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Neuroregulation of Appetite

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Treatment of the Obese Patient

Abstract

This chapter reviews current literature on hormonal and neural signals critical for the regulation of individual meals and body fat. Body weight is regulated via an ongoing process called energy homeostasis, or the long-term matching of food intake to energy expenditure. Reductions from an individual’s “normal” weight due to lack of sufficient food lowers levels of adiposity signals (leptin and insulin) reaching the brain from the blood, activates anabolic hormones that stimulate food intake, and decreases the efficacy of meal-generated signals (such as cholecystokinin or CCK) that normally reduce meal size. A converse sequence of events happens when individuals gain weight, adiposity signals are increased, catabolic hormones are stimulated, and the consequence is a reduction in food intake and a normalization of body weight. The brain also functions as a “fuel sensor” and thereby senses nutrients and generates signals and activation of neuronal systems and circuits that regulate energy homeostasis. This chapter focuses on how these signals are received and integrated by the central nervous system (CNS).

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Reizes, O., Benoit, S.C., Clegg, D.J. (2014). Neuroregulation of Appetite. In: Kushner, R., Bessesen, D. (eds) Treatment of the Obese Patient. Springer, New York, NY. https://doi.org/10.1007/978-1-4939-1203-2_1

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