title: Effect of pioglitazone on glucose metabolism and luteinizing hormone secretion in women with polycystic ovary syndrome.
abstract: OBJECTIVE
  To thoroughly examine the mechanisms for insulin resistance in polycystic ovary syndrome (PCOS) and to evaluate the effects of pioglitazone treatment on insulin resistance, beta-cell function, LH secretion, and glucose metabolism.
  
  
  METHODS
  Randomized, blinded, placebo-controlled study.
  
  
  METHODS
  Outpatient clinic, at a university hospital in Denmark.
  
  
  METHODS
  Thirty obese women with PCOS and 14 weight-matched healthy females.
  
  
  METHODS
  Sixteen weeks of blinded treatment with pioglitazone (30 mg/d) or placebo.
  
  
  METHODS
  Fasting blood samples, 24-hour 20-minute integrated blood sampling (LH, insulin, and C-peptide), euglycemic hyperinsulinemic clamps including 3-(3)H glucose, and indirect calorimetry were performed before and after the intervention period.
  
  
  RESULTS
  Patients with PCOS had significantly lower insulin sensitivity compared with controls, including significantly decreased insulin-stimulated oxidative and nonoxidative glucose metabolism. Pioglitazone treatment resulted in significantly lower levels of fasting insulin and significantly higher insulin sensitivity, increased insulin-stimulated glucose oxidation, and increased insulin-stimulated inhibition of lipid oxidation. During 24-hour blood sampling, significantly lower area under-the-curve insulin and lower median insulin levels were observed. Secretion profiles of LH and E(2) and T levels did not change significantly.
  
  
  CONCLUSIONS
  Insulin resistance in PCOS was characterized by hyperinsulinemia, impaired insulin-stimulated oxidative and nonoxidative glucose metabolism, which was partly reversed by pioglitazone treatment.
authors.affiliation: Department of Endocrinology and Metabolism, Odense University Hospital, Odense, Denmark. dorte.glintborg@dadlnet.dk
authors.forename: Dorte
authors.initials: D
authors.lastname: Glintborg
authors.forename: Anne Pernille
authors.initials: AP
authors.lastname: Hermann
authors.forename: Marianne
authors.initials: M
authors.lastname: Andersen
authors.forename: Claus
authors.initials: C
authors.lastname: Hagen
authors.forename: Henning
authors.initials: H
authors.lastname: Beck-Nielsen
authors.forename: Johannes D
authors.initials: JD
authors.lastname: Veldhuis
authors.forename: Jan Erik
authors.initials: JE
authors.lastname: Henriksen
mesh_terms: D000328:Adult; D001786:Blood Glucose / Q000378:metabolism*; D004311:Double-Blind Method; D005215:Fasting / Q000097:blood; D005260:Female; D015309:Glucose Clamp Technique; D006728:Hormones / Q000097:blood; D006801:Humans; D006946:Hyperinsulinism / Q000209:etiology; D007004:Hypoglycemic Agents / Q000627:therapeutic use*; D007328:Insulin / Q000378:metabolism / Q000494:pharmacology; D007333:Insulin Resistance; D000078790:Insulin Secretion; D050417:Insulin-Secreting Cells / Q000187:drug effects / Q000378:metabolism; D007986:Luteinizing Hormone / Q000378:metabolism*; D008597:Menstrual Cycle / Q000187:drug effects; D010084:Oxidation-Reduction; D000077205:Pioglitazone; D011085:Polycystic Ovary Syndrome / Q000150:complications / Q000188:drug therapy* / Q000378:metabolism* / Q000503:physiopathology; D045162:Thiazolidinediones / Q000627:therapeutic use*
chemical_list: D001786:Blood Glucose; D006728:Hormones; D007004:Hypoglycemic Agents; D007328:Insulin; D045162:Thiazolidinediones; D007986:Luteinizing Hormone; D000077205:Pioglitazone