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Leptin and the obesity hypoventilation syndrome: a leap of faith?
  1. M Fitzpatrick
  1. Division of Respiratory and Critical Care Medicine, Queen's University, Kingston, Ontario K7L 3N6, Canada
  1. Correspondence to:
    Dr M Fitzpatrick;
    mf19{at}post.qeensu.ca

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A possible role for leptin or its analogues in the treatment of the obesity hypoventilation syndrome

The discovery of the anti-obesity hormone leptin (the name is derived from the Greek “leptos” meaning “thin”), the product of the ob gene,1 has fuelled a recent surge of interest in the mechanisms regulating mammalian fat stores. Leptin, a 16 kD protein of 167 amino acids with a similar crystal structure to cytokines,2 is produced primarily by white adipose tissue.3 The hormone elicits appetite suppression and weight loss.4,5 Leptin circulates in the plasma in the free and protein bound forms. Circulating plasma leptin levels reflect the amount of energy storage in adipose tissue and increase exponentially with increasing fat mass.6 Plasma leptin levels also respond to short term energy imbalance, increasing during periods of overfeeding and decreasing with fasting.7,8 The hormone activates specific receptors9 located at several sites throughout the brain, but plays a key role at the hypothalamus, in particular, where it alters the expression of several hypothalamic neuropeptides.10,11 One of these, neuropeptide Y (NPY), is a potent stimulator of food intake and activator of the hypothalamic-pituitary-gonadal axis. Leptin inhibits synthesis of hypothalamic NPY and downregulation of NPY is associated with appetite suppression, increased sympathetic nervous system outflow, and increased energy expenditure.12 Increasing leptin levels activate the thyroid hormone, gonadal, and growth hormone axes and suppress the pituitary-adrenal axis.13 It must be emphasised that human obesity is a complex disorder, probably resulting from both …

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