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Hyperleptinaemia, respiratory drive and hypercapnic response in obese patients

Depts of ¹ Pulmonary Medicine, ² Endocrinology, and ³ Neurophysiology, Clinica Universitaria de Navarra, University of Navarra, Pamplona, and ⁴ Dept of Pulmonary Medicine, Hospital de Cruces, Vizcaya, Spain.

CORRESPONDENCE: A. Campo, Pulmonary Medicine, Clinica Universitaria de Navarra, Avda. Pío XII, 36, 31008 Pamplona, Spain. Fax: 34 948296500. E-mail: acampoe{at}unav.es

Keywords: Control of breathing, hypoventilation, leptin, obesity, respiratory centre, respiratory function tests

Received: August 31, 2006
Accepted April 10, 2007

Leptin is a powerful stimulant of ventilation in rodents. In humans, resistance to leptin has been consistently associated with obesity. Raised leptin levels have been reported in subjects with sleep apnoea or obesity–hypoventilation syndrome. The aim of the present study was to assess, by multivariate analysis, the possible association between respiratory centre impairment and levels of serum leptin.

In total, 364 obese subjects (body mass index 30 kg·m^–2) underwent the following tests: sleep studies, respiratory function tests, baseline and hypercapnic response (mouth occlusion pressure (P_0.1), minute ventilation), fasting leptin levels, body composition and anthropometric measures. Subjects with airways obstruction on spirometry were excluded.

Out of the 346 subjects undergoing testing, 245 were included in the current analysis. Lung volumes, age, log leptin levels, end-tidal carbon dioxide tension, percentage body fat and minimal nocturnal saturation were predictors for baseline P_0.1. The hypercapnic response test was performed by 186 subjects; log leptin levels were predictors for hypercapnic response in males, but not in females.

Hyperleptinaemia is associated with a reduction in respiratory drive and hypercapnic response, irrespective of the amount of body fat. These data suggest the extension of leptin resistance to the respiratory centre.

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