Traditionally it has been thought that appetite is influenced solely by body components or by metabolism. These influences are commonly referred to as the glucostatic, aminostatic, thermostatic, or lipostatic hypotheses. Each suggests that a single variable such as glucose, amino acids, heat generation, or adipose tissue stores plays the major role in modulating the expression of appetite. It can be accepted that all four variables can be monitored and each can exert some influences over food consumption. In the last few years research has given renewed support to the lipostatic hypothesis, specifically, the identification of the adipose signal lep-tin. The short-term consequences of food ingestion generated by a meal also produce a powerful inhibition on further intake (satiety). We can draw a distinction between short-term satiety signals generated by the physiological consequences of meal intake (episodic), and the long-term signals generated by the body's constant metabolic need for energy (tonic). This distinction may be a useful starting point in our examination of the integration of the CNS systems responsible for the expression of appetite.
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