title: Subcutaneous adipocytes from obese hyperinsulinemic women with polycystic ovary syndrome exhibit normal insulin sensitivity but reduced maximal insulin responsiveness.
abstract: BACKGROUND
  Polycystic ovary syndrome (PCOS) has a high prevalence in women and is often associated with insulin resistance and hence with aspects of the so-called metabolic syndrome.
  
  
  METHODS
  Ten women diagnosed with PCOS were consecutively included (aged 21-39 years, average 30.2 +/- 1.9 years; body mass index 28.4-42.5 kg/m2, average 37.5 +/- 1.7 kg/m2 (mean +/- s.e.)). Adipocytes were isolated from the subcutaneous fat and, after overnight incubation to recover from insulin resistance due to the surgical cell isolation procedures, they were analyzed for insulin sensitivity.
  
  
  RESULTS
  The patients with PCOS exhibited marked clinical hyperinsulinemia with 3.6-fold higher blood levels of C-peptide than a healthy lean control group (1.7 +/- 0.2 and 0.5 +/- 0.02 nmol/l respectively, P < 0.0001). The patients with PCOS also exhibited 2.4-fold higher concentrations of serum triacylglycerol (2.1 +/- 0.3 and 0.9 +/- 0.06 mmol/l respectively, P < 0.0001), but only slightly elevated blood pressure (118 +/- 12/76 +/- 6 and 113 +/- 7/72 +/- 6 mmHg respectively, P = 0.055/0.046). However, insulin sensitivity for stimulation of glucose transport in the isolated adipocytes was indistinguishable from a non-PCOS, non-diabetic control group, while the maximal insulin effect on glucose uptake was significantly lower (2.2 +/- 0.2- and 3.8 +/- 0.8-fold respectively, P = 0.02).
  
  
  CONCLUSIONS
  Subcutaneous adipocytes from patients with PCOS do not display reduced insulin sensitivity. The findings show that the insulin resistance of PCOS is qualitatively different from that of type 2 diabetes.
authors.affiliation: Department of Cell Biology and Diabetes Research Centre, University of Linköping, SE58185 Linköping, Sweden.
authors.forename: Erika
authors.initials: E
authors.lastname: Lystedt
authors.forename: Hanna
authors.initials: H
authors.lastname: Westergren
authors.forename: Jan
authors.initials: J
authors.lastname: Brynhildsen
authors.forename: Lotta
authors.initials: L
authors.lastname: Lindh-Astrand
authors.forename: Johanna
authors.initials: J
authors.lastname: Gustavsson
authors.forename: Fredrik H
authors.initials: FH
authors.lastname: Nystrom
authors.forename: Mats
authors.initials: M
authors.lastname: Hammar
authors.forename: Peter
authors.initials: P
authors.lastname: Strålfors
mesh_terms: D050153:Abdominal Fat / Q000166:cytology / Q000187:drug effects / Q000502:physiology; D017667:Adipocytes / Q000187:drug effects / Q000502:physiology*; D000328:Adult; D003924:Diabetes Mellitus, Type 2 / Q000503:physiopathology; D005260:Female; D005947:Glucose / Q000378:metabolism; D006801:Humans; D006946:Hyperinsulinism / Q000150:complications* / Q000503:physiopathology*; D007328:Insulin / Q000494:pharmacology*; D007333:Insulin Resistance / Q000502:physiology; D009765:Obesity / Q000150:complications* / Q000503:physiopathology*; D011085:Polycystic Ovary Syndrome / Q000150:complications* / Q000503:physiopathology*
chemical_list: D007328:Insulin; D005947:Glucose