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Selenium Supplementation during Puberty and Young Adulthood Mitigates Obesity-Induced Metabolic, Cellular and Epigenetic Alterations in Male Rat Physiology
Selenium (Se) role in obesity is not clear. In addition, information on Se’s role in male physiology, specifically in obesity, is scarce. We conducted this study to evaluate the efficacy of Se supplementation, specifically during puberty until young adulthood, against obesity-induced deregulation of...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9138167/ https://www.ncbi.nlm.nih.gov/pubmed/35624758 http://dx.doi.org/10.3390/antiox11050895 |
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author | Pascoal, Gabriela de Freitas Laiber Novaes, Gabriela Machado Sobrinho, Monique de Paula Hirayama, André Bubna Castro, Inar Alves Ong, Thomas Prates |
author_facet | Pascoal, Gabriela de Freitas Laiber Novaes, Gabriela Machado Sobrinho, Monique de Paula Hirayama, André Bubna Castro, Inar Alves Ong, Thomas Prates |
author_sort | Pascoal, Gabriela de Freitas Laiber |
collection | PubMed |
description | Selenium (Se) role in obesity is not clear. In addition, information on Se’s role in male physiology, specifically in obesity, is scarce. We conducted this study to evaluate the efficacy of Se supplementation, specifically during puberty until young adulthood, against obesity-induced deregulation of metabolic, cellular, and epigenetic parameters in epididymal fat and/or sperm cells in a rat model. High-fat-diet consumption by male rats during puberty and young adulthood significantly increased body weight, adipocyte size, oxidative stress, deregulated expression of genes associated with inflammation (Adiponectin, IL-6, TNF-α), adipogenesis (CEBPα), estrogen biosynthesis (CYP19) and epigenetic processes in epididymal adipose tissue (Dnmt3a), as well as altered microRNA expression vital for spermatogenesis in sperm cells (miR-15b and miR-497). On the other hand, Se supplementation significantly decreased oxidative stress and mitigated these molecular/epigenetic alterations in epididymal adipose tissue or sperm cells. Our results indicate that selenium supplementation during puberty/young adulthood could improve male physiology in the context of obesity. In addition, it suggests that Se could potentially positively affect offspring health. |
format | Online Article Text |
id | pubmed-9138167 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-91381672022-05-28 Selenium Supplementation during Puberty and Young Adulthood Mitigates Obesity-Induced Metabolic, Cellular and Epigenetic Alterations in Male Rat Physiology Pascoal, Gabriela de Freitas Laiber Novaes, Gabriela Machado Sobrinho, Monique de Paula Hirayama, André Bubna Castro, Inar Alves Ong, Thomas Prates Antioxidants (Basel) Article Selenium (Se) role in obesity is not clear. In addition, information on Se’s role in male physiology, specifically in obesity, is scarce. We conducted this study to evaluate the efficacy of Se supplementation, specifically during puberty until young adulthood, against obesity-induced deregulation of metabolic, cellular, and epigenetic parameters in epididymal fat and/or sperm cells in a rat model. High-fat-diet consumption by male rats during puberty and young adulthood significantly increased body weight, adipocyte size, oxidative stress, deregulated expression of genes associated with inflammation (Adiponectin, IL-6, TNF-α), adipogenesis (CEBPα), estrogen biosynthesis (CYP19) and epigenetic processes in epididymal adipose tissue (Dnmt3a), as well as altered microRNA expression vital for spermatogenesis in sperm cells (miR-15b and miR-497). On the other hand, Se supplementation significantly decreased oxidative stress and mitigated these molecular/epigenetic alterations in epididymal adipose tissue or sperm cells. Our results indicate that selenium supplementation during puberty/young adulthood could improve male physiology in the context of obesity. In addition, it suggests that Se could potentially positively affect offspring health. MDPI 2022-04-30 /pmc/articles/PMC9138167/ /pubmed/35624758 http://dx.doi.org/10.3390/antiox11050895 Text en © 2022 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Pascoal, Gabriela de Freitas Laiber Novaes, Gabriela Machado Sobrinho, Monique de Paula Hirayama, André Bubna Castro, Inar Alves Ong, Thomas Prates Selenium Supplementation during Puberty and Young Adulthood Mitigates Obesity-Induced Metabolic, Cellular and Epigenetic Alterations in Male Rat Physiology |
title | Selenium Supplementation during Puberty and Young Adulthood Mitigates Obesity-Induced Metabolic, Cellular and Epigenetic Alterations in Male Rat Physiology |
title_full | Selenium Supplementation during Puberty and Young Adulthood Mitigates Obesity-Induced Metabolic, Cellular and Epigenetic Alterations in Male Rat Physiology |
title_fullStr | Selenium Supplementation during Puberty and Young Adulthood Mitigates Obesity-Induced Metabolic, Cellular and Epigenetic Alterations in Male Rat Physiology |
title_full_unstemmed | Selenium Supplementation during Puberty and Young Adulthood Mitigates Obesity-Induced Metabolic, Cellular and Epigenetic Alterations in Male Rat Physiology |
title_short | Selenium Supplementation during Puberty and Young Adulthood Mitigates Obesity-Induced Metabolic, Cellular and Epigenetic Alterations in Male Rat Physiology |
title_sort | selenium supplementation during puberty and young adulthood mitigates obesity-induced metabolic, cellular and epigenetic alterations in male rat physiology |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9138167/ https://www.ncbi.nlm.nih.gov/pubmed/35624758 http://dx.doi.org/10.3390/antiox11050895 |
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