title: Integration of satiety signals by the central nervous system.
abstract: Individual meals are products of a complex interaction of signals related to both short-term and long-term availability of energy stores. In addition to maintaining the metabolic demands of the individual in the short term, levels of energy intake must also maintain and defend body weight over longer periods. To accomplish this, satiety pathways are regulated by a sophisticated network of endocrine and neuroendocrine pathways. Higher brain centers modulate meal size through descending inputs to caudal brainstem regions responsible for the motor pattern generators associated with ingestion. Gastric and intestinal signals interact with central nervous system pathways to terminate food intake. These inputs can be modified as a function of internal metabolic signals, external environmental influences, and learning to regulate meal size.
authors: Metabolic Diseases Institute, University of Cincinnati, 2170 E. Galbraith Road, Bldg E, 3rd Floor, ML 0503, Cincinnati, OH 45237, USA. adam.chambers@uc.edu
authors: Adam P
authors: AP
authors: Chambers
authors: Darleen A
authors: DA
authors: Sandoval
authors: Randy J
authors: RJ
authors: Seeley
mesh_terms: D000818:Animals; D002490:Central Nervous System / Q000502:physiology*; D004435:Eating; D002149:Energy Intake; D006728:Hormones / Q000378:metabolism; D006801:Humans; D051379:Mice; D009490:Neurosecretory Systems / Q000502:physiology*; D051381:Rats; D012527:Satiation; D015398:Signal Transduction
chemical_list: D006728:Hormones
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