ArticleFrontiers in endocrinology2026
Divergent pathophysiological drivers of polycystic ovary syndrome: insulin resistance independently fuels the hyperandrogenic phenotype whilst neuroendocrine factors dominate non-hyperandrogenic presentations.
Article in Frontiers in endocrinology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Polycystic Ovary Syndrome (PCOS) manifests as a heterogeneous disorder, yet the extent to which metabolic dysfunction drives specific phenotypes independent of obesity remains debated. This study aimed to delineate the distinct clinical and pathophysiological characteristics of Hyperandrogenic (HA) versus 38 Non-Hyperandrogenic (Non-HA) phenotypes, with a specific focus on disentangling the roles of insulin resistance and adiposity in driving androgen excess. Methods: A retrospective cross-sectional study was conducted involving 301 women with PCOS and 144 controls. Patients were stratified into Non-HA ( Results: The HA phenotype was characterised by significantly more severe oligo-anovulation and metabolic disturbance compared to the Non-HA group, despite comparable age ( Conclusion: Our findings demonstrate that PCOS encompasses two pathophysiologically distinct entities. The Non-HA phenotype appears driven primarily by neuroendocrine dysregulation, whereas the HA phenotype is intrinsically linked to metabolic dysfunction, specifically insulin resistance. Most importantly, we confirm that insulin resistance drives the hyperandrogenic phenotype independently of obesity. These data support a paradigm shift towards phenotype-specific management, necessitating aggressive insulin-sensitising strategies for hyperandrogenic patients regardless of their BMI.
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