title: Fat accumulation, leptin, and hypercapnia in obstructive sleep apnea-hypopnea syndrome.
abstract: BACKGROUND
  Obesity and visceral fat accumulation (VFA) are risk factors for the development of obstructive sleep apnea-hypopnea syndrome (OSAHS), and a subgroup of OSAHS patients acquire hypoventilation. Circulating leptin, an adipocyte-derived signaling factor, increases in accordance with body mass index (BMI); under experimental conditions, leptin selectively decreases visceral adiposity and it is also a respiratory stimulant.
  
  
  OBJECTIVE
  To investigate whether the location of body fat deposits, ie, the distribution of VFA and subcutaneous fat accumulation (SFA), contributes to hypoventilation and whether circulating levels of leptin are involved in the pathogenesis of hypoventilation, which is often observed in OSAHS.
  
  
  METHODS
  We assessed VFA and SFA by abdominal CT scan, and measured lung function and circulating levels of leptin in 106 eucapnic and 79 hypercapnic male patients with OSAHS.
  
  
  RESULTS
  In the whole study group, circulating leptin levels correlated with BMI (r = 0.56), VFA (r = 0.24), and SFA (r = 0.47), but not with Po(2) or sleep mean arterial oxygen saturation (Sao(2)). BMI, percentage of predicted vital capacity, FEV(1)/FVC ratio, apnea-hypopnea index, sleep mean Sao(2), VFA, and SFA were not significantly different between two groups. Circulating leptin levels were higher in the hypercapnic group than in the eucapnic group. Logistic regression analysis indicated that serum leptin was the only predictor for the presence of hypercapnia (beta = 0.21, p < 0.01).
  
  
  CONCLUSIONS
  These results suggest that the location of body fat deposits may not contribute to the pathogenesis of hypoventilation, and circulating leptin may fail to maintain alveolar ventilation in hypercapnic patients with OSAHS.
authors.affiliation: Department of Respirology, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuou-ku, Chiba 260-8670, Japan.
authors.forename: Ryuhi
authors.initials: R
authors.lastname: Shimura
authors.forename: Koichiro
authors.initials: K
authors.lastname: Tatsumi
authors.forename: Akira
authors.initials: A
authors.lastname: Nakamura
authors.forename: Yasunori
authors.initials: Y
authors.lastname: Kasahara
authors.forename: Nobuhiro
authors.initials: N
authors.lastname: Tanabe
authors.forename: Yuichi
authors.initials: Y
authors.lastname: Takiguchi
authors.forename: Takayuki
authors.initials: T
authors.lastname: Kuriyama
mesh_terms: D000273:Adipose Tissue / Q000503:physiopathology*; D000328:Adult; D000368:Aged; D001823:Body Composition / Q000502:physiology*; D015992:Body Mass Index; D006801:Humans; D006935:Hypercapnia / Q000503:physiopathology*; D007040:Hypoventilation / Q000503:physiopathology; D020738:Leptin / Q000097:blood*; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D010100:Oxygen / Q000097:blood; D017286:Polysomnography; D012307:Risk Factors; D012885:Skinfold Thickness; D020181:Sleep Apnea, Obstructive / Q000175:diagnosis / Q000503:physiopathology*; D013223:Statistics as Topic
chemical_list: D020738:Leptin; D010100:Oxygen