Abstract
Polycystic Ovary Syndrome (PCOS) is a prevalent endocrine and metabolic disorder among women of reproductive age. Although the traditional mechanistic framework has focused on dysregulation of the hypothalamic-pituitary-ovarian axis (HPOA), emerging evidence suggests that PCOS-associated metabolic disturbances predominantly originate from dysregulation of the hypothalamic-sympathetic nerve-adipose tissue axis (HSF axis). This article systematically reviews the mechanisms by which hypothalamic nuclei (including the arcuate nucleus and paraventricular nucleus) regulate adipose tissue metabolism through sympathetic neural pathways. Furthermore, it explores how HSF axis dysfunction exacerbates both metabolic and reproductive abnormalities in PCOS through pathophysiological pathways such as chronic low-grade inflammation and energy sensing dysregulation. This synthesis offers novel insights into PCOS pathogenesis by bridging the gap between neuroendocrine regulation and systemic metabolic dysfunction.