Polycystic ovary syndrome (PCOS) is an exceedingly complex endocrine, reproductive and metabolic disorder of a diverse and still unclear pathogenesis. PCOS affects approximately 10% of women of reproductive age and is considered one of the most common endocrine and reproductive disturbances in its group (1)(2). The syndrome is clinically characterised by oligo/anovulation and infertility, hirsutism and abdominal obesity (3). However, the absence of clearly defined causative factors and mechanisms has historically made research and collaboration regarding PCOS difficult. Nevertheless, recently, European and American communities have come to a consensus regarding the definition of PCOS. The current requirement for diagnosis of PCOS necessitates that at least two of the following criteria are present: ultrasound evidence of polycystic ovaries, oligo/anovulation and/or biochemical evidence of hyperandrogenism after the exclusion of other conditions which cause the same features (4)(2). In addition to the reproductive abnormalities, most women diagnosed with PCOS are predisposed to obesity and insulin resistance as well as dyslipidemia and hypertension (5). In other words, there is a high incidence of metabolic syndrome in patients with PCOS. This encompasses the development of type 2 diabetes and cardiovascular disease. Clearly it is the high incidence as well as the yet unknown mechanisms linking PCOS to metabolic and vascular abnormalities which make PCOS of high socioeconomic importance. Additionally, the amelioration of these metabolic and vascular abnormalities has been shown to improve hyperandrogenism and fertility and subsequently requires more scientific elucidation (5). Recent studies have focused on the role of obesity, or more specifically the role of various adipocytes in PCOS. It has been shown that adipocytes are secretory cells that produce a number of proteins with hormonal type functions, collectively referred to as adipokines. In this review we see that a number of studies have shown that the secretion of various adipokines is disrupted in PCOS (6)(7) and that it is considered that this disruption of adipokine secretion could be a significant predictor of metabolic and vascular disease in patients with PCOS (8)(5)(9). Current research is aimed at further elucidating this connection because the early detection of these associated diseases would allow preventative treatment and subsequently result in improved clinical outcome, and improved quality of life for patients with PCOS.