title: Improvement of endothelial function with metformin and rosiglitazone treatment in women with polycystic ovary syndrome.
abstract: OBJECTIVE
  There is evidence of preclinical cardiovascular disease even in young women with polycystic ovary syndrome (PCOS). The aim of our study was to assess and compare the effects of metformin (MET) and rosiglitazone (ROSI) on endothelial function in PCOS patients.
  
  
  METHODS
  For 6 months, 26 women with PCOS received either MET or ROSI. Blood samples for assessment of androgens, lipids, and high-sensitive C-reactive protein were taken at baseline and at endpoint. Endothelium-dependent flow-mediated dilation (FMD) and glyceryl trinitrate-induced endothelium-independent dilation of brachial artery were studied before and after treatment. Homeostasis model assessment (HOMA(IR)) calculation was applied as a measure of insulin resistance (IR).
  
  
  RESULTS
  With treatment, FMD of brachial artery improved significantly from 4.2+/-6.6 to 10.2+/-5.9% in MET group (P=0.036) and from 2.9+/-3.2 to 7.6+/-4.9% in ROSI group (P=0.026), MET being as effective as ROSI (P=0.70). The endothelium-independent dilation did not change. Additionally, administration of MET was associated with a significant decrease in HOMA(IR) (P=0.003), serum total and serum-free testosterone (P=0.045 and P=0.008 respectively) and significantly higher frequencies of menstrual bleeding (P=0.006).
  
  
  CONCLUSIONS
  A 6-month therapy with insulin sensitizers, MET and ROSI, resulted in marked improvement of endothelial function in young PCOS patients without clinically evident atherosclerosis who were not severely insulin resistant. Neither drug was superior to the other. We conclude that therapeutic intervention with either insulin sensitizer may reverse the atherosclerotic process in PCOS patients at its early stage.
authors.affiliation: Department of Endocrinology, Diabetes and Metabolic Diseases, University Medical Centre, Zaloska 7, SI-1000 Ljubljana, Slovenia.
authors.forename: Mojca
authors.initials: M
authors.lastname: Jensterle
authors.forename: Miran
authors.initials: M
authors.lastname: Sebestjen
authors.forename: Andrej
authors.initials: A
authors.lastname: Janez
authors.forename: Janez
authors.initials: J
authors.lastname: Prezelj
authors.forename: Tomaz
authors.initials: T
authors.lastname: Kocjan
authors.forename: Irena
authors.initials: I
authors.lastname: Keber
authors.forename: Marija
authors.initials: M
authors.lastname: Pfeifer
mesh_terms: D000728:Androgens / Q000097:blood; D001916:Brachial Artery / Q000502:physiology; D002097:C-Reactive Protein / Q000378:metabolism; D002318:Cardiovascular Diseases / Q000517:prevention & control; D004730:Endothelium, Vascular / Q000187:drug effects* / Q000502:physiology; D005260:Female; D006706:Homeostasis / Q000187:drug effects; D006801:Humans; D007004:Hypoglycemic Agents / Q000008:administration & dosage*; D007333:Insulin Resistance; D008055:Lipids / Q000097:blood; D008597:Menstrual Cycle / Q000187:drug effects; D008687:Metformin / Q000008:administration & dosage*; D011085:Polycystic Ovary Syndrome / Q000188:drug therapy*; D000077154:Rosiglitazone; D045162:Thiazolidinediones / Q000008:administration & dosage*; D014664:Vasodilation / Q000187:drug effects
chemical_list: D000728:Androgens; D007004:Hypoglycemic Agents; D008055:Lipids; D045162:Thiazolidinediones; D000077154:Rosiglitazone; D002097:C-Reactive Protein; D008687:Metformin