Segundo Ángel Gómez-Abril, Dolores Periañez-Gómez, Carlos Morillas, Víctor M. Víctor and Milagros Rocha
Antioxidants 2020, 9(9), 892; https://doi.org/10.3390/antiox9090892 - 21 Sep 2020
Cited by 14 | Viewed by 3258
Abstract
Obesity is a low-grade inflammatory condition affecting a range of individuals, from metabolically healthy obese (MHO) subjects to type 2 diabetes (T2D) patients. Metformin has been shown to display anti-inflammatory properties, though the underlying molecular mechanisms are unclear. To study whether the effects [...] Read more.
Obesity is a low-grade inflammatory condition affecting a range of individuals, from metabolically healthy obese (MHO) subjects to type 2 diabetes (T2D) patients. Metformin has been shown to display anti-inflammatory properties, though the underlying molecular mechanisms are unclear. To study whether the effects of metformin are mediated by changes in the inflammasome complex and autophagy in visceral adipose tissue (VAT) of obese patients, a biopsy of VAT was obtained from a total of 68 obese patients undergoing gastric bypass surgery. The patients were clustered into two groups: MHO patients and T2D patients treated with metformin. Patients treated with metformin showed decreased levels of all analyzed serum pro-inflammatory markers (TNFα, IL6, IL1β and MCP1) and a downwards trend in IL18 levels associated with a lower production of oxidative stress markers in leukocytes (mitochondrial ROS and myeloperoxidase (MPO)). A reduction in protein levels of MCP1, NFκB, NLRP3, ASC, ATG5, Beclin1 and CHOP and an increase in p62 were also observed in the VAT of the diabetic group. This downregulation of both the NLRP3 inflammasome and autophagy in VAT may be associated with the improved inflammatory profile and leukocyte homeostasis seen in obese T2D patients treated with metformin with respect to MHO subjects and endorses the cardiometabolic protective effect of this drug. Full article
(This article belongs to the Special Issue Oxidative Stress in Obesity)
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14 pages, 1090 KiB  
Article
Effect of Roux-en-Y Bariatric Bypass Surgery on Subclinical Atherosclerosis and Oxidative Stress Markers in Leukocytes of Obese Patients: A One-Year Follow-Up Study
by Zaida Abad-Jiménez, Sandra López-Domènech, Segundo Ángel Gómez-Abril, Dolores Periañez-Gómez, Aranzazu M. de Marañón, Celia Bañuls, Carlos Morillas, Víctor M. Víctor and Milagros Rocha
Antioxidants 2020, 9(8), 734; https://doi.org/10.3390/antiox9080734 - 11 Aug 2020
Cited by 11 | Viewed by 2418
Abstract
Little is known about the mechanisms underlying the cardioprotective effect of Roux en-Y gastric bypass (RYGB) surgery. Therefore, the aim of the present study was to investigate whether weight loss associated with RYGB improves the oxidative status of leukocytes and ameliorates subclinical atherosclerotic [...] Read more.
Little is known about the mechanisms underlying the cardioprotective effect of Roux en-Y gastric bypass (RYGB) surgery. Therefore, the aim of the present study was to investigate whether weight loss associated with RYGB improves the oxidative status of leukocytes and ameliorates subclinical atherosclerotic markers. This is an interventional study of 57 obese subjects who underwent RYGB surgery. We determined biochemical parameters and qualitative analysis of cholesterol, leukocyte and systemic oxidative stress markers —superoxide production, glutathione peroxidase 1 (GPX1), superoxide dismutase (SOD) activity and protein carbonylation—, soluble cellular adhesion molecules —sICAM-1 and sP-selectin—, myeloperoxidase (MPO) and leukocyte-endothelium cell interactions—rolling flux, velocity and adhesion. RYGB induced an improvement in metabolic parameters, including hsCRP and leukocyte count (p < 0.001, for both). This was associated with an amelioration in oxidative stress, since superoxide production and protein carbonylation were reduced (p < 0.05 and p < 0.01, respectively) and antioxidant systems were enhanced (GPX1; p < 0.05 and SOD; p < 0.01). In addition, a significant reduction of the following parameters was observed one year after RYGB: MPO and sICAM (p < 0.05, for both), sPselectin and pattern B of LDL particles (p < 0.001, for both), and rolling flux and adhesion of leukocytes (p < 0.05 and p < 0.01, respectively). Our results suggest that patients undergoing RYGB benefit from an amelioration of the prooxidant status of leukocytes, metabolic outcomes, and subclinical markers of atherosclerosis. Full article
(This article belongs to the Special Issue Oxidative Stress in Obesity)
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15 pages, 3385 KiB  
Article
The Interaction between Mitochondrial Oxidative Stress and Gut Microbiota in the Cardiometabolic Consequences in Diet-Induced Obese Rats
by Adriana Ortega-Hernández, Ernesto Martínez-Martínez, Ruben Gómez-Gordo, Natalia López-Andrés, Amaya Fernández-Celis, Beatriz Gutiérrrez-Miranda, María Luisa Nieto, Teresa Alarcón, Claudio Alba, Dulcenombre Gómez-Garre and Victoria Cachofeiro
Antioxidants 2020, 9(7), 640; https://doi.org/10.3390/antiox9070640 - 21 Jul 2020
Cited by 23 | Viewed by 3753
Abstract
Background: The objective of this study is to determine the role of mitochondrial oxidative stress in the dysbiosis associated with a high fat diet in rats. In addition, the impact of gut microbiota (GM) in the cardiometabolic consequences of diet-induced obesity in rats [...] Read more.
