title: Continuous positive airway pressure therapy improves hypoadiponectinemia in severe obese men with obstructive sleep apnea without changes in insulin resistance.
abstract: BACKGROUND
  Obstructive sleep apnea (OSA) is associated with several conditions that could facilitate the onset of cardiovascular and metabolic dysfunctions. Continuous positive airway pressure (CPAP) therapy has been shown to improve cardiovascular morbidity and mortality related to OSA, but the mechanisms underlying this association are not fully understood.
  
  
  OBJECTIVE
  The aim of the present study was to evaluate whether sleep apnea contributes to insulin resistance and inflammatory marker alterations and to evaluate the benefits of nasal CPAP therapy in severe obese patients with OSA.
  
  
  METHODS
  Plasma inflammatory cytokines and the homeostasis model assessment of insulin resistance index (HOMA-IR, Insulin Sensitivity Index [ISI]) were measured in severe obese male with OSA (n = 16) and compared with body mass index (BMI)-matched male controls without OSA (n = 13). Seven patients with severe sleep apnea (apnea-hypopnea index >30 events/h) were reevaluated after 3 months of nasal CPAP therapy.
  
  
  RESULTS
  OSA patients had a significantly lower adiponectin levels than obese controls (8.7 +/- 1.18 ng/mL vs. 15.0 +/- 2.55 ng/mL, P = 0.025). HOMA-IR, ISI, tumor necrosis factor-alpha (TNF-alpha, C-reactive protein (CRP), and interleukin-6 (IL-6) levels were not different between groups. Although insulin resistance index and BMI values did not change after 3 months of nCPAP therapy, adiponectin levels increased (P = 0.036) and the levels of TNF-alpha tended to decrease (P = 0.065). Changes in adiponectin levels during nCPAP therapy were positively correlated with an improvement in minimum oxygen saturation (r = 0.773; P = 0.041) and negatively correlated with changes in TNF-alpha levels (r = -0.885; P = 0.008).
  
  
  CONCLUSIONS
  nCPAP therapy reverses hypoadiponectinemia levels present in obese men with OSA, probably through reductions in hypoxia and inflammation activity.
authors: Department of Medicine, Division of Endocrinology, Universidade Federal de São Paulo, São Paulo, Brazil. glauciacarneiro@uol.com.br
authors: Gláucia
authors: G
authors: Carneiro
authors: Sônia Maria
authors: SM
authors: Togeiro
authors: Fernando Flexa
authors: FF
authors: Ribeiro-Filho
authors: Eveli
authors: E
authors: Truksinas
authors: Artur Beltrame
authors: AB
authors: Ribeiro
authors: Maria Teresa
authors: MT
authors: Zanella
authors: Sérgio
authors: S
authors: Tufik
mesh_terms: D052242:Adiponectin / Q000097:blood* / Q000172:deficiency; D002097:C-Reactive Protein / Q000378:metabolism; D002318:Cardiovascular Diseases / Q000517:prevention & control; D016022:Case-Control Studies; D045422:Continuous Positive Airway Pressure; D006801:Humans; D007333:Insulin Resistance; D015850:Interleukin-6 / Q000097:blood; D008297:Male; D008875:Middle Aged; D009767:Obesity, Morbid / Q000150:complications* / Q000503:physiopathology; D010100:Oxygen / Q000097:blood; D020181:Sleep Apnea, Obstructive / Q000150:complications* / Q000503:physiopathology / Q000628:therapy*; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D052242:Adiponectin; C508600:IL6 protein, human; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D002097:C-Reactive Protein; D010100:Oxygen