Vol. 7, Issue 1, Part B (2025)

Polycystic ovary syndrome (PCOS) is a prevalent endocrine-metabolic condition in reproductive-aged women and is frequently accompanied by ovulatory dysfunction and biochemical or clinical hyperandrogenism. The syndrome also increases susceptibility to metabolic complications such as insulin resistance, dyslipidemia, and fatty liver. Adipose tissue particularly visceral white adipose tissue (WAT) plays a central role in these abnormalities. Although traditionally viewed as an energy-storage depot, adipose tissue is now recognized as an active endocrine organ with pivotal functions in metabolic homeostasis.
In PCOS, disturbances in adipocyte biology, including altered fat distribution, increased visceral adiposity, and adipocyte hypertrophy, worsen insulin resistance and perpetuate hyperandrogenism. In contrast, brown adipose tissue (BAT) characterized by uncoupling protein 1 (UCP-1) supports energy expenditure and thermogenesis. BAT activity and mass are diminished in women with PCOS, contributing to impaired post-prandial thermogenesis and adverse metabolic profiles. The suppression of UCP-1 expression by excess androgens further links hyperandrogenism to disrupted mitochondrial function.
This review synthesizes current evidence on WAT and BAT dysfunction in PCOS, highlights the mechanistic relevance of UCP-1, and examines emerging therapeutic possibilities, including strategies aimed at activating BAT or promoting WAT browning.