title: Pioglitazone treatment increases spontaneous growth hormone (GH) secretion and stimulated GH levels in polycystic ovary syndrome.
abstract: BACKGROUND
  Low GH levels, probably due to insulin resistance and increased abdominal fat mass, are well described in polycystic ovary syndrome (PCOS). GH acts as an important ovarian cogonadotropin, and GH disturbances may be an additional pathogenic factor in PCOS. Decreased abdominal fat mass and improved insulin sensitivity during pioglitazone treatment may affect GH secretion.
  
  
  OBJECTIVE
  The objective of the study was to investigate the effect of pioglitazone on GH levels in PCOS.
  
  
  METHODS
  Thirty insulin-resistant PCOS patients were randomized to either 16 wk pioglitazone (30 mg/d) or placebo treatment. Before and after intervention, levels of fasting insulin, GH, total IGF-I, free IGF-I, IGF binding protein-1, IGF-II, free fatty acids, testosterone, and SHBG were measured. Patients underwent whole-body dual x-ray absorptiometry scans, pyridostigmine-GHRH tests, and 24-h 20-min integrated blood sampling for measurement of GH.
  
  
  RESULTS
  Peak GH and area under the curve for GH in pyridostigmine-GHRH tests and 24-h mean GH concentrations and pulsatile GH secretion significantly increased after pioglitazone treatment. No significant changes were observed in GH pulse frequency, pulse duration, approximate entropy levels, or basal GH release. Levels of IGF binding protein-1 significantly increased, whereas no significant differences were measured in total IGF-I and free IGF-I. Pioglitazone treatment significantly decreased fasting insulin and homeostasis model assessment levels. No significant changes were observed in Ferriman Gallwey score or androgen levels.
  
  
  CONCLUSIONS
  Pioglitazone treatment significantly increased GHRH-stimulated GH levels and 24-h pulsatile GH secretion, probably directly or indirectly due to improved insulin sensitivity.
authors.affiliation: Department of Endocrinology and Metabolism, Odense University Hospital, Denmark. dorte.glintborg@dadlnet.dk
authors.forename: Dorte
authors.initials: D
authors.lastname: Glintborg
authors.forename: René Klinkby
authors.initials: RK
authors.lastname: Støving
authors.forename: Claus
authors.initials: C
authors.lastname: Hagen
authors.forename: Anne Pernille
authors.initials: AP
authors.lastname: Hermann
authors.forename: Jan
authors.initials: J
authors.lastname: Frystyk
authors.forename: Johannes D
authors.initials: JD
authors.lastname: Veldhuis
authors.forename: Allan
authors.initials: A
authors.lastname: Flyvbjerg
authors.forename: Marianne
authors.initials: M
authors.lastname: Andersen
mesh_terms: D015502:Absorptiometry, Photon; D000328:Adult; D019540:Area Under Curve; D001823:Body Composition / Q000187:drug effects; D002800:Cholinesterase Inhibitors / Q000494:pharmacology; D004311:Double-Blind Method; D005260:Female; D012739:Gonadal Steroid Hormones / Q000097:blood; D013007:Growth Hormone-Releasing Hormone / Q000097:blood; D019382:Human Growth Hormone / Q000097:blood*; D006801:Humans; D007004:Hypoglycemic Agents / Q000627:therapeutic use*; D007328:Insulin / Q000378:metabolism; D007333:Insulin Resistance / Q000502:physiology; D007334:Insulin-Like Growth Factor I / Q000378:metabolism; D008598:Menstruation / Q000502:physiology; D047495:PPAR gamma / Q000819:agonists; D000077205:Pioglitazone; D011085:Polycystic Ovary Syndrome / Q000097:blood*; D011729:Pyridostigmine Bromide / Q000494:pharmacology; D013268:Stimulation, Chemical; D045162:Thiazolidinediones / Q000627:therapeutic use*
chemical_list: D002800:Cholinesterase Inhibitors; D012739:Gonadal Steroid Hormones; D007004:Hypoglycemic Agents; D007328:Insulin; D047495:PPAR gamma; D045162:Thiazolidinediones; D019382:Human Growth Hormone; D007334:Insulin-Like Growth Factor I; D013007:Growth Hormone-Releasing Hormone; D011729:Pyridostigmine Bromide; D000077205:Pioglitazone