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However, far greater concentrations of leptin
receptors are present in the arcuate nucleus than in these other hypothalamic sites. Satiety signals control meal size It is self-evident that either the amount of food consumed during individual meals, the frequency of meals, or both, must be regulated if energy homeostasis is to be achieved. The major determinant of meal size is the onset of satiety, a biological state induced by neurohumoral stimuli generated during food ingestion that leads to meal termination. To clarify how the decision to terminate a meal once it has begun is controlled in the regulation of energy homeostasis, we proposethathypothalamicpathwaysinvolvedinenergyhomeostasis interact with a distinctly different set of pathways involved in the response to satiety signals65,87. In contrast to the timing of meal initiation, which can be influenced by many external and internal variables (for example, emotional factors, time of day, availability and palatability of foods, and threats from the environment), meal terminationtendstobeamorebiologicallycontrolledprocess88.Several findings indicate that control of meal size is a component of the feeding response induced by changes of body fuel stores or adiposity signalling. The hyperphagic response to central administration of NPY, for example, arises predominantly from the consumption of larger meals89. Conversely, leptin-treated animals consume the same number of meals as vehicle-treated controls, but the meals are smaller90. These observations indicate that signals involved in energy homeostasis may control food intake primarily by adjusting the size of individual meals. One way that this could be accomplished is by modulating the response to satiety signals in brain areas that process thisinformation. In contrast to its major role in mediating the response to adiposity signals, the hypothalamus is probably not the site that processes

satiety signals. Rather, satiety information generated during the course of a meal is largely conveyed to the hindbrain by means of afferent fibres of the vagus nerve and by afferents passing into the spinal cord from the upper gastrointestinal tract91.