Background: The objective of this study is to determine the role of mitochondrial oxidative stress in the dysbiosis associated with a high fat diet in rats. In addition, the impact of gut microbiota (GM) in the cardiometabolic consequences of diet-induced obesity in rats has been evaluated. Methods: Male Wistar rats were fed either a high fat diet (HFD) or a control (CT) one for 6 weeks. At the third week, one-half of the animals of each group were treated with the mitochondrial antioxidant MitoTempo (MT; 0.7 mgKg−1day−1 i.p). Results: Animals fed an HFD showed a lower microbiota evenness and diversity in comparison to CT rats. This dysbiosis is characterized by a decrease in Firmicutes/Bacteroidetes ratio and relevant changes at family and genera compared with the CT group. This was accompanied by a reduction in colonic mucin-secreting goblet cells. These changes were reversed by MT treatment. The abundance of certain genera could also be relevant in the metabolic consequences of obesity, as well as in the occurrence of cardiac fibrosis associated with obesity. Conclusions: These results support an interaction between GM and mitochondrial oxidative stress and its relation with development of cardiac fibrosis, suggesting new approaches in the management of obesity-related cardiometabolic consequences. Full article
(This article belongs to the Special Issue Oxidative Stress in Obesity)
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24 pages, 2328 KiB  
Review
Natural Antioxidant Application on Fat Accumulation: Preclinical Evidence
by Proshanta Roy, Daniele Tomassoni, Enea Traini, Ilenia Martinelli, Maria Vittoria Micioni Di Bonaventura, Carlo Cifani, Francesco Amenta and Seyed Khosrow Tayebati
Antioxidants 2021, 10(6), 858; https://doi.org/10.3390/antiox10060858 - 27 May 2021
Cited by 9 | Viewed by 3102
Abstract
Obesity represents one of the most important challenges in the contemporary world that must be overcome. Different pathological consequences of these physical conditions have been studied for more than 30 years. The most nagging effects were found early in the cardiovascular system. However, [...] Read more.
Obesity represents one of the most important challenges in the contemporary world that must be overcome. Different pathological consequences of these physical conditions have been studied for more than 30 years. The most nagging effects were found early in the cardiovascular system. However, later, its negative impact was also investigated in several other organs. Damage at cellular structures due to overexpression of reactive oxygen species together with mechanisms that cause under-production of antioxidants leads to the development of obesity-related complications. In this view, the negative results of oxidant molecules due to obesity were studied in various districts of the body. In the last ten years, scientific literature has reported reasonable evidence regarding natural and synthetic compounds’ supplementation, which showed benefits in reducing oxidative stress and inflammatory processes in animal models of obesity. This article attempts to clarify the role of oxidative stress due to obesity and the opposing role of antioxidants to counter it, reported in preclinical studies. This analysis aims to clear-up different mechanisms that lead to the build-up of pro-oxidants during obesity and how various molecules of different origins hinder this phenomenon, behaving as antioxidants. Full article
(This article belongs to the Special Issue Oxidative Stress in Obesity)
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13 pages, 7374 KiB  
Review
Oxidized Albumin as a Mediator of Kidney Disease
by Stefanny M. Figueroa, Patricio Araos, Javier Reyes, Basile Gravez, Jonatan Barrera-Chimal and Cristián A. Amador
Antioxidants 2021, 10(3), 404; https://doi.org/10.3390/antiox10030404 - 8 Mar 2021
Cited by 14 | Viewed by 4327
Abstract
Renal diseases are a global health concern, and nearly 24% of kidney disease patients are overweight or obese. Particularly, increased body mass index has been correlated with oxidative stress and urinary albumin excretion in kidney disease patients, also contributing to increased cardiovascular risk. [...] Read more.
