Unravelling the metabolic complexity of polycystic ovary syndrome: Understanding the interplay of GLP-1 and UCP-1 a comprehensive review

Abstract

Polycystic Ovary Syndrome (PCOS) is a multifactorial endocrine disorder affecting 5-10% of women globally, with prevalence rates as high as 22.5% in India. Characterized by hyperandrogenism, insulin resistance, and visceral adiposity, PCOS manifests in various phenotypes, contributing to reproductive and metabolic complications. This review explores the emerging therapeutic potential of glucagon-like peptide-1 (GLP-1) and uncoupling protein-1 (UCP-1) in managing PCOS. GLP-1 enhances insulin sensitivity, regulates gonadotropin release, and increases sex hormone-binding globulin (SHBG) levels, mitigating hyperandrogenism. UCP-1, primarily involved in thermogenesis, facilitates the conversion of white adipose tissue (WAT) into brown adipose tissue (BAT), reducing visceral fat accumulation. The downregulation of GLP-1 and UCP-1 exacerbates PCOS by promoting insulin resistance, hyperandrogenism, and metabolic dysfunction. Understanding the central and peripheral actions of GLP-1 and UCP-1 highlights their interplay in modulating energy homeostasis and hormonal balance, making them promising targets for future PCOS therapies. This review underscores the need for further research into GLP-1 and UCP-1 agonists to optimize treatment strategies and improve patient outcomes in PCOS.