INSULIN RESISTANCE IN POLYCYSTIC OVARY SYNDROME — A NARRATIVE REVIEW OF MECHANISMS AND MANAGEMENT

Abstract

Polycystic ovary syndrome (PCOS) affects 11–13% of women of reproductive age worldwide and combines hyperandrogenism, ovulatory dysfunction and polycystic ovarian morphology. Once viewed as a purely reproductive disorder, PCOS is now also recognised as a metabolic one, with insulin resistance (IR) and compensatory hyperinsulinaemia linking its reproductive and metabolic features. In a 2026 international consensus published in The Lancet, the condition was formally renamed polyendocrine metabolic ovarian syndrome (PMOS); the term PCOS remains widely used during the announced three-year transition period. This narrative review synthesises current evidence on the role of insulin resistance in the pathophysiology of PCOS, with a focus on the 2023 International Evidence-based Guideline and recent pharmacological developments. We searched PubMed, Scopus and Google Scholar for peer-reviewed literature published in English between January 2004 and April 2026, prioritising original studies, systematic reviews, meta-analyses and current clinical guidelines. Hyperinsulinaemia stimulates ovarian theca-cell androgen production and lowers hepatic sex hormone-binding globulin synthesis, raising bioavailable androgens. A pathway-selective insulin signalling defect — impaired PI3K/Akt with relatively preserved MAPK signalling — has been proposed as a unifying molecular mechanism. Lifestyle modification remains first-line therapy; metformin and inositol improve metabolic and ovulatory parameters, and glucagon-like peptide-1 receptor agonists produce greater reductions in body weight and HOMA-IR than metformin in head-to-head studies. Insulin resistance is a key driver of both reproductive and metabolic outcomes, and early identification is essential for reducing long-term cardiometabolic morbidity.