title: Hypothalamic dopaminergic tone and prolactin bioactivity in women with polycystic ovary syndrome.
abstract: BACKGROUND
  The present study was carried out to investigate the functional significance of the reduced dopaminergic tone in subjects affected with polycystic ovary syndrome (PCOS).
  
  
  METHODS
  Our group evaluated the response of pituitary PRL, LH, FSH, and TSH to the administration of a single 10-mg oral dose of the dopamine (DA) receptor antagonist metoclopramide in lean (n = 7) and obese (n = 8) PCOS women and in 11 regularly cycling age- and weight-matched controls (six lean and five obese). In addition, circulating PRL bioactivity was evaluated by its mitogenic activity on a lymphoma cell bioassay.
  
  
  RESULTS
  Oral administration of metoclopramide resulted in a significant increase in serum PRL in all subjects; however, the highest increments, regardless of body mass index (BMI), were observed in control women (p <0.005). Measurements of PRL mitogenic activity on the Nb2 lymphoma cell bioassay revealed a significant increase in the bioactive/immunoreactive (B/I) ratio of PRL under basal and stimulated conditions in obese PCOS subjects (p <0.05). Mean fasting glucose/insulin and glucose/insulin-AUC ratios were significantly lower (p <0.001) in obese PCOS when compared with all other groups.
  
  
  CONCLUSIONS
  These data support the existence of low DA hypothalamic tone in PCOS women that is likely involved in the inappropriate LH and PRL secretion frequently seen in this syndrome. In addition, our results suggest changes in PRL bioactivity in obese PCOS that may play a role in the development of hyperinsulinemia; however, whether PRL has a functional significance in the development of the metabolic disturbances frequently seen in PCOS remains to be elucidated.
authors.affiliation: Departamento de Biología de la Reproducción, Instituto Nacional de la Nutrición Salvador Zubirán, México, D.F., Mexico.
authors.forename: I
authors.initials: I
authors.lastname: Hernández
authors.forename: A
authors.initials: A
authors.lastname: Parra
authors.forename: I
authors.initials: I
authors.lastname: Méndez
authors.forename: V
authors.initials: V
authors.lastname: Cabrera
authors.forename: M C
authors.initials: MC
authors.lastname: Cravioto
authors.forename: M
authors.initials: M
authors.lastname: Mercado
authors.forename: V
authors.initials: V
authors.lastname: Díaz-Sánchez
authors.forename: F
authors.initials: F
authors.lastname: Larrea
mesh_terms: D000293:Adolescent; D000328:Adult; D019540:Area Under Curve; D001786:Blood Glucose / Q000032:analysis; D019314:Dehydroepiandrosterone Sulfate / Q000097:blood; D004298:Dopamine / Q000502:physiology*; D018492:Dopamine Antagonists; D004958:Estradiol / Q000378:metabolism; D005215:Fasting / Q000097:blood; D005260:Female; D005640:Follicle Stimulating Hormone / Q000378:metabolism; D006801:Humans; D007030:Hypothalamo-Hypophyseal System / Q000503:physiopathology*; D007031:Hypothalamus / Q000503:physiopathology*; D007328:Insulin / Q000097:blood; D007986:Luteinizing Hormone / Q000378:metabolism; D008223:Lymphoma / Q000473:pathology; D008787:Metoclopramide; D009765:Obesity / Q000150:complications / Q000503:physiopathology; D011085:Polycystic Ovary Syndrome / Q000150:complications / Q000503:physiopathology*; D011388:Prolactin / Q000097:blood / Q000378:metabolism* / Q000494:pharmacology; D012636:Secretory Rate / Q000187:drug effects; D013739:Testosterone / Q000378:metabolism; D013972:Thyrotropin / Q000378:metabolism; D014407:Tumor Cells, Cultured / Q000187:drug effects
chemical_list: D001786:Blood Glucose; D018492:Dopamine Antagonists; D007328:Insulin; D013739:Testosterone; D004958:Estradiol; D019314:Dehydroepiandrosterone Sulfate; D011388:Prolactin; D007986:Luteinizing Hormone; D005640:Follicle Stimulating Hormone; D013972:Thyrotropin; D008787:Metoclopramide; D004298:Dopamine