Obesogens and male fertility

Abstract

In the last decades, several studies evidenced a decrease in male fertility in developed countries. Although the aetiology of this trend in male reproductive health remains a matter of debate, environmental compounds that predispose to weight gain, namely obesogens, are appointed as contributors because of their action as endocrine disruptors. Obesogens favour adipogenesis by an imbalance of metabolic processes and can be found virtually everywhere. These compounds easily accumulate in tissues with high lipid content. Obesogens change the functioning of male reproductive axis, and, consequently, the testicular physiology and metabolism that are pivotal for spermatogenesis. The disruption of these tightly regulated metabolic pathways leads to adverse reproductive outcomes. Notably, adverse effects of obesogens may also promote disturbances in the metabolic performance of the following generations, through epigenetic modifications passed by male gametes. Thus, unveiling the molecular pathways by which obesogens induce toxicity that may end up in epigenetic modifications is imperative. Otherwise, a transgenerational susceptibility to metabolic diseases may be favoured. We present an up-to-date overview of the impact of obesogens on testicular physiology, with a particular focus on testicular metabolism. We also address the effects of obesogens on male reproductive parameters and the subsequent consequences for male fertility.

Maternal diethylhexyl phthalate exposure affects adiposity and insulin tolerance in offspring in a PCNA-dependent manner

“…As a lack of exercise and a calorie-rich diet cannot fully explain the high occurrence of obesity and metabolic syndrome prevalent in the US population, we sought to examine ubiquitous environmental factors, specifically endocrine disruptors, for their ability to exacerbate weight gain and metabolic phenotypes. In particular, exposure to phthalates, a common chemical found in plasticizers, has been increasingly associated with obesity (Hurst and Waxman 2003, Snyder, Westerhoff et al 2003, Bility, Thompson et al 2004, Casals-Casas and Desvergne 2011, Janesick and Blumberg 2011, Heindel, Newbold et al 2015, Barakat, Lin et al 2017, Cardoso, Alves et al 2017), and recent studies suggest that phthalate exposure during the fetal period may increase this risk (Hatch, Nelson et al 2008). The underlying mechanism associated with the early effect of phthalate exposure on obesity has not been well established and is a topic of intensive investigation.…”

“…A subset of endocrine disruptors leads to metabolic deregulation, manifested by increased adipose deposition and disorder of glucose metabolism (Casals-Casas and Desvergne 2011, Heindel, Newbold et al 2015). However, much of the current knowledge about in utero and postnatal exposure to endocrine disruptors have been focused on development, particularly of reproductive systems (Barakat, Lin et al 2017, Cardoso, Alves et al 2017). The potential impact of interaction between endocrine disruptors and diet on global metabolic programming remains understudied.…”

Long term impact of the endocrine disruptor tributyltin on male fertility following a single acute exposure

“…Male infertility is one of the challenging problems encountered by the human society worldwide . Emerging reports indicate the involvement of various environmental factors in inducing male infertility . Impact of environmental factors are complicated to understand due to the large number of variables (exposure route, extent, duration, and many others) and also partly due to weak correlation between infertility and the methods to ascertain it .…”

“…1 Emerging reports indicate the involvement of various environmental factors in inducing male infertility. 2,3 Impact of environmental factors are complicated to understand due to the large number of variables (exposure route, extent, duration, and many others) and also partly due to weak correlation between infertility and the methods to ascertain it. 1 Apart from some well-known endocrine disruptors (like bisphenol A, phthalates, and polychlorinated biphenyls), organotin compounds like tributyltin (TBT) has also been reported to interfere with the endocrine system and induce imposex in female gastropods.…”

Effect of aerobic exercise, low‐fat and high‐fat diet on the testis tissue and sperm parameters in obese and nonobese mice model

“…Among social–environmental bases or lifestyle habits, overconsumption of high‐energy diets that rich in sugars and saturated fats along with low physical activity could have negative feedback on male fertility potential. In addition, environmental pollutant can adversely affect various parameter of adipose tissue functions (Cardoso et al, ). Most of these compositions are lipophilic and can disrupt male reproductive function due to high lipid content of this tissue which in turn affect testis physiology especially testicular metabolism and germ cell development, and ultimately reduces sperm quality (Cardoso et al, ; Skakkebaek, Rajpert‐De Meyts, & Main, ).…”