title: Treatment of obesity hypoventilation syndrome and serum leptin.
abstract: BACKGROUND
  Leptin is a protein produced by adipose tissue that circulates to the brain and interacts with receptors in the hypothalamus to inhibit eating. In obese humans, serum leptin is up to four times higher than in lean subjects, indicating that human obesity is associated with a central resistance to the weight-lowering effects of leptin. Although the leptin-deficient mouse (ob/ob) develops obesity hypoventilation syndrome (OHS), in humans with OHS, serum leptin is a better predictor of awake hypercapnia in obesity than the body mass index (BMI). This suggests that central leptin resistance may promote the development of OHS in humans. We speculated that the reversal of OHS by regular non-invasive ventilation (NIV) therapy decreases leptin levels.
  
  
  OBJECTIVE
  The aim of this study was to investigate whether ventilatory treatment of OHS would alter circulating leptin concentrations.
  
  
  METHODS
  We measured fasting serum leptin levels, BMI, spirometry and arterial blood gases in 14 obese hypercapnic subjects undergoing a diagnostic sleep study.
  
  
  RESULTS
  The average age of the subjects was (mean +/- SE) 62 +/- 13 years, BMI 40.9 +/- 2.2 kg/m(2), PaCO(2) 6.7 +/- 0.2 kPa, PaO(2 )8.9 +/- 0.4 kPa and total respiratory disturbance index 44 +/- 35 events/hour. Subjects were clinically reviewed after a median of 2.3 years (range 1.6-3) with repeat investigations. Nine patients were regular NIV users and 5 were non-users. NIV users had a significant reduction in serum leptin levels (p = 0.001), without a change in BMI. In these patients, there was a trend towards an improved daytime hypercapnia and hypoxemia, while in the 5 non-users, no changes in serum leptin, BMI or arterial blood gases occurred.
  
  
  CONCLUSIONS
  Regular NIV use reduces serum leptin in OHS. Leptin may be a modulator of respiratory drive in patients with OHS.
authors.affiliation: Sleep Research Group, Woolcock Institute of Medical Research, Royal Prince Alfred Hospital, Camperdown, Sydney, Australia.
authors.forename: Brendon J
authors.initials: BJ
authors.lastname: Yee
authors.forename: Jane
authors.initials: J
authors.lastname: Cheung
authors.forename: Paul
authors.initials: P
authors.lastname: Phipps
authors.forename: Dev
authors.initials: D
authors.lastname: Banerjee
authors.forename: Amanda J
authors.initials: AJ
authors.lastname: Piper
authors.forename: Ronald R
authors.initials: RR
authors.lastname: Grunstein
mesh_terms: D015992:Body Mass Index; D002245:Carbon Dioxide / Q000097:blood; D045422:Continuous Positive Airway Pressure; D005260:Female; D006801:Humans; D006935:Hypercapnia / Q000209:etiology / Q000517:prevention & control; D007040:Hypoventilation / Q000097:blood / Q000209:etiology / Q000628:therapy*; D000860:Hypoxia / Q000209:etiology / Q000517:prevention & control; D020738:Leptin / Q000097:blood*; D008297:Male; D008875:Middle Aged; D009765:Obesity / Q000097:blood / Q000150:complications*; D010100:Oxygen / Q000097:blood; D017286:Polysomnography; D011175:Positive-Pressure Respiration; D011446:Prospective Studies; D020181:Sleep Apnea, Obstructive / Q000097:blood / Q000209:etiology / Q000628:therapy*; D013577:Syndrome
chemical_list: D020738:Leptin; D002245:Carbon Dioxide; D010100:Oxygen