adipose tissue as an endocrine organ has emerged (Mohamed- Ali et al 1998; Spiegelman and Flier 1996; Fruhbeck 2004). Adipocytes are metabolically active cells which secrete tumor necrosis factor alpha, interleukin 6, plasminogen activator inhibitor-1, leptin, resistin, adiponectin, and angiotensinogen (Rondinone 2006; Yu and Ginsberg 2005). Leptin is secreted mainly by adipose tissue and deﬁciency in leptin results in hyperphagia, decreased energy expenditure and morbid obesity (Friedman and Halaas 1998). However, in terms of human obesity, leptin deﬁciency is rare. It has been postulated that leptin activates the sympathetic nervous system and is involved in blood pressure regulation, brain and bone development, hematopoiesis and wound healing (Ahima and Flier 2000). It has been suggested that the function of leptin is to control the deposition of fat and this modulates its harmful accumulation in tissues such as heart, liver and kidneys. Leptin is involved in the control of vascular tone by stimutaneously producing a pressor action and opposing the nitric oxide mediated relaxing function (Fruhbeck and Gomez-Ambrosi 2001). This may contribute to the hypertension associated with cardiometabolic syndrome. A positive relationship between insulin resistant PCOS women (both obese and non-obese) and hyperlep- tinemia, regardless of the BMI has been suggested in one study (Calvar et al 2003). Increasing adipose tissue mass is associated with increasing levels of angiotensin II from the increased secretion of angio- tensinogen by adipose tissue. Increase in angiotensin II could contribute to hypertension and aggravate insulin resistance (Engeli et al 2003). IL-6 inhibits liproprotein lipase activity, enhances aromatase activity and increases the hepatic production of triglycerides (Nonogaki et al 1995). IL-6 is stimulated by TNF-alpha: TNF stimulates C-reactive protein that has been found to be correlated with obesity, insulin resistance, endothelial dysfunction, and therefore cardiovascular risk, and patients with PCOS have been shown to have a higher level of CRP (Kelly et al 2001; Bahceci et al 2004). TNF-alpha also suppresses lipoprotein lipase and its release is inhibited by the thiazolidinediones and in PCOS, serum TNF-alpha is increased irrespective of obesity (Gonzalez et al 1999). Elevation of these inﬂammatory markers are in ac- cord with the hypothesis that atheroma formation is primarily an inﬂammatory condition. Adiponectin is secreted exclusively by adipocytes and levels are reduced in obesity, type 2 diabetes and coronary heart disease. Studies suggest an important link with insulin resistance (Steppan et al 2001) and adiponectin also inhibits vascular smooth muscle proliferation and the expression of Vascular Health and Risk Management 2007:3(1) Cardiometabolic aspects of POCS adhesion molecules. Levels of adiponectin are increased by weight reduction and by thiazoledinediones (Yu et al 2002). It has recently been shown that a signiﬁcant reciprocal cor- relation exists between adiponectin and resistin independent of insulin resistance in women with PCOS (Lewandowski et al 2005). Resistin is implicated in the pathogenesis of Type 2 diabetes and obesity (Seow et al 2004) where circulating resistin levels and resistin expression in adipocytes are increased. However, the role of resistin in patients with PCOS and thus cardiovascular risk in this group is still debatable. In one study, serum resistin level in patients with PCOS were no different to matched controls but resistin mRNA levels were 2-fold higher in omental adipocytes from PCOS patients (Seow et al 2004). Others have reported that there is an in- crease in serum resistin level in patients with PCOS (Munir et al 2005), although it has been suggested that this increase is dependent on BMI (Panidis et al 2004). Against this ar- gument is that in BMI matched patients, serum resistin was found not to be different compared with controls (Carmina et al 2005, 2006). Therefore more studies will be required to determine its importance in patients with PCOS. Therapy of PCOS The effective treatment of patients with PCOS requires that the speciﬁc goal(s) of the therapy be ﬁrst established. Indi- vidual goals may include fertility, treatment for hirsutism and/or acne, achieving a regular menstrual cycle, weight reduction, and the prevention of the long-term consequences associated with PCOS (type 2 diabetes, dyslipidemia, and possibly cardiovascular disease) or all of the above! Treatments discussed here will focus on those aimed at modifying the cardiometabolic aspects of PCOS. Exercise and diet Although obesity is not thought to be the cause for PCOS, it may exacerbate this dysfunction (Holte 1996). Loss of signiﬁcant weight has been reported to result in spontaneous resumption of ovulation (Crosignani et al 2003), improve- ment in fertility (Norman et al 2004), increased SHBG, and reduced basal level of insulin (Huber-Buchholz et al 1999; Tolino et al 2005). Data from the Diabetes Prevention Program (DPP) showed the importance of weight reduction in patients with impaired glucose tolerance that were at high risk of developing diabetes This study showed that both metformin therapy and intensive lifestyle intervention reduced the risk of developing diabetes (by 31% and 58%, respectively, in comparison with placebo), and both interventions were 59