Peripheral Physiological Determinants
of Eating and Body Weight
GERARD P. SMITH
The relative importance of the peripheral controls of eating and body weight has increased significantly in the past 5 years. This has been due to the realization that peripheral controls function at every meal, that so-called long-term controls of food intake act by modulating the potency of the peripheral controls, and the discovery of a new genetic obesity in rats that is due to spontaneous mutation of a mechanism of a peripheral control. All of this is the result of using meals as the functional unit of nalysis for investigating the control of eating.
The experimental focus on the controls of eating has not only led to a better understanding of peripheral controls but also to a paradigm shift from seeing eating as a problem of how intake serves metabolism to seeing eating as a problem in behavioral neuroscience. Using this larger view, recent research has revealed a coherent neural network composed of peripheral feedbacks and central mechanisms for distributed processing that use amines, peptides, and steroids (see Chapter 1). This network is sensitive to genetic change, sexual differences, and prior experience. The new view also provides a more relevant basic science of eating for clinical eating disorders in which abnormally large meals can occur in patients with high, normal, or low body weight.
All of the recent progress has occurred in analyzing the controls of the size of meals (i.e., what maintains eating once it has begun and what terminates it). Much less has been discovered about the peripheral controls of meal number (i.e., what initiates eating).
Meal size is determined by the integration of the positive and negative feedbacks produced by ingested food stimuli (Figure 2.1). Positive feedback stimulates the central net