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Antioxidants
Special Issues
Antioxidant Therapy for Obesity-Related Diseases
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Antioxidant Therapy for Obesity-Related Diseases

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Natural and Synthetic Antioxidants".

Deadline for manuscript submissions: 28 February 2025 | Viewed by 3681

Special Issue Editor

Dr. Seyed Khosrow Tayebati

E-Mail Website
Guest Editor
School of Pharmacy, University of Camerino, 62032 Camerino, Italy
Interests: obesity; hypertension; neuroinflammation; neurodegeneration; neuroprotection; natural and synthetic antioxidants
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Obesity-related diseases affect different districts of the body, including cardiovascular, renal, retinal, urogenital, and cerebrovascular disorders. It is widely documented that obesity and being overweight lead to severe inflammatory status involving every part of the organism, but some areas are particularly damaged. In this context, the role of oxidative stress and inflammation in this process is well-known. Therefore, the identification of antioxidants and their correct therapeutical use is crucial to addressing the inauspicious effects of obesity.

This Special Issue will showcase a range of papers or reviews to increase the general know-how relative to this topic. We would particularly like to include papers that analyze natural or synthetic antioxidants, explaining their deep mechanisms of action, opportunities for use in obesity-related diseases, and their therapeutical approaches.

There may be different reasons to actively participate in this project. Among them, in my opinion, is that this Special Issue has an intriguing theme and the support of Antioxidants, one of the journals with a high reputation in this field.   

Therefore, I encourage the participation of colleagues who study obesity, oxidative stress, and antioxidant therapy.

Dr. Seyed Khosrow Tayebati
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.

Keywords

  • obesity
  • inflammation
  • oxidative stress
  • organ damage
  • natural antioxidants
  • synthetic antioxidants
  • mechanisms of action
  • therapeutical approaches

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Further information on MDPI's Special Issue polices can be found here.

Published Papers (3 papers)

