An endocrinological perspective on polycystic ovarian syndrome

Polycystic ovarian syndrome (PCOS) is a complex endocrinological disorder that involves dysfunctions across multiple endocrine axes, including the hypothalamic-pituitary-gonadal (HPG), hypothalamic-pituitary-adrenal (HPA) and hypothalamic-pituitary-thyroid (HPT) axes. Our review focuses on understanding the pathophysiology of PCOS through an endocrinological perspective, emphasizing the complex interactions between multiple endocrine axes. We have discussed the roles of the HPG, HPA, and HPT axes in PCOS. Dysregulation of the HPG axis, particularly the altered gonadotropin-releasing hormone pulse frequency resulting in elevated ratio of luteinizing hormone to follicle stimulating hormone, is central to the hyperandrogenism and anovulation, observed in PCOS. We have further highlighted the contributions of the HPA and HPT axes, where elevated adrenal androgen levels and hypothyroidism intensifies the phenotypes of PCOS. Additionally, insulin resistance and hyperinsulinemia, commonly associated with PCOS, aggravates hormonal disturbances and heighten the risk of metabolic complications such as type 2 diabetes and cardiovascular diseases. Elevated levels of anti-Müllerian hormone have also been emphasized as a key factor in inhibiting follicular growth, leading to impaired ovarian function and hyperandrogenism. This review further supports that PCOS is a multifactorial condition involving complex feedback mechanisms between the endocrine, metabolic, and reproductive systems. Furthermore, there remains a huge scope for deciphering the precise molecular interactions between the HPG, HPA, and HPT axes in PCOS, which could pave the way for targeted therapies for better management of both the endocrine and metabolic aspects of this disorder. This review will benefit researchers to get an endocrine perspective on PCOS.