?Leptin is not simply an appetite suppressant.
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 whether leptin modulates this circuitry and to what extent. Appetite is chemically coordinated in the hypothalamus (Kalra, 1997), in a complex network of connections between various hypothalamic nuclei.
Leptin receptors, Ob-Rb, are found mainly in nuclei of the hypothalamus, including the arcuate nucleus (ARC), the paraventricular nucleus (PVN), the dorsomedial hypothalamic nucleus (DMH), the ventromedial nucleus (VMN), and the lateral hypothalamic nucleus (LH). Each of these nuclei is important in regulating body weight (Kalra, 1997). Lesions of these structures (apart from LH) all produce permanently enhanced appetite and hyperphagia. The arcuate nucleus is thought to be one of the main hypothalamic sites that regulates energy expenditure, because it has the highest density of neurons that produce orexigenic peptides, such as NPY,-endorphin, galanin, GABA and glutamate.
