The satiety effect of cholecystokinin: A progress report

G. P. Smith; J. Gibbs; C. Jerome; F. X. Pi-Sunyer; H. R. Kissileff; J. Thornton

doi:10.1016/0196-9781(81)90011-5

The satiety effect of cholecystokinin: A progress report

G. P. Smith, J. Gibbs, C. Jerome, F. X. Pi-Sunyer, H. R. Kissileff, J. Thornton

Research output: Contribution to journal › Article › peer-review

92 Scopus citations

Abstract

The satiety effect of cholecystokinin (CCK) that was first observed in rats has now been extended to chickens, rabbits, pigs, sheep, rhesus monkeys, lean mice, genetically obese mice and rats, neurologically obese rats, lean men and women, and obese men. The effect is specific and can be obtained in animals and humans without reports or signs of sickness. The mechanism of the effect is unknown, but the gastric vagal fibers are necessary for the effect. This has led to the hypothesis that the satiety effect is due to activation of vagal afferent fibers that inhibit the central control system of feeding by CCK acting directly on recently described vagal CCK receptors and/or indirectly through a gastric smooth muscle effect that vagal receptors are sensitive to.

Original language	English
Pages (from-to)	57-59
Number of pages	3
Journal	Peptides
Volume	2
Issue number	SUPPL. 2
DOIs	https://doi.org/10.1016/0196-9781(81)90011-5
State	Published - 1981

Keywords

Cholecystokinin
Cholecystokinin receptors
Feeding behavior
Food intake
Gastric emptying
Genetic obesity
Obesity
Satiety
Vagal afferents
Vagal receptors
Vagus

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title = "The satiety effect of cholecystokinin: A progress report",

abstract = "The satiety effect of cholecystokinin (CCK) that was first observed in rats has now been extended to chickens, rabbits, pigs, sheep, rhesus monkeys, lean mice, genetically obese mice and rats, neurologically obese rats, lean men and women, and obese men. The effect is specific and can be obtained in animals and humans without reports or signs of sickness. The mechanism of the effect is unknown, but the gastric vagal fibers are necessary for the effect. This has led to the hypothesis that the satiety effect is due to activation of vagal afferent