title: Early metabolic derangements in daughters of women with polycystic ovary syndrome.
abstract: BACKGROUND
  Polycystic ovary syndrome (PCOS) is a familial endocrine-metabolic dysfunction, increasingly recognized in adolescent girls with hyperandrogenism. However, it is difficult to establish whether the metabolic abnormalities described in PCOS are present before the onset of hyperandrogenism. In children, a strong association of adiponectin levels with metabolic parameters of insulin resistance has been described.
  
  
  OBJECTIVE
  The objective of the study was to evaluate adiponectin serum concentrations and metabolic parameters in prepubertal and pubertal daughters of women with PCOS to identify girls with increased metabolic risk.
  
  
  METHODS
  Fifty-three prepubertal and 22 pubertal (Tanner stages II-V) daughters of PCOS women (PCOSd) and 32 prepubertal and 17 pubertal daughters of control women (Cd) were studied. In both groups, an oral glucose tolerance test was performed with measurement of glucose and insulin. Adiponectin, leptin, C-reactive protein, SHBG, sex steroids, and lipids were determined in the fasting sample.
  
  
  RESULTS
  Both groups had similar chronological ages, body mass index sd score, and Tanner stage distribution. In the prepubertal girls, 2-h insulin was higher (P = 0.023) and adiponectin levels were lower (P = 0.004) in the PCOSd group, compared with the Cd group. In the pubertal girls, triglycerides (P = 0.03), 2-h insulin (P = 0.01), and serum testosterone concentrations were higher (P = 0.012) and SHBG lower (P = 0.009) in PCOSd, compared with Cd, but adiponectin levels were similar in both groups.
  
  
  CONCLUSIONS
  Some of the metabolic features of PCOS are present in daughters of PCOS women before the onset of hyperandrogenism. Adiponectin appears to be one of the early markers of metabolic derangement in these girls.
authors.affiliation: Endocrinology and Metabolism Laboratory, University of Chile, Santiago, Chile. tsir@med.uchile.cl
authors.forename: Teresa
authors.initials: T
authors.lastname: Sir-Petermann
authors.forename: Manuel
authors.initials: M
authors.lastname: Maliqueo
authors.forename: Ethel
authors.initials: E
authors.lastname: Codner
authors.forename: Bárbara
authors.initials: B
authors.lastname: Echiburú
authors.forename: Nicolás
authors.initials: N
authors.lastname: Crisosto
authors.forename: Virginia
authors.initials: V
authors.lastname: Pérez
authors.forename: Francisco
authors.initials: F
authors.lastname: Pérez-Bravo
authors.forename: Fernando
authors.initials: F
authors.lastname: Cassorla
mesh_terms: D052242:Adiponectin / Q000097:blood; D000328:Adult; D000886:Anthropometry; D015415:Biomarkers; D001786:Blood Glucose / Q000378:metabolism; D002097:C-Reactive Protein / Q000032:analysis / Q000378:metabolism; D002648:Child; D002675:Child, Preschool; D004958:Estradiol / Q000097:blood; D005260:Female; D005951:Glucose Tolerance Test; D006801:Humans; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance; D020738:Leptin / Q000097:blood; D008055:Lipids / Q000097:blood; D010641:Phenotype; D011085:Polycystic Ovary Syndrome / Q000235:genetics* / Q000378:metabolism*; D011863:Radioimmunoassay; D018570:Risk Assessment; D012738:Sex Hormone-Binding Globulin / Q000378:metabolism; D013739:Testosterone / Q000097:blood
chemical_list: D052242:Adiponectin; D015415:Biomarkers; D001786:Blood Glucose; D007328:Insulin; D020738:Leptin; D008055:Lipids; D012738:Sex Hormone-Binding Globulin; D013739:Testosterone; D004958:Estradiol; D002097:C-Reactive Protein