Insulin Resistance, Thyroid Dysregulation, and Androgen Excess in Polycystic Ovary Syndrome: A Narrative Review of a Triangular Hormonal–Metabolic Model

Abstract

Background: Polycystic ovary syndrome (PCOS) is a heterogeneous endocrine–metabolic disorder characterized by reproductive dysfunction, androgen excess, and variable metabolic risk. Although insulin resistance, thyroid dysfunction, and hyperandrogenism are frequently discussed as separate abnormalities, their interaction may better explain the diversity of PCOS phenotypes and long-term cardiometabolic consequences. Objective: This narrative review aims to synthesize current evidence on the interrelationship among insulin resistance, thyroid dysregulation, and androgen excess in PCOS and to present these mechanisms as an integrated triangular hormonal–metabolic model. Methods: A targeted narrative literature search was conducted using PubMed, Google Scholar, and Scopus. Search terms included combinations of “polycystic ovary syndrome,” “PCOS,” “insulin resistance,” “hyperinsulinemia,” “hyperandrogenism,” “thyroid dysfunction,” “subclinical hypothyroidism,” “autoimmune thyroiditis,” and “cardiometabolic risk.” Priority was given to international guidelines, systematic reviews, meta-analyses, mechanistic studies, observational studies, and clinically relevant interventional evidence. The synthesis was organized thematically around epidemiology, pathophysiology, clinical manifestations, and phenotype-directed management. Results: The reviewed evidence supports insulin resistance as a central metabolic driver of PCOS through compensatory hyperinsulinemia, increased ovarian androgen synthesis, reduced sex hormone-binding globulin, and impaired ovulatory function. Hyperandrogenism may further aggravate insulin resistance through visceral adiposity and adipose dysfunction. Thyroid dysfunction, particularly subclinical hypothyroidism and thyroid autoimmunity, appears to modify metabolic and reproductive severity in selected patients by influencing insulin sensitivity, lipid metabolism, inflammation, and follicular function. Conclusion: PCOS should be approached as an integrated endocrine–metabolic syndrome in which insulin resistance, androgen excess, and thyroid dysfunction may interact bidirectionally. Integrated assessment and phenotype-directed management may improve clinical care, although further longitudinal and interventional studies are needed.