Polycystic Ovary Syndrome as a Metabolic Disorder Involving Insulin Resistance, Chronic Inflammation and Adipose Dysfunction

Polycystic ovary syndrome is a heterogeneous reproductive and metabolic disorder in which insulin resistance, androgen excess and adipose dysfunction can reinforce one another. Human physiological studies, experimental models, longitudinal cohorts and intervention trials were considered together to clarify these relationships. Clamp studies support impaired insulin action in important PCOS subgroups, while adipocyte morphology, adiponectin and local androgen metabolism connect body-fat biology to systemic metabolic risk. Inflammatory and oxidative responses may amplify these abnormalities, but their contribution varies with adiposity and phenotype. Clinical studies indicate increased vulnerability to dysglycemia and other long-term health problems, although reproductive diagnostic criteria do not fully describe metabolic severity. Lifestyle interventions, metformin and treatments targeting obesity address overlapping but nonidentical components of the disorder. Trials of glucagon-like peptide-1 receptor agonists provide evidence for improvements in selected weight and metabolic outcomes, while reproductive and long-term safety questions require separate evaluation. Experimental microbiome and cell-based approaches remain preliminary. The review concludes that PCOS should be assessed as a multidimensional condition, with treatment goals defined by metabolic risk, symptoms and reproductive plans rather than by a single biomarker.