<![CDATA[Polycystic ovary syndrome (PCOS) is a prevalent endocrine disorder with complex reproductive and metabolic consequences that remain insufficiently addressed by symptom-oriented management strategies. This study aims to review and synthesize recent evidence on the metabolic basis of PCOS, emphasizing the importance of insulin resistance and hyperinsulinemia as central mechanisms underlying both metabolic and reproductive abnormalities. A narrative review method was employed by analyzing peer-reviewed literature published in recent years, focusing on studies examining insulin signaling disturbances, mitochondrial dysfunction, oxidative stress, inflammatory pathways, and emerging therapeutic approaches in PCOS. The main findings indicate that insulin resistance and hyperinsulinemia act as key drivers of PCOS across diverse phenotypes, including non-obese women, while mitochondrial dysfunction and chronic inflammation further amplify metabolic–reproductive impairment. The results also show that improvements in metabolic parameters do not consistently align with normalization of reproductive hormones, underscoring the heterogeneous and multifactorial nature of PCOS. These findings have important implications for clinical practice, supporting the adoption of personalized, mechanism-based management strategies that integrate metabolic profiling with reproductive goals. The originality of this review lies in its integrative metabolic–reproductive framework, which consolidates emerging mechanistic insights and novel therapeutic perspectives to reconceptualize PCOS as a systemic metabolic–reproductive disorder.]]>
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