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Submitted on May 5, 2005
Accepted on August 4, 2005
Division of Endocrinology, Diabetes and Clinical Nutrition (JJP, SV, MK, UK, BM), Division of Gynecological Endocrinology and Reproductive Medicine (CDG), University Hospital, CH-4031 Basel, Switzerland
* To whom correspondence should be addressed. E-mail: Puderj{at}uhbs.ch.
Background: It is controversial whether the polycystic ovary syndrome (PCOS) per se increases low-grade chronic inflammation and whether this relates to central fat excess. In addition, the association between circulating sex hormones and body fat distribution in premenopausal women is debated.
Methods: Blood was drawn in 20 patients with PCOS and compared with 15 controls, matched for body mass index and age. Regional fat distribution was assessed using dual x-ray absorptiometry.
Results: Compared with controls, patients with PCOS had a higher trunk to extremity fat ratio (T/E fat), were more insulin-resistant (higher HOMA-IR [homeostasis model assessment of insulin resistance] and lower SHBG concentrations) and had higher levels of highly sensitive C-reactive protein (hs-CRP), tumor necrosis factor-
, procalcitonin and white blood cell count (WBC); all P 
0.04), even after adjusting for total body fat. However, additional adjusting for T/E fat eliminated or attenuated the effect of PCOS status on estimates of insulin resistance, on inflammatory mediators and on WBC, but not on circulating sex hormones. Independently of each other, both total body fat as well as T/E fat correlated with estimates of insulin resistance and most inflammatory mediators (P 0.04). However, the correlations between T/E fat and circulating sex hormones (P 0.02) were greatly reduced after adjustment for the presence of PCOS.
Conclusion: The increase in low-grade chronic inflammation and in insulin resistance in women with PCOS is primarily associated with increased central fat excess rather than PCOS status per se. Procalcitonin represents a novel marker of the inflammatory activity of body fat and of PCOS.
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