Signals to Feed: Biological and Associative Mechanisms

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A longstanding idea is that the regulation of energy intake and body weight depends on the integrative control by external food-related cues in the environment and physiological signals arising from the internal milieu. In fact, according to several accounts the ability of such environmental food cues to evoke appetitive and consummatory responding is held in check by interoceptive satiety signals that inhibit those behaviors. Within this framework, energy dysregulation leading to obesity can be seen as a failure of interoceptive satiety cues to adequately counter response evocation by food cues in the environment. This type of failure would presumably be an important contributor to what has been termed the “obesogenic” environment. The purpose of research proposed in this application is to elucidate the factors that contribute, to and the mechanisms that underlie, the weakening of internal stimulus control of appetitive behavior relative to control by external food-related stimuli. Based on recent research from our laboratory and elsewhere, we propose that both the ability of environmental cues to evoke eating and the ability of physiological cues to inhibit intake are dependent on learning and memory. However, both types of cues involve different types of learning and memory processes that rely on distinct brain structures and circuits are involved with the evocation, compared to the inhibition, of appetitive and consummatory behavior. The research we plan to do will evaluate a specific, mechanistic, and testable account that explains how consuming a diet high in saturated fat and sugar (a.k.a. “Western diet” (WD)) can disturb the function and physiology of the hippocampus (a brain structure long-identified with learning and memory). These disturbances reduce the ability of internal satiety signals to inhibit eating behavior evoked by signals in the environment related to food. Research planned in this application will advance knowledge about the operation of this mechanism, along with its neural substrates, in both male and female rats and will investigate the implications of this model for interventions that could both prevent excess intake and body weight gain and restore normal regulatory function following consumption of WD.