title: Inverse relationship between luteinizing hormone and body mass index in polycystic ovarian syndrome: investigation of hypothalamic and pituitary contributions.
abstract: BACKGROUND
  Patients with polycystic ovarian syndrome (PCOS) have increased LH relative to FSH, but LH is modified by body mass index (BMI).
  
  
  OBJECTIVE
  The objective of the study was to determine whether the impact of BMI on neuroendocrine dysregulation in PCOS is mediated at the hypothalamic or pituitary level. PARTICIPANTS/INTERVENTIONS/SETTING: Twenty-four women with PCOS across a spectrum of BMIs underwent frequent blood sampling, iv administration of GnRH (75 ng/kg), and sc administration of the NAL-GLU GnRH antagonist (5 microg/kg) in the General Clinical Research Center at an academic hospital.
  
  
  METHODS
  LH pulse frequency and LH response to submaximal GnRH receptor blockade were used as measures of hypothalamic function; LH response to GnRH was used as a measure of pituitary responsiveness.
  
  
  RESULTS
  BMI was negatively correlated with mean LH, LH/FSH, and LH pulse amplitude. There was no effect of BMI on LH pulse frequency. Percent inhibition of LH was decreased in PCOS, compared with normal women (53.9 +/- 1.5 vs. 63.1 +/- 4.1, respectively; P < 0.01), suggesting an increase in the amount of endogenous GnRH, but was not influenced by BMI. Pituitary responsiveness to GnRH was inversely correlated with BMI (peak LH, R = -0.475, P < 0.02; and LH area under the curve R = -0.412, P < 0.02).
  
  
  CONCLUSIONS
  LH pulse frequency and quantity of GnRH are increased in PCOS, but there is no influence of BMI on either marker of hypothalamic function. The pituitary response to a weight-based dose of GnRH is inversely related to BMI in PCOS. These studies suggest that the effect of BMI on LH is mediated at a pituitary and not a hypothalamic level in PCOS.
authors.affiliation: Reproductive Endocrine Unit, BHX-5, Massachusetts General Hospital, 55 Fruit Street, Boston, MA 02114, USA.
authors.forename: Yanira L
authors.initials: YL
authors.lastname: Pagán
authors.forename: Serene S
authors.initials: SS
authors.lastname: Srouji
authors.forename: Yarisie
authors.initials: Y
authors.lastname: Jimenez
authors.forename: Anne
authors.initials: A
authors.lastname: Emerson
authors.forename: Sabrina
authors.initials: S
authors.lastname: Gill
authors.forename: Janet E
authors.initials: JE
authors.lastname: Hall
mesh_terms: D000328:Adult; D019540:Area Under Curve; D015992:Body Mass Index; D004958:Estradiol / Q000097:blood; D005260:Female; D005640:Follicle Stimulating Hormone / Q000097:blood; D012739:Gonadal Steroid Hormones / Q000097:blood; D007987:Gonadotropin-Releasing Hormone / Q000037:antagonists & inhibitors / Q000627:therapeutic use; D006801:Humans; D007031:Hypothalamus / Q000378:metabolism / Q000503:physiopathology*; D007328:Insulin / Q000097:blood; D007986:Luteinizing Hormone / Q000097:blood*; D009490:Neurosecretory Systems / Q000502:physiology; D009765:Obesity / Q000503:physiopathology; D010902:Pituitary Gland / Q000378:metabolism / Q000503:physiopathology*; D011085:Polycystic Ovary Syndrome / Q000097:blood / Q000503:physiopathology*; D012738:Sex Hormone-Binding Globulin / Q000378:metabolism; D013739:Testosterone / Q000097:blood
chemical_list: D012739:Gonadal Steroid Hormones; D007328:Insulin; D012738:Sex Hormone-Binding Globulin; D007987:Gonadotropin-Releasing Hormone; D013739:Testosterone; D004958:Estradiol; D007986:Luteinizing Hormone; D005640:Follicle Stimulating Hormone