Physiological interplay among obesity, male fertility, and aryl hydrocarbon receptor in human and mice: A mini review.

According to the most recent World Health Organization report in 2022, approximately 16% of people were classified as obese. Obesity is an inflammatory-mediated condition manifested by accelerated lipogenesis and excessive fat accumulation around the viscera and, in some cases, surrounding the male gonads. Thus, obesity is considered a major cause of male infertility. Many environmental toxicants, known as obesogens, are connected to obesity progression by disrupting the hormonal profile, interrupting cellular metabolism, and subsequently leading to the development of sue. Such toxicants, such as bisphenol A, a plastic derivative, and dioxins, which are byproducts of incomplete combustion or industrial processes. Interestingly, these types of toxicants, in addition to others like polycyclic aromatic hydrocarbons (PAHs) and polychlorinated biphenyls, are defined as ligands of aryl hydrocarbon receptor (AhR). AhR has critical roles in immunity, metabolism, reproduction, and cancer biology, and it is expressed in immune cells such as T/B lymphocytes, macrophages, and dendritic cells. The effect of AhR on immunity is dependent on the ligand, which could activate macrophage-induced obesity. Many AhR ligands (e.g., kynurenine and indole derivatives) can be exogenous or endogenous and affect reproductive functions, such as spermatogenesis and oocyte maturation. There are also natural antagonists to AhR, including resveratrol, which have the potential to play a role in fertility. Currently, to connect the roles of AhR in obesity-induced male infertility. This review aims to elucidate the physiological and toxicological roles of AhR in the initiation of obesity and male infertility.