title: Decreased soluble leptin receptor levels in women with polycystic ovary syndrome.
abstract: OBJECTIVE
  Polycystic ovary syndrome (PCOS) is associated with insulin resistance and a high incidence of obesity. Leptin, the product of the ob gene, is involved in the regulation of energy balance and obesity and circulates in both free and bound forms. The soluble leptin receptor (sOB-R) is the most important leptin-binding protein, thus influencing the biologically active free leptin level.
  
  
  METHODS
  We assessed the correlation of metabolic and endocrine parameters with leptin and sOB-R levels in 122 PCOS women (aged 27 +/- 5.7 years) and 81 healthy controls (aged 25 +/- 4.0 years).
  
  
  METHODS
  Leptin and sOB-R levels were measured using ELISA kits. In addition, anthropometric variables, body fat and endocrine parameters were evaluated and a glucose tolerance test performed to assess indices of insulin resistance and glucose metabolism.
  
  
  RESULTS
  In PCOS patients, no correlation was found between leptin or sOB-R and parameters of hyper-androgenism. However, as expected, body mass index (BMI), body fat, waist circumference and indices of insulin resistance were significantly correlated with leptin in PCOS subjects and controls. In a subgroup analysis of lean, overweight and obese PCOS patients, significant differences were found in leptin (29.7 +/- 20.7 vs 45.4 +/- 25.0 vs 67.7 +/- 28.8 ng/ml, P < 0.0001) and sOB-R (8.0 +/- 3.4 vs 6.4 +/- 2.5 vs 5.7 +/- 2.3 ng/ml, P < 0.05). Compared with BMI-matched controls, lean PCOS patients had lower sOB-R levels (8.0 +/- 3.4 vs 12.7 +/- 4.7 ng/ml, P < 0.0001) and higher free leptin indices (4.5 +/- 3.9 vs 2.8 +/- 2.2, P = 0.0285).
  
  
  CONCLUSIONS
  Taking into account that low sOB-R levels supposedly compensate diminished leptin action, PCOS per se might cause leptin resistance.
authors.affiliation: Division of Endocrinology, Department of Medicine, University of Duisburg-Essen, Essen, Germany.
authors.forename: Susanne
authors.initials: S
authors.lastname: Hahn
authors.forename: Uwe
authors.initials: U
authors.lastname: Haselhorst
authors.forename: Beate
authors.initials: B
authors.lastname: Quadbeck
authors.forename: Susanne
authors.initials: S
authors.lastname: Tan
authors.forename: Rainer
authors.initials: R
authors.lastname: Kimmig
authors.forename: Klaus
authors.initials: K
authors.lastname: Mann
authors.forename: Onno E
authors.initials: OE
authors.lastname: Janssen
mesh_terms: D000328:Adult; D000735:Androstenedione / Q000097:blood; D001786:Blood Glucose / Q000378:metabolism; D001823:Body Composition / Q000502:physiology; D015992:Body Mass Index; D002784:Cholesterol / Q000097:blood; D004958:Estradiol / Q000097:blood; D005260:Female; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D007333:Insulin Resistance / Q000502:physiology*; D007334:Insulin-Like Growth Factor I / Q000378:metabolism; D020738:Leptin / Q000097:blood / Q000378:metabolism; D009765:Obesity / Q000378:metabolism; D011085:Polycystic Ovary Syndrome / Q000378:metabolism*; D011956:Receptors, Cell Surface / Q000097:blood / Q000378:metabolism*; D054411:Receptors, Leptin; D012738:Sex Hormone-Binding Globulin / Q000378:metabolism; D018709:Statistics, Nonparametric; D013739:Testosterone / Q000097:blood; D013972:Thyrotropin / Q000097:blood
chemical_list: D001786:Blood Glucose; C515448:LEPR protein, human; D020738:Leptin; D011956:Receptors, Cell Surface; D054411:Receptors, Leptin; D012738:Sex Hormone-Binding Globulin; D013739:Testosterone; D000735:Androstenedione; D004958:Estradiol; D007334:Insulin-Like Growth Factor I; D013972:Thyrotropin; D002784:Cholesterol; D006854:Hydrocortisone