TITLE

Association of serum leptin with hypoventilation in human obesity

AUTHOR(S)
Phipps, P. R.; Starritt, E.; Caterson, I.; Grunstein, R. R.
PUB. DATE
January 2002
SOURCE
Thorax;Jan2002, Vol. 57 Issue 1, p75
SOURCE TYPE
Academic Journal
DOC. TYPE
Article
ABSTRACT
Background: Leptin is a protein hormone produced by fat cells of mammals. It acts within the hypothalamus via a specific receptor to reduce appetite and increase energy expenditure. Plasma leptin levels correlate closely with total body fat mass operating via a central feedback mechanism. In human obesity serum leptin levels are up to four times higher than in lean subjects, indicating a failure of the feed- back loop and central leptin resistance. In leptin deficient obese mice (ob/ob mice) leptin infusion reverses hypoventilation. It was hypothesised that a relative deficiency in CNS leptin, indicated by high circulating leptin levels, may be implicated in the pathogenesis of obesity hypoventilation syndrome (OHS). Methods: Fasting morning leptin levels were measured in obese and non-obese patients with and without daytime hypercapnia (n=56). Sleep studies, anthropometric data, spirometric parameters, and awake arterial blood gas tensions were measured in each patient. Results: In the whole group serum leptin levels correlated closely with % body fat (r=0.77). Obese hypercapnic patients (mean (SD) % body fat 43.8 (6.0)%) had higher fasting serum leptin levels than eucapnic patients (mean % body fat 40.8 (6.2)%), with mean (SD) leptin levels of 39.1 (17.9) and 21 .4 (11 .4) ng/ml, respectively (p<0.005). Serum leptin (odds ratio (OR) 1.12, 95% Cl 1.03 to 1 .22) was a better predictor than % body fat (OR 0.92, 95% CI 0.76 to 1 .1) for the presence of hypercapnia. Conclusions: Hyperleptinaemia is associated with hypercapnic respiratory failure in obesity. Treatment with leptin or its analogues may have a role in OHS provided central leptin resistance can be overcome.
ACCESSION #
12941012

 

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