Leptin, a protein secreted by fat cells, seems to be involved in mechanisms of ventilatory control in humans. Leptin induces satiation and reduction of appetite, and increases the rate of metabolism. This leads to the maintenance or reduction of weight (from the Greek leptos, meaning thin). Since most obese people have very high levels of leptin, obesity has been postulated as a state of leptin resistance.

There is previous evidence that this protein is also a ventilatory stimulant in rodents. In humans, however, there are only a few studies that show indirect relationships, such as the presence of higher levels of serum leptin in patients with sleep apnoea syndrome or in obese patients with associated hypoventilation disorders.
Patients suffering from the obesity-hypoventilation syndrome develop severe consequences, such as respiratory failure, pulmonary hypertension and heart failure. Otherwise, the pathogenesis of hypoventilation in obese people is not completely understood and it has been suggested that neural control impairment plays a role in these phenomena.

Arantza Campo (University Clinic, Pamplona, Spain) and her colleagues found a relationship between high levels of leptin and reduced measurements of ventilation control in a sample of 364 patients seeking treatment for obesity.
The relationship was stronger in men compared with women.
Other variables were taken into account, such as the severity of obesity, percentage and distribution of fat, presence of sleep apnoea, nocturnal oxygen desaturation and impairment in respiratory mechanics caused by obesity.

The results of this study suggest that in obese patients, leptin resistance could affect not only appetite, but also the neurological centres for ventilatory control. The consequences of these findings include the possibility of treating these patients with the administration of supplementary leptin or leptin sensitisers.

European Respiratory Journal