title: Differential gene expression profile in omental adipose tissue in women with polycystic ovary syndrome.
abstract: BACKGROUND
  The polycystic ovary syndrome (PCOS) is frequently associated with visceral obesity, suggesting that omental adipose tissue might play an important role in the pathogenesis of the syndrome.
  
  
  OBJECTIVE
  The objective was to study the expression profiles of omental fat biopsy samples obtained from morbidly obese women with or without PCOS at the time of bariatric surgery.
  
  
  METHODS
  This was a case-control study.
  
  
  METHODS
  We conducted the study in an academic hospital.
  
  
  METHODS
  Eight PCOS patients and seven nonhyperandrogenic women submitted to bariatric surgery because of morbid obesity.
  
  
  METHODS
  Biopsy samples of omental fat were obtained during bariatric surgery.
  
  
  METHODS
  The main outcome measure was high-density oligonucleotide arrays.
  
  
  RESULTS
  After statistical analysis, we identified changes in the expression patterns of 63 genes between PCOS and control samples. Gene classification was assessed through data mining of Gene Ontology annotations and cluster analysis of dysregulated genes between both groups. These methods highlighted abnormal expression of genes encoding certain components of several biological pathways related to insulin signaling and Wnt signaling, oxidative stress, inflammation, immune function, and lipid metabolism, as well as other genes previously related to PCOS or to the metabolic syndrome.
  
  
  CONCLUSIONS
  The differences in the gene expression profiles in visceral adipose tissue of PCOS patients compared with nonhyperandrogenic women involve multiple genes related to several biological pathways, suggesting that the involvement of abdominal obesity in the pathogenesis of PCOS is more ample than previously thought and is not restricted to the induction of insulin resistance.
authors.affiliation: Instituto de Investigaciones Biomédicas, Consejo Superior de Investigaciones Científicas and Universidad Autónoma de Madrid, E-28029 Madrid, Spain.
authors.forename: Marta
authors.initials: M
authors.lastname: Cortón
authors.forename: José I
authors.initials: JI
authors.lastname: Botella-Carretero
authors.forename: Alberto
authors.initials: A
authors.lastname: Benguría
authors.forename: Gemma
authors.initials: G
authors.lastname: Villuendas
authors.forename: Angel
authors.initials: A
authors.lastname: Zaballos
authors.forename: José L
authors.initials: JL
authors.lastname: San Millán
authors.forename: Héctor F
authors.initials: HF
authors.lastname: Escobar-Morreale
authors.forename: Belén
authors.initials: B
authors.lastname: Peral
mesh_terms: D000273:Adipose Tissue / Q000378:metabolism*; D000328:Adult; D000367:Age Factors; D016022:Case-Control Studies; D005260:Female; D020869:Gene Expression Profiling; D006801:Humans; D017588:Hyperandrogenism / Q000378:metabolism; D007328:Insulin / Q000502:physiology; D007333:Insulin Resistance; D008066:Lipolysis / Q000235:genetics; D024821:Metabolic Syndrome / Q000235:genetics; D009852:Omentum / Q000378:metabolism*; D018384:Oxidative Stress; D010727:Phosphoric Diester Hydrolases / Q000235:genetics; D011085:Polycystic Ovary Syndrome / Q000276:immunology / Q000378:metabolism*; D011755:Pyrophosphatases / Q000235:genetics; D015398:Signal Transduction; D051153:Wnt Proteins / Q000502:physiology
chemical_list: D007328:Insulin; D051153:Wnt Proteins; D010727:Phosphoric Diester Hydrolases; C065962:ectonucleotide pyrophosphatase phosphodiesterase 1; D011755:Pyrophosphatases