Peripheral Signals in the Control of Feeding Behavior

Abstract

Eating requires at least two basic decisions: what to eat, which is a decision about food choice, and how much to eat, which is a decision about food intake. This distinction is important because food choice and intake involve different behaviors, different controlling signals and different physiological mechanisms. Feeding behavior is controlled by a variety of signals. ‘Cephalic’ signals, such as the taste, smell, sound and sight of food, control food choice and can influence the amount of food consumed in the shortterm. Gastrointestinal signals resulting from changes in distention or the release of gut peptides may play a role in the control of shortterm intake within a meal or across several meals. Metabolic signals generated by the supply and utilization of metabolic fuels not only influence food choice, but also how much food is consumed in the short-term. Metabolic signals also determine food intake in the longterm and are important in maintaining energy balance over a nutritionally significant interval. Traditionally, research emphasized separate signals associated with glucose and fat metabolism. ‘Glucostatic’ hypotheses about these signals have focused on either changes in the circulating level of glucose or on intracellular glucose utilization, whereas ‘lipostatic’ hypotheses have targeted the amount of body fat or, more recently, the adipose hormone, leptin. A less well known line of research has looked to metabolic processes common to the metabolism of both glucose and fat for metabolic signals controlling food intake. This perspective was initially proposed by Ugolev and Kassil (1961), who investigated the tricarboxylic acid cycle as a source of a common, ‘oxidative’ metabolic signal. More recently, research in this area has focused on aspects of ATP production. Our approach to the study of the metabolic controls of food intake addresses questions that are usually associated with the study of sensory systems: Where are receptors/detectors that monitor metabolic events to control food intake? What stimulus is adequate to activate the receptor? How is this stimulus transduced into a neural signal? And how is this signal transmitted to and within the central nervous system? Here, we review our laboratory’s work on each of these issues in turn.