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Metabolic signals and food intake. Forty years of progress
1Department of Psychiatry and Behavioral Neuroscience, University of Cincinnati, 2170 East Galbraith Road, Cincinnati, OH 45237, United States.
Abstract:
The Columbia Appetitive Seminar, which began in 1972, has been a huge success in bringing together scholars interested in appetitive behavior, stimulating research and new ideas, and encouraging collaborations. At the time of the Seminar's inception, predominant views were that energy derived acutely from the utilization of glucose was a primary causative factor in determining the initiation (hunger) and offset (satiation) of meals; and that specific nuclei in the hypothalamus controlled unique aspects of motivated behaviors, such as stimulating water intake or creating a feeling of satiety. Over the ensuing 40 years, these views have given way to models of appetitive behavior utilizing complex interacting neural circuits responding to diverse signals emanating from the gastrointestinal tract, the external environment, cognitive, learned and social factors, and many more. Pivotal reports include the 1973 demonstration that cholecystokinin reduces meal size, and the discovery of leptin in 1994.
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