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Research

15 pages, 18551 KiB  
Article
Inhibiting Ferroptosis Prevents the Progression of Steatotic Liver Disease in Obese Mice
by Gi Cheol Park, Soo-Young Bang, Ji Min Kim, Sung-Chan Shin, Yong-il Cheon, Kwang Min Kim, Hanaro Park, Eui-Suk Sung, Minhyung Lee, Jin-Choon Lee and Byung-Joo Lee
Antioxidants 2024, 13(11), 1336; https://doi.org/10.3390/antiox13111336 - 31 Oct 2024
Viewed by 613
Abstract
Ferroptosis, a form of regulated cell death characterized by lipid peroxidation and iron accumulation, has been implicated in the progression of metabolic-dysfunction-associated steatohepatitis (MASH) in obesity. This study investigated the role of ferroptosis in the development of hepatic steatosis and MASH in obese [...] Read more.
Ferroptosis, a form of regulated cell death characterized by lipid peroxidation and iron accumulation, has been implicated in the progression of metabolic-dysfunction-associated steatohepatitis (MASH) in obesity. This study investigated the role of ferroptosis in the development of hepatic steatosis and MASH in obese mice and assessed the therapeutic potential of ferrostatin-1, a ferroptosis inhibitor. C57BL/6J wild-type (n = 8) and ob/ob mice (n = 16) were maintained on a standard chow diet. Mice were divided into three groups that included C57BL/6 (n = 8), ob/ob (n = 8), and ob/ob + ferrostatin-1 (FER) (n = 8), with the latter group receiving an intraperitoneal injection of 5 μM/kg ferrostatin three times per week for eight weeks. Following treatment, serum and tissue samples were collected for analysis. Significant hepatic steatosis and increased lipogenesis markers were observed in ob/ob mice, which were restored to baseline levels in the ob/ob + FER group treated with ferrostatin-1. Elevated oxidative stress was indicated by increased reactive oxygen species (ROS) and malondialdehyde (MDA) levels in the ob/ob group, while glutathione peroxidase 4 (GPX4) activity was significantly reduced. Ferrostatin-1 treatment decreases MDA levels and restores GPX4 activity. Additionally, ferrostatin mitigates iron overload and promotes macrophage polarization from M1 to M2, thereby reducing liver inflammation and fibrosis. Ferrostatin treatment reversed mitochondrial dysfunction in ob/ob mice. Our findings revealed that ferroptosis plays a significant role in the progression of obesity to hepatic steatosis and MASH. Inhibiting ferroptosis using ferrostatin-1 effectively improves liver histology, reduces oxidative stress, normalizes lipogenesis, and modulates macrophage polarization. This study highlights the potential of targeting ferroptosis as a therapeutic strategy for obesity-related liver diseases, warranting further investigation in clinical settings. Full article
(This article belongs to the Special Issue Antioxidant Therapy for Obesity-Related Diseases)
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14 pages, 6218 KiB  
Article
Sodium Houttuybonate Promotes the Browning of White Adipose Tissue by Inhibiting Ferroptosis via the AMPK-NRF2-HO1 Pathway
by Wenhui Liu, Huren Zou, Danming You, Huijie Zhang and Lingling Xu
Antioxidants 2024, 13(9), 1057; https://doi.org/10.3390/antiox13091057 - 30 Aug 2024
Viewed by 822
Abstract
The rising prevalence of obesity has resulted in an increased demand for innovative and effective treatment strategies. Houttuynia cordata Thunb. (H. cordata) has demonstrated promising potential in preventing obesity. However, the mechanism underlying the anti-obesity effects of H. cordata and its bioactive component, [...] Read more.
The rising prevalence of obesity has resulted in an increased demand for innovative and effective treatment strategies. Houttuynia cordata Thunb. (H. cordata) has demonstrated promising potential in preventing obesity. However, the mechanism underlying the anti-obesity effects of H. cordata and its bioactive component, sodium houttuybonate (SH), remains unclear. Our study reveals that SH treatment promotes the browning of inguinal white adipose tissue (iWAT) and prevents the obesity induced by a high-fat diet. SH significantly mitigates ferroptosis by upregulating glutathione peroxidase 4 (Gpx4) and decreasing malondialdehyde (MDA) levels, while also enhancing superoxide dismutase (SOD) levels. Furthermore, SH promotes the phosphorylation of AMP-activated protein kinase (AMPK), which subsequently increases the expression of nuclear factor erythroid 2-related factor 2 (NRF2) and heme oxygenase-1 (HO-1) in the iWAT. However, the effects of SH were attenuated by ML385, an Nrf2 inhibitor. Collectively, our findings suggest that SH induces iWAT browning and prevents diet-induced obesity primarily through the AMPK/NRF2/HO-1 pathway by inhibiting ferroptosis. Full article
(This article belongs to the Special Issue Antioxidant Therapy for Obesity-Related Diseases)
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18 pages, 5198 KiB  
Article
Dysfunction of the Brown Adipose Organ in HFD-Obese Rats and Effect of Tart Cherry Supplementation
by Vincenzo Bellitto, Maria Gabriella Gabrielli, Ilenia Martinelli, Proshanta Roy, Giulio Nittari, Paolo Cocci, Francesco Alessandro Palermo, Francesco Amenta, Maria Vittoria Micioni Di Bonaventura, Carlo Cifani, Daniele Tomassoni and Seyed Khosrow Tayebati
Antioxidants 2024, 13(4), 388; https://doi.org/10.3390/antiox13040388 - 23 Mar 2024
Viewed by 1628
Abstract
Obesity has a great impact on adipose tissue biology, based on its function as a master regulator of energy balance. Brown adipose tissue (BAT) undergoes remodeling, and its activity declines in obese subjects due to a whitening process. The anti-obesity properties of fruit [...] Read more.
Obesity has a great impact on adipose tissue biology, based on its function as a master regulator of energy balance. Brown adipose tissue (BAT) undergoes remodeling, and its activity declines in obese subjects due to a whitening process. The anti-obesity properties of fruit extracts have been reported. The effects of tart cherry against oxidative stress, inflammation, and the whitening process in the BAT of obese rats were investigated. Intrascapular BAT (iBAT) alterations and effects of Prunus cerasus L. were debated in rats fed for 17 weeks with a high-fat diet (DIO), in DIO supplemented with seed powder (DS), and with seed powder plus the juice (DJS) of tart cherry compared to CHOW rats fed with a normo-caloric diet. iBAT histologic observations revealed a whitening process in DIO rats that was reduced in the DS and DJS groups. A modulation of uncoupling protein-1 (UCP-1) protein and gene expression specifically were detected in the obese phenotype. An upregulation of UCP-1 and related thermogenic genes after tart cherry intake was detected compared to the DIO group. Metabolic adjustment, endoplasmic reticulum stress, protein carbonylation, and the inflammatory microenvironment in the iBAT were reported in DIO rats. The analysis demonstrated an iBAT modulation that tart cherry promoted. In addition to our previous results, these data confirm the protective impact of tart cherry consumption on obesity. Full article
(This article belongs to the Special Issue Antioxidant Therapy for Obesity-Related Diseases)
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