title: Increased body iron stores of obese women with polycystic ovary syndrome are a consequence of insulin resistance and hyperinsulinism and are not a result of reduced menstrual losses.
abstract: OBJECTIVE
  Increased serum ferritin levels, indicating increased body iron stores, have been found in overweight and obese women with polycystic ovary syndrome (PCOS). This finding might result from reduced menstrual losses secondary to oligo- or amenorrhea or from hyperinsulinism secondary to insulin resistance, because insulin favors the intestinal absorption and the tissue deposition of iron. To explore which of these mechanisms is responsible for the increase in body iron stores in women with PCOS, we have monitored the changes in serum ferritin levels during treatment with an antiandrogenic oral contraceptive or an insulin sensitizer.
  
  
  METHODS
  Thirty-four consecutive PCOS patients were randomized to an oral contraceptive containing 35 microg ethinyl-estradiol plus 2 mg cyproterone acetate (Diane(35) Diario) or metformin (850 mg twice daily), and their serum ferritin levels were evaluated at baseline and after 12 and 24 weeks of treatment.
  
  
  RESULTS
  Despite the fact that treatment with Diane(35) Diario restored regular menstrual cycles in all the patients, whereas metformin only did so in 50% of them, serum ferritin levels decreased at 12 and 24 weeks of treatment only with metformin, in association with a marked increase in insulin sensitivity. On the contrary, no changes in ferritin and insulin sensitivity were observed with Diane(35) Diario.
  
  
  CONCLUSIONS
  Our present results suggest that insulin resistance and hyperinsulinism, and not the reduced menstrual losses secondary to from oligo- or amenorrhea, are responsible of the increased ferritin levels and body iron stores found in overweight and obese women with PCOS.
authors.affiliation: Department of Endocrinology and Molecular Genetics, Hospital Universitario Ramón y Cajal and Universidad de Alcalá, Madrid, Spain.
authors.forename: Manuel
authors.initials: M
authors.lastname: Luque-Ramírez
authors.forename: Francisco
authors.initials: F
authors.lastname: Alvarez-Blasco
authors.forename: José I
authors.initials: JI
authors.lastname: Botella-Carretero
authors.forename: Raul
authors.initials: R
authors.lastname: Sanchón
authors.forename: José L
authors.initials: JL
authors.lastname: San Millán
authors.forename: Héctor F
authors.initials: HF
authors.lastname: Escobar-Morreale
mesh_terms: D000293:Adolescent; D000328:Adult; D000726:Androgen Antagonists / Q000627:therapeutic use; D017373:Cyproterone Acetate / Q000627:therapeutic use; D004338:Drug Combinations; D004997:Ethinyl Estradiol / Q000627:therapeutic use; D005260:Female; D005293:Ferritins / Q000097:blood; D006801:Humans; D006946:Hyperinsulinism / Q000503:physiopathology*; D007004:Hypoglycemic Agents / Q000627:therapeutic use; D007333:Insulin Resistance / Q000502:physiology*; D007501:Iron / Q000378:metabolism; D008687:Metformin / Q000627:therapeutic use; D009765:Obesity / Q000150:complications / Q000378:metabolism*; D009839:Oligomenorrhea / Q000503:physiopathology*; D011085:Polycystic Ovary Syndrome / Q000150:complications / Q000188:drug therapy / Q000378:metabolism*
chemical_list: D000726:Androgen Antagonists; D004338:Drug Combinations; D007004:Hypoglycemic Agents; D004997:Ethinyl Estradiol; D017373:Cyproterone Acetate; C032640:Cyproterone acetate, ethinyl estradiol drug combination; D005293:Ferritins; D008687:Metformin; D007501:Iron