title: Hyperandrogenism exerts an anti-inflammatory effect in obese women with polycystic ovary syndrome.
abstract: We determined the effect of chronic androgen suppression on inflammation in women with polycystic ovary syndrome (PCOS) compared to weight-matched controls. We performed a pilot project using samples from previous prospective, controlled studies. Nine women with PCOS (5 obese, 4 lean) and 9 ovulatory controls (5 obese, 4 lean) participated in the study. Androgens, C-reactive protein (CRP), interleukin-6 (IL-6), free fatty acids (FFA) and body weight were measured before and after 3 and 6 months of gonadotropin-releasing hormone (GnRH) agonist administration. GnRH agonist treatment decreased estradiol, testosterone and androstenedione to similar levels in all subjects. CRP and IL-6 increased in obese women with PCOS, was unaltered in lean women with PCOS and obese controls, and decreased in lean controls after 6 months of treatment. FFA decreased and body weight increased in obese women with PCOS, but did not change significantly in lean women with PCOS and in either control group after 6 months of treatment. The testosterone reduction was related to increases in weight and IL-6. The fall in FFA was related to the rise in CRP. The increases in weight and IL-6 were related to the rise in CRP. We propose that hyperandrogenism in PCOS may exert an anti-inflammatory effect when obesity is present, but may not promote inflammation in the disorder; and that circulating androgens have a pleiotropic effect on inflammation depending on the combination of PCOS and weight status in a given individual.
authors: Department of Obstetrics and Gynecology, Indiana University School of Medicine, AOC Room 6046, 550 N. University Boulevard, Indianapolis, IN 46202, USA. gonzalef@iupui.edu
authors: Frank
authors: F
authors: González
authors: Chang Ling
authors: CL
authors: Sia
authors: Frank Z
authors: FZ
authors: Stanczyk
authors: Hilary E
authors: HE
authors: Blair
authors: Michelle E
authors: ME
authors: Krupa
mesh_terms: D000726:Androgen Antagonists / Q000627:therapeutic use; D000728:Androgens / Q000097:blood; D015415:Biomarkers / Q000097:blood; D001823:Body Composition / Q000502:physiology; D001835:Body Weight / Q000187:drug effects / Q000502:physiology; D002097:C-Reactive Protein / Q000378:metabolism; D005230:Fatty Acids, Nonesterified / Q000097:blood; D005260:Female; D007987:Gonadotropin-Releasing Hormone / Q000627:therapeutic use; D006801:Humans; D017588:Hyperandrogenism / Q000503:physiopathology*; D007249:Inflammation / Q000503:physiopathology*; D018836:Inflammation Mediators / Q000097:blood; D015850:Interleukin-6 / Q000097:blood; D008066:Lipolysis / Q000502:physiology; D009765:Obesity / Q000150:complications / Q000503:physiopathology*; D010865:Pilot Projects; D011085:Polycystic Ovary Syndrome / Q000150:complications / Q000503:physiopathology*; D055815:Young Adult
chemical_list: D000726:Androgen Antagonists; D000728:Androgens; D015415:Biomarkers; D005230:Fatty Acids, Nonesterified; D018836:Inflammation Mediators; D015850:Interleukin-6; D007987:Gonadotropin-Releasing Hormone; D002097:C-Reactive Protein