Epigenetic Mechanisms of Endocrine-Disrupting Chemicals in Obesity

Abstract

The incidence of obesity has dramatically increased over the last decades. Recently, there has been a growing interest in the possible association between the pandemics of obesity and some endocrine-disrupting chemicals (EDCs), termed “obesogens”. These are a heterogeneous group of exogenous compounds that can interfere in the endocrine regulation of energy metabolism and adipose tissue structure. Oral intake, inhalation, and dermal absorption represent the major sources of human exposure to these EDCs. Recently, epigenetic changes such as the methylation of cytosine residues on DNA, post-translational modification of histones, and microRNA expression have been considered to act as an intermediary between deleterious effects of EDCs and obesity development in susceptible individuals. Specifically, EDCs exposure during early-life development can detrimentally affect individuals via inducing epigenetic modifications that can permanently change the epigenome in the germline, enabling changes to be transmitted to the next generations and predisposing them to a multitude of diseases. The purpose of this review is to analyze the epigenetic alterations putatively induced by chemical exposures and their ability to interfere with the control of energy metabolism and adipose tissue regulation, resulting in imbalances in the control of body weight, which can lead to obesity.

Obesity and Thyroid Cancer Risk: An Update

“…The onset of IR can be influenced by several factors, including genetic and epigenetic factors, obesity and diabetes, or exposure to EDCs [94,95]. IR has also been associated with elevated TNF-α levels [84].…”

Epigenome Modulation Induced by Ketogenic Diets

“…Similarly, obesity, higher mortality, and age-related memory loss were prevented in mice fed a cyclic (every two weeks) ketogenic diet [ 83 ]. These effects have been linked to the downregulation of genes involved in fatty acid metabolism and the upregulation of Peroxisome Proliferator-Activated Receptor alpha (PPAR-) target genes [ 83 ], mechanisms that have been shown to be closely linked to epigenetic changes, at least in adipose tissue [ 64 , 86 ].…”

Endocrine Disruption of the Follicle-Stimulating Hormone Receptor Signaling During the Human Antral Follicle Growth

“…Exposure of female mice to DEHP has been shown to disrupt steriodogenic enzymes in F2 and F3 generations and altered DNA methylation in the ovaries ( 99 , 100 ). In fact, it is known that EDs may alter the epigenetic profile ( 101 ), as a disrupting event that was described to occur at the level of non coding RNAs, such as the transfer RNA (tRNA) possibly impacting protein expression levels ( 102 ). Certain studies have used a mixture of chemical compounds to evaluate their conjoint effect on female reproductive health.…”