title: Metformin administration improves endothelial function in women with polycystic ovary syndrome.
abstract: OBJECTIVE
  The aim of this study was to investigate the endothelial status in young women with polycystic ovary syndrome (PCOS), using a simple and easily reproducible hemodynamic method combined with a biological marker and to evaluate the effect of metformin treatment on these parameters.
  
  
  METHODS
  Descriptive clinical trial.
  
  
  METHODS
  Forty young women, 20 with PCOS and 20 normal women of similar age and body mass index were studied. Metformin (1700 mg daily) was administered for 6 months to the PCOS group. The endothelium status and the metabolic and hormonal profile were studied in both groups, as well as after metformin, by flow-mediated dilatation (FMD) on the brachial artery and by measurements of plasma endothelin-1 (ET-1) levels.
  
  
  RESULTS
  FMD was impaired in the PCOS group when compared with controls (3.24+/-0.71% vs 8.81+/-1.07% respectively, P<0.0001), but this difference normalized after metformin treatment (PCOS(post-metformin) vs controls: 8.17+/-1.26 vs 8.81+/-1.07%, P = 0.70) since the values significantly improved after metformin treatment (PCOS(pre-metformin) vs PCOS(post-metformin): 3.24+/-0.71 vs 8.17+/-1.26%, P=0.003). ET-1 levels were significantly higher in the PCOS women compared with the control group (7.23+/-0.50 vs 4.99+/-0.69 fmol/l, P=0.01), they improved significantly after metformin treatment (PCOS(pre-metformin) vs PCOS(post-metformin): 7.23+/-0.50 vs 3.57+/-0.60 fmol/l, P<0.0001) and their difference compared with the control group was reversed (PCOS(post-metformin) vs controls: 3.57+/-0.60 vs 4.99+/-0.69 fmol/l, P=0.13). Metformin administration improved hyperandrogenemia. However, in this study, mathematical methods used to assess insulin resistance failed to show any detected alteration after treatment with metformin.
  
  
  CONCLUSIONS
  PCOS women were found to exhibit endothelial dysfunction compared with controls, which was reversed 6 months after metformin administration.
authors.affiliation: Laiko Hospital, Medical School, University of Athens, Endocrine Section, First Department of Medicine, Athens, Greece. akandara@otenet.gr
authors.forename: E
authors.initials: E
authors.lastname: Diamanti-Kandarakis
authors.forename: K
authors.initials: K
authors.lastname: Alexandraki
authors.forename: A
authors.initials: A
authors.lastname: Protogerou
authors.forename: C
authors.initials: C
authors.lastname: Piperi
authors.forename: C
authors.initials: C
authors.lastname: Papamichael
authors.forename: A
authors.initials: A
authors.lastname: Aessopos
authors.forename: J
authors.initials: J
authors.lastname: Lekakis
authors.forename: M
authors.initials: M
authors.lastname: Mavrikakis
mesh_terms: D000328:Adult; D001916:Brachial Artery / Q000502:physiology; D019332:Endothelin-1 / Q000097:blood; D004730:Endothelium, Vascular / Q000187:drug effects* / Q000502:physiology; D005260:Female; D018149:Glucose Intolerance / Q000188:drug therapy / Q000503:physiopathology; D006801:Humans; D007004:Hypoglycemic Agents / Q000008:administration & dosage*; D007333:Insulin Resistance; D008687:Metformin / Q000008:administration & dosage*; D011085:Polycystic Ovary Syndrome / Q000188:drug therapy* / Q000503:physiopathology; D013739:Testosterone / Q000097:blood; D014664:Vasodilation / Q000187:drug effects* / Q000502:physiology
chemical_list: D019332:Endothelin-1; D007004:Hypoglycemic Agents; D013739:Testosterone; D008687:Metformin