Selenium Supplementation during Puberty and Young Adulthood Mitigates Obesity-Induced Metabolic, Cellular and Epigenetic Alterations in Male Rat Physiology

Abstract

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.

Effect of Paternal Diet on Spermatogenesis and Offspring Health: Focus on Epigenetics and Interventions with Food Bioactive Compounds

“…One explanation would be the fact that the animals were lean and not submitted to any metabolic challenge. It has been highlighted that oxidative stress background could be a key interfering factor in selenium efficacy [ 146 ]. Thus, we [ 146 ] recently found that, when selenium was supplemented to obese fathers (a condition previously shown to program increased breast cancer risk [ 119 ]), during puberty and young adulthood, it led to amelioration of epididymal fat tissue obesity-induced oxidative stress and inflammation and reprogrammed sperm microRNA vital for spermatogenesis.…”

“…It has been highlighted that oxidative stress background could be a key interfering factor in selenium efficacy [ 146 ]. Thus, we [ 146 ] recently found that, when selenium was supplemented to obese fathers (a condition previously shown to program increased breast cancer risk [ 119 ]), during puberty and young adulthood, it led to amelioration of epididymal fat tissue obesity-induced oxidative stress and inflammation and reprogrammed sperm microRNA vital for spermatogenesis. This suggests that selenium supplementation during puberty and during these developmental stages could affect male physiology in the context of obesity, and it suggests that it could, potentially, positively affect offspring health [ 146 ].…”

“…Thus, we [ 146 ] recently found that, when selenium was supplemented to obese fathers (a condition previously shown to program increased breast cancer risk [ 119 ]), during puberty and young adulthood, it led to amelioration of epididymal fat tissue obesity-induced oxidative stress and inflammation and reprogrammed sperm microRNA vital for spermatogenesis. This suggests that selenium supplementation during puberty and during these developmental stages could affect male physiology in the context of obesity, and it suggests that it could, potentially, positively affect offspring health [ 146 ]. These results suggest that the preconception stage is an important developmental window of opportunity to initiate nutritional preventive strategies for breast cancer, focusing on the future father´s diet during preconception.…”

Dietary Selenium and Its Antioxidant Properties Related to Growth, Lipid and Energy Metabolism

“…GPxs and TXNRDs are essential for correct β-cell function and insulin secretion; furthermore, Se regulates the transcription levels of the hypothalamic and GH/IGF axis-related genes responsible for growth promotion [ 1 ]. Apart from these endocrine actions, which affect lipid, protein and glucose homeostasis, Se modulates adipogenesis via GPx1 SREBP1, SelP and SelW, since this is a process where reactive oxygen species (ROS) are used as transmitters [ 2 , 3 ]. These effects are even more important during intense growth periods, such as gestation, lactation, adolescent and embryogenic periods, where tissues are growing and in some cases developing [ 1 , 2 ].…”

“…Apart from these endocrine actions, which affect lipid, protein and glucose homeostasis, Se modulates adipogenesis via GPx1 SREBP1, SelP and SelW, since this is a process where reactive oxygen species (ROS) are used as transmitters [ 2 , 3 ]. These effects are even more important during intense growth periods, such as gestation, lactation, adolescent and embryogenic periods, where tissues are growing and in some cases developing [ 1 , 2 ].…”