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Antioxidants
Special Issues
Cross Talk between Hormones, Programming and Oxidative Stress
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Cross Talk between Hormones, Programming and Oxidative Stress

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 (30 November 2022) | Viewed by 5801

Special Issue Editors

Dr. Patricia Cristina Lisboa

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Guest Editor
Researcher in the Laboratory of Endocrine Physiology, Department of Physiology, Institute of Biology Roberto Alcantara Gomes, State University of Rio de Janeiro, Rio de Janeiro, Brazil
Interests: hormones; obesity; metabolic programing; DOHaD concept; malnutrition; overfeeding; early weaning
Special Issues, Collections and Topics in MDPI journals
Dr. Gustavo Casimiro-Lopes

E-Mail Website
Guest Editor
Associate Professor in the Department of Gymnastics, Researcher in the Laboratory of Exercise Pathophysiology, Institute of Physical Education and Sports, State University of Rio de Janeiro, Rio de Janeiro, Brazil
Interests: Oxidative stress; Hormones; Exercise biochemistry; Metabolic Programming

Special Issue Information

Dear Colleagues,

Increased oxidative stress has been associated with diseases such as metabolic syndrome, characterized by increased abdominal fat, insulin resistance, cardiovascular disease and dyslipidemia. On the other hand, obesity, type 2 diabetes mellitus and arterial hypertension in adulthood can originate early in life due to nutritional, hormonal and environmental insults—a phenomenon called metabolic programming. Since obesity is recognized as a global pandemic, it is important to know the key role of oxidative stress in cell damage and dysfunction in this situation. The present research topic “Cross Talk between Hormones, Programming and Oxidative Stress” intends to stimulate discussion on animal and human studies highlighting the central role of oxidative stress on both endocrine disorders and programming. In addition, discussions on non-pharmacological strategies such as physical exercise are also welcome, as they have great therapeutic potential in health and related pathophysiological mechanisms. Therefore, we are pleased to invite you to submit an original research or review article for this Special Issue. We believe that this topic is current and can generate new insights into therapeutic strategies for obesity.

We look forward to your contributions.

Dr. Patricia Cristina Lisboa
Dr. Gustavo Casimiro-Lopes
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

  • metabolism
  • diabetes
  • obesity
  • antioxidants

Published Papers (3 papers)

