Obesity: A Doorway to a Molecular Path Leading to Infertility

The dramatic rise in obesity has recently made it a global health issue. About 1.9 billion were overweight, and 650 million global populations were obese in 2016. Obese women suffer longer conception time, lowered fertility rates, and greater rates of miscarriage. Obesity alters hormones such as adiponectin and leptin, affecting all levels within the hypothalamic-pituitary-gonadal axis. Advanced glycation end products (AGEs) and monocyte chemotactic protein-1 (MCP-1) are inflammatory cytokines that may play an important role in the pathophysiology of ovarian dysfunction in obesity. In obese males, there are altered sperm parameters, reduced testosterone, increased estradiol, hypogonadism, and epigenetic modifications transmitted to offspring. The focus of this article is on the possible adverse effects on reproductive health resulting from obesity and sheds light on different molecular pathways linking obesity with infertility in both female and male subjects. Electronic databases such as Google Scholar, Embase, Science Direct, PubMed, and Google Search Engine were utilized to find obesity and infertility-related papers. The search strategy is detailed in the method section. Even though multiple research work has shown that obesity impacts fertility in both male and female negatively, it is significant to perform extensive research on the molecular mechanisms that link obesity to infertility. This is to find therapeutics that may be developed aiming at these mechanisms to manage and prevent the negative effects of obesity on the reproductive system.