Obesity and fertility

Objective Reproductive function is intrinsically linked to body metabolism, as both energy deficiency and excess significantly impact pubertal onset and fertility. Obesity leads to secondary hypogonadism in males, also called “male obesity-related secondary hypogonadism” (MOSH)—a complex condition driven by systemic inflammation, insulin resistance, and suppressed gonadotropin secretion. In females, obesity is a primary risk factor for polycystic ovary syndrome (PCOS), the most prevalent anovulatory disorder. Furthermore, obesity can trigger non-PCOS ovulatory dysfunction, recently conceptualized as “female obesity-related secondary hypogonadism” (FOSH). Notably, even metabolically healthy obese (MHO) women exhibit a heightened risk of infertility. Consequently, managing obesity is fundamental to preserving reproductive health. In this context, glucagon-like peptide-1 receptor agonists (GLP-1 RAs) have emerged as promising therapeutic agents. Design and Methods Based on this framework, this review evaluates: (i) the physiological interplay between metabolism and reproduction; (ii) the contemporary pathophysiological model of obesity-related male infertility; and (iii) the clinical challenges of obesity-related reproductive dysfunction in females. Results and Conclusions Ultimately, while weight loss remains a cornerstone of fertility preservation, GLP-1 RAs represent a significant advancement, potentially offering reproductive benefits beyond weight reduction, whether used alone or in combination with lifestyle interventions or surgery.