[Satiation Mechanism]

Overview

Journal Z Ernahrungswiss

Specialty Nutritional Sciences

Date 1984 Dec 1

PMID 6098086

Authors

E Scharrer

Affiliations

Soon will be listed here.

Abstract

Food intake in man and animals occurs as meals. Because changes in daily food intake in laboratory animals are often associated with corresponding changes in meal size, while meal frequency is less affected, food intake appears to be regulated mainly by the satiety mechanism. Meal size is controlled by feedback or satiety signals originating from the stomach, the small intestine, the liver and the fat depots. Both neural and hormonal (Bombesin?, Cholecystokinin?) feedback signals are elicited in the stomach and intestine. The feedback signals of the liver apparently originate from hepatic chemoreceptors, whose activity is modulated by certain metabolites, in particular glucose. The satiety effect of pancreatic glucagon, whose plasma concentration in the portal vein increases during a meal, also appears to be mediated by the hepatic chemoreceptors. Unmyelated nerve endings are probably the morphological substrate of the hepatic chemoreceptors. There is some evidence that circulating fat metabolites (fatty acids, ketone bodies, glycerol), whose plasma levels are related to the size of the fat depots, function as lipostatic feedback signals. The signal transfer from the gastrointestinal chemo- and mechanoreceptors and from the hepatic chemoreceptors to the central nervous system occurs mainly through vagal afferents. The first relay for this afferents is the nucleus tractus solitarii in the medulla oblongata. The next relay is at the pons, from where neurons project to the hypothalamus and other forebrain areas. The hypothalamus has important integrative functions in the control of food intake.

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