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Research

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22 pages, 4222 KiB  
Article
Resveratrol Supplementation in Obese Pregnant Rats Improves Maternal Metabolism and Prevents Increased Placental Oxidative Stress
by Guadalupe L. Rodríguez-González, Lilia Vargas-Hernández, Luis A. Reyes-Castro, Carlos A. Ibáñez, Claudia J. Bautista, Consuelo Lomas-Soria, Nozomi Itani, Guadalupe Estrada-Gutierrez, Aurora Espejel-Nuñez, Arturo Flores-Pliego, Araceli Montoya-Estrada, Enrique Reyes-Muñoz, Paul D. Taylor, Peter W. Nathanielsz and Elena Zambrano
Antioxidants 2022, 11(10), 1871; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox11101871 - 21 Sep 2022
Cited by 7 | Viewed by 1926
Abstract
Maternal obesity (MO) causes maternal and fetal oxidative stress (OS) and metabolic dysfunction. We investigated whether supplementing obese mothers with resveratrol improves maternal metabolic alterations and reduces OS in the placenta and maternal and fetal liver. From weaning through pregnancy female Wistar rats [...] Read more.
Maternal obesity (MO) causes maternal and fetal oxidative stress (OS) and metabolic dysfunction. We investigated whether supplementing obese mothers with resveratrol improves maternal metabolic alterations and reduces OS in the placenta and maternal and fetal liver. From weaning through pregnancy female Wistar rats ate chow (C) or a high-fat diet (MO). One month before mating until 19 days’ gestation (dG), half the rats received 20 mg resveratrol/kg/d orally (Cres and MOres). At 19dG, maternal body weight, retroperitoneal fat adipocyte size, metabolic parameters, and OS biomarkers in the placenta and liver were determined. MO mothers showed higher body weight, triglycerides and leptin serum concentrations, insulin resistance (IR), decreased small and increased large adipocytes, liver fat accumulation, and hepatic upregulation of genes related to IR and inflammatory processes. Placenta, maternal and fetal liver OS biomarkers were augmented in MO. MOres mothers showed more small and fewer large adipocytes, lower triglycerides serum concentrations, IR and liver fat accumulation, downregulation of genes related to IR and inflammatory processes, and lowered OS in mothers, placentas, and female fetal liver. Maternal resveratrol supplementation in obese rats improves maternal metabolism and reduces placental and liver OS of mothers and fetuses in a sex-dependent manner. Full article
(This article belongs to the Special Issue Cross Talk between Hormones, Programming and Oxidative Stress)
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16 pages, 2592 KiB  
Article
Hippocampal Endoplasmic Reticulum Stress Hastens Motor and Cognitive Decline in Adult Male Rats Sustainedly Exposed to High-Sucrose Diet
by Bruno Araújo Serra Pinto, Thamys Marinho Melo, Karla Frida Torres Flister, Lucas Martins França, Vanessa Ribeiro Moreira, Daniela Kajihara, Nelmar Oliveira Mendes, Silma Regina Pereira, Francisco Rafael Martins Laurindo and Antonio Marcus Andrade Paes
Antioxidants 2022, 11(7), 1395; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox11071395 - 19 Jul 2022
Cited by 2 | Viewed by 1929
Abstract
Metabolic dysfunctions, such as hyperglycemia and insulin resistance, have been associated to cognitive impairment and dementia regardless of advanced age, although the underlying mechanisms are still elusive. Thus, this study investigates the deleterious effects of metabolic syndrome (MetS) induced by long-term exposure to [...] Read more.
Metabolic dysfunctions, such as hyperglycemia and insulin resistance, have been associated to cognitive impairment and dementia regardless of advanced age, although the underlying mechanisms are still elusive. Thus, this study investigates the deleterious effects of metabolic syndrome (MetS) induced by long-term exposure to a high-sucrose diet on motor and cognitive functions of male adult rats and its relationship with hippocampal endoplasmic reticulum (ER) stress. Weaned Wistar male rats were fed a high-sucrose diet until adulthood (HSD; 6 months old) and compared to both age-matched (CTR; 6 months old) and middle-aged chow-fed rats (OLD; 20 months old). MetS development, serum redox profile, behavioral, motor, and cognitive functions, and hippocampal gene/protein expressions for ER stress pro-adaptive and pro-apoptotic pathways, as well as senescence markers were assessed. Prolonged exposure to HSD induced MetS hallmarked by body weight gain associated to central obesity, hypertriglyceridemia, insulin resistance, and oxidative stress. Furthermore, HSD rats showed motor and cognitive decline similar to that in OLD animals. Noteworthy, HSD rats presented marked hippocampal ER stress characterized by failure of pro-adaptive signaling and increased expression of Chop, p21, and Parp-1 cleavage, markers of cell death and aging. This panorama resembles that found in OLD rats. In toto, our data showed that early and sustained exposure to a high-sucrose diet induced MetS, which subsequently led to hippocampus homeostasis disruption and premature impairment of motor and cognitive functions in adult rats. Full article
(This article belongs to the Special Issue Cross Talk between Hormones, Programming and Oxidative Stress)
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Review

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12 pages, 3235 KiB  
Review
The Common Single Cause of Chronic Multi-Hormonal Resistance in Oxidative Stress
by István Wittmann
Antioxidants 2023, 12(1), 75; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox12010075 - 29 Dec 2022
Cited by 1 | Viewed by 1271
Abstract
In diseases with concomitant oxidative stress, chronic multi-hormonal resistances could be detected. The most conspicuous component of these resistances is insulin resistance, but also leptin, erythropoietin, acetylcholine, triiodothyronine and glucagon-like peptide-1 resistances also occur. On the other hand, in oxidative stress, abnormal tyrosines, [...] Read more.
In diseases with concomitant oxidative stress, chronic multi-hormonal resistances could be detected. The most conspicuous component of these resistances is insulin resistance, but also leptin, erythropoietin, acetylcholine, triiodothyronine and glucagon-like peptide-1 resistances also occur. On the other hand, in oxidative stress, abnormal tyrosines, for instance, meta- and ortho-tyrosine are also produced and incorporated into the proteins through the translational process. In case these modified proteins are components of the intracellular signalling pathways, a hormonal resistance may develop. The above-mentioned hormones, owning overlapping signalling pathways at the insulin receptor substrate, develop an abnormal tyrosine phosphorylation dependent chronic multi-hormonal resistance. A few weeks free of oxidative stress or the use of antioxidant therapy are required to provide a return from this resistance, which return may be further supported by the supplementation of physiological para-tyrosine and by the add-on therapy of a pharmacological dose of glucagon-like peptide-1 receptor agonist, which is able to bypass the critical insulin receptor substrate signalling. Full article
(This article belongs to the Special Issue Cross Talk between Hormones, Programming and Oxidative Stress)
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