Leptin research has exploded in the last five years, meaning that our understanding of the roles of this hormone are emerging as much more complex than originally proposed. At present, there seems to be many theories as to the function of leptin, most of which are related in some way to energy homeostasis. However, energy homeostasis is a complex system that as yet is not fully understood, therefore where exactly leptin fits in is still difficult to characterise. If one defines appetite as simply the desire for food, then no, leptin is not simply an appetite suppressant. This is too simplistic a description of leptin?s actions. While the control of appetite is one aspect that will lead to energy homeostasis, evidence obtained so far certainly indicates that the role of leptin is far more complex than being an appetite suppressant, and I shall attempt to describe here the main emerging theories of leptin?s actions.

Firstly, leptin as an appetite suppressant. In order for us to include leptin as an anorexigenic molecule, one must first have an understanding of the circuitry that regulates appetite, and then investigate whet

Leptin as an adipostatic signal, acting via negative feedback to brain centres that control energy homeostasis, may act to limit obesity in times of nutritional abundance, supported by the evidence that mice that either lack leptin or are resistant to it are obese.

Neural elements in the VMN and DMN complex tonically restrain the orexigenic signals, aided by leptins? action on diminution of NPY orexigenic signals or augmentation of anorexigenic signals (?MSH, CART and GLP-1), as seen by the fact that lesions of the VMN lead to both hyperphagia and leptin resistance. While the VMN-DMN-PVN connection is thought to integrate the timing of appetite mechanism, seen by the loss of regulated feeing when lesioned, evidence points towards the PVN as being the primary site for release and action of the various orexigenic and anorexigenic signals.

Treatment with leptin reduces weight is all mammals tested (Friedman, 1998), in a weight loss pattern that differences from food-deprived weight loss as only the adipose tissue is lost, and not lean body mass. The complications comes when most obese people already have high leptin levels, therefore further administration is not expected to lead to weight loss, as they are resistant. Clinical trials of leptin as an anti-obesity drug are currently in phase I and II trials, and one might say that so far, the results are positive, but at least at the doses used, leptin is by no means the wonder drug it was predicted to be to treat obesity.

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