Abstract
PCOS is a common endocrine-metabolic disorder with serious health consequences for women, including alarming rates of infertility. Although the exact cause is unknown, several hormonal imbalances are known to be involved, including hyperandrogenemia, insulin resistance (IR), and hyperinsulinemia. Insulin appears to disrupt all components of the hypothalamus-hypophysis-ovary axis, resulting in impaired metabolic signalling but intact mitogenic and steroidogenic activity, favouring hyperandrogenemia, which appears to be the primary cause of the PCOS clinical picture. Androgens, in turn, may contribute to IR by increasing free fatty acid levels and changing the composition and functionality of muscle tissue, perpetuating the IR-hyperinsulinemia-hyperandrogenemia cycle. Nonobese women with PCOS have distinct biochemical and hormonal profiles, among other characteristics. However, both lean and obese patients have chronic inflammation, which mediates the long-term cardiometabolic problems and comorbidities seen in women with PCOS, such as dyslipidemia, metabolic syndrome, type 2 diabetes, and cardiovascular disease. Given these serious consequences, it is critical to fully understand the pathophysiologic connections that underpin PCOS in order to develop superior therapeutic approaches and ensure improved quality of life for women suffering from this illness.