Hyperleptinemia, respiratory drive and hypercapnic response in obese patients

¹ Depts of Pulmonary Medicine
² Endocrinology
³ Neurophysiology, Clínica Universitaria; Universidad de Navarra, Pamplona, Spain
⁴ Dept of Pulmonary Medicine, Hospital de Cruces, Vizcaya, Spain

^* To whom correspondence should be addressed. E-mail: acampoe{at}unav.es.

	Abstract

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.

To assess by multivariate analysis the possible association between respiratory center impairment and levels of serum leptin.

Three hundred and sixty four obese subjects (BMI 30 kg·m^-2) had the following tests: sleep studies, respiratory function tests, baseline and hypercapnic response (P0.1, minute ventilation), fasting leptin levels, body composition and anthropometric measures. Subjects with airways obstruction by spirometry were excluded.

Two hundred and forty-five subjects were included in the analysis. Lung volumes, age, log leptin levels, PetCO2, % body fat and minimal nocturnal saturation were predictors for baseline P0.1 (R²=0.222; p<0.001). One hundred and eighty six subjects performed hypercapnic response test; log leptin levels were predictors for hypercapnic response in men (R²=0.051; p=0.027 for P0.1), but not in women.

Hyperleptinemia 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 center.

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