Renal diseases are a global health concern, and nearly 24% of kidney disease patients are overweight or obese. Particularly, increased body mass index has been correlated with oxidative stress and urinary albumin excretion in kidney disease patients, also contributing to increased cardiovascular risk. Albumin is the main plasma protein and is able to partially cross the glomerular filtration barrier, being reabsorbed mainly by the proximal tubule through different mechanisms. However, it has been demonstrated that albumin suffers different posttranslational modifications, including oxidation, which appears to be tightly linked to kidney damage progression and is increased in obese patients. Plasma-oxidized albumin levels correlate with a decrease in estimated glomerular filtration rate and an increase in blood urea nitrogen in patients with chronic kidney disease. Moreover, oxidized albumin in kidney disease patients is independently correlated with higher plasma levels of transforming growth factor beta (TGF-β1), tumor necrosis factor (TNF-α), and interleukin (IL)-1β and IL-6. In addition, oxidized albumin exerts a direct effect on neutrophils by augmenting the levels of neutrophil gelatinase-associated lipocalin, a well-accepted biomarker for renal damage in patients and in different experimental settings. Moreover, it has been suggested that albumin oxidation occurs at early stages of chronic kidney disease, accelerating the patient requirements for dialytic treatment during disease progression. In this review, we summarize the evidence supporting the role of overweight- and obesity-induced oxidative stress as a critical factor for the progression of renal disease and cardiovascular morbimortality through albumin oxidation. Full article
(This article belongs to the Special Issue Oxidative Stress in Obesity)
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14 pages, 10399 KiB  
Review
Targeting Autophagy to Counteract Obesity-Associated Oxidative Stress
by Federico Pietrocola and José Manuel Bravo-San Pedro
Antioxidants 2021, 10(1), 102; https://doi.org/10.3390/antiox10010102 - 12 Jan 2021
Cited by 36 | Viewed by 3357
Abstract
Reactive oxygen species (ROS) operate as key regulators of cellular homeostasis within a physiological range of concentrations, yet they turn into cytotoxic entities when their levels exceed a threshold limit. Accordingly, ROS are an important etiological cue for obesity, which in turn represents [...] Read more.
Reactive oxygen species (ROS) operate as key regulators of cellular homeostasis within a physiological range of concentrations, yet they turn into cytotoxic entities when their levels exceed a threshold limit. Accordingly, ROS are an important etiological cue for obesity, which in turn represents a major risk factor for multiple diseases, including diabetes, cardiovascular disorders, non-alcoholic fatty liver disease, and cancer. Therefore, the implementation of novel therapeutic strategies to improve the obese phenotype by targeting oxidative stress is of great interest for the scientific community. To this end, it is of high importance to shed light on the mechanisms through which cells curtail ROS production or limit their toxic effects, in order to harness them in anti-obesity therapy. In this review, we specifically discuss the role of autophagy in redox biology, focusing on its implication in the pathogenesis of obesity. Because autophagy is specifically triggered in response to redox imbalance as a quintessential cytoprotective mechanism, maneuvers based on the activation of autophagy hold promises of efficacy for the prevention and treatment of obesity and obesity-related morbidities. Full article
(This article belongs to the Special Issue Oxidative Stress in Obesity)
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20 pages, 1243 KiB  
Review
N-Acetyl Cysteine Targets Hepatic Lipid Accumulation to Curb Oxidative Stress and Inflammation in NAFLD: A Comprehensive Analysis of the Literature
by Phiwayinkosi V. Dludla, Bongani B. Nkambule, Sithandiwe E. Mazibuko-Mbeje, Tawanda M. Nyambuya, Fabio Marcheggiani, Ilenia Cirilli, Khanyisani Ziqubu, Samukelisiwe C. Shabalala, Rabia Johnson, Johan Louw, Elisabetta Damiani and Luca Tiano
Antioxidants 2020, 9(12), 1283; https://doi.org/10.3390/antiox9121283 - 16 Dec 2020
Cited by 40 | Viewed by 6511
Abstract
Impaired adipose tissue function and insulin resistance remain instrumental in promoting hepatic lipid accumulation in conditions of metabolic syndrome. In fact, enhanced lipid accumulation together with oxidative stress and an abnormal inflammatory response underpin the development and severity of non-alcoholic fatty liver disease [...] Read more.
Impaired adipose tissue function and insulin resistance remain instrumental in promoting hepatic lipid accumulation in conditions of metabolic syndrome. In fact, enhanced lipid accumulation together with oxidative stress and an abnormal inflammatory response underpin the development and severity of non-alcoholic fatty liver disease (NAFLD). There are currently no specific protective drugs against NAFLD, and effective interventions involving regular exercise and healthy diets have proved difficult to achieve and maintain. Alternatively, due to its antioxidant and anti-inflammatory properties, there has been growing interest in understanding the therapeutic effects of N-acetyl cysteine (NAC) against metabolic complications, including NAFLD. Here, reviewed evidence suggests that NAC blocks hepatic lipid accumulation in preclinical models of NAFLD. This is in part through the effective regulation of a fatty acid scavenger molecule (CD36) and transcriptional factors such as sterol regulatory element-binding protein (SREBP)-1c/-2 and peroxisome proliferator-activated receptor gamma (PPARγ). Importantly, NAC appears effective in improving liver function by reducing pro-inflammatory markers such as interleukin (IL)-6 IL-1β, tumour necrosis factor alpha (TNF-α) and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB). This was primarily through the attenuation of lipid peroxidation and enhancements in intracellular response antioxidants, particularly glutathione. Very few clinical studies support the beneficial effects of NAC against NAFLD-related complications, thus well-organized randomized clinical trials are still necessary to confirm its therapeutic potential. Full article
(This article belongs to the Special Issue Oxidative Stress in Obesity)
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21 pages, 616 KiB  
Review
Neural Underpinnings of Obesity: The Role of Oxidative Stress and Inflammation in the Brain
by Caitlyn A. Mullins, Ritchel B. Gannaban, Md Shahjalal Khan, Harsh Shah, Md Abu B. Siddik, Vijay K. Hegde, P. Hemachandra Reddy and Andrew C. Shin
Antioxidants 2020, 9(10), 1018; https://doi.org/10.3390/antiox9101018 - 20 Oct 2020
Cited by 31 | Viewed by 4433
Abstract
Obesity prevalence is increasing at an unprecedented rate throughout the world, and is a strong risk factor for metabolic, cardiovascular, and neurological/neurodegenerative disorders. While low-grade systemic inflammation triggered primarily by adipose tissue dysfunction is closely linked to obesity, inflammation is also observed in [...] Read more.
Obesity prevalence is increasing at an unprecedented rate throughout the world, and is a strong risk factor for metabolic, cardiovascular, and neurological/neurodegenerative disorders. While low-grade systemic inflammation triggered primarily by adipose tissue dysfunction is closely linked to obesity, inflammation is also observed in the brain or the central nervous system (CNS). Considering that the hypothalamus, a classical homeostatic center, and other higher cortical areas (e.g. prefrontal cortex, dorsal striatum, hippocampus, etc.) also actively participate in regulating energy homeostasis by engaging in inhibitory control, reward calculation, and memory retrieval, understanding the role of CNS oxidative stress and inflammation in obesity and their underlying mechanisms would greatly help develop novel therapeutic interventions to correct obesity and related comorbidities. Here we review accumulating evidence for the association between ER stress and mitochondrial dysfunction, the main culprits responsible for oxidative stress and inflammation in various brain regions, and energy imbalance that leads to the development of obesity. Potential beneficial effects of natural antioxidant and anti-inflammatory compounds on CNS health and obesity are also discussed. Full article
(This article belongs to the Special Issue Oxidative Stress in Obesity)
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18 pages, 2450 KiB  
Review
The Interplay between Oxidative Stress and miRNAs in Obesity-Associated Hepatic and Vascular Complications
by Jorge Infante-Menéndez, Andrea R. López-Pastor, Paula González-López, Almudena Gómez-Hernández and Oscar Escribano
Antioxidants 2020, 9(7), 607; https://doi.org/10.3390/antiox9070607 - 10 Jul 2020
Cited by 11 | Viewed by 3519
Abstract
Nowadays, the obesity pandemic is one of the most relevant health issues worldwide. This condition is tightly related to comorbidities such as non-alcoholic fatty liver disease (NAFLD) and cardiovascular diseases (CVDs), namely atherosclerosis. Dysregulated lipid metabolism and inflammation link these three diseases, leading [...] Read more.
Nowadays, the obesity pandemic is one of the most relevant health issues worldwide. This condition is tightly related to comorbidities such as non-alcoholic fatty liver disease (NAFLD) and cardiovascular diseases (CVDs), namely atherosclerosis. Dysregulated lipid metabolism and inflammation link these three diseases, leading to a subsequent increase of oxidative stress (OS) causing severe cellular damage. On the other hand, microRNAs (miRNAs) are short, single-stranded, non-coding RNAs that act as post-transcriptional negative regulators of gene expression, thus being involved in the molecular mechanisms that promote the development of many pathologies including obesity and its comorbidities. The involvement of miRNAs in promoting or opposing OS in disease progression is becoming more evident. Some miRNAs, such as miR-200a and miR.421, seem to play important roles in OS control in NAFLD. On the other hand, miR-92a and miR-133, among others, are important in the development of atherosclerosis. Moreover, since both diseases are linked to obesity, they share common altered miRNAs, being miR-34a and miR-21 related to OS. This review summarizes the latest advances in the knowledge about the mechanisms of oxidative stress (OS) generation in obesity-associated NAFLD and atherosclerosis, as well as the role played by miRNAs in the regulation of such mechanisms. Full article
(This article belongs to the Special Issue Oxidative Stress in Obesity)
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