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Updated: May 11, 2026

Real-time Analysis of Gut-brain Neural Communication: Cortex wide Calcium Dynamics in Response to Intestinal Glucose Stimulation
Published on: December 29, 2023
Integration of satiety signals by the central nervous system
Adam P Chambers1, Darleen A Sandoval, Randy J Seeley
1Metabolic Diseases Institute, University of Cincinnati, 2170 E. Galbraith Road, Bldg E, 3rd Floor, ML 0503, Cincinnati, OH 45237, USA. adam.chambers@uc.edu
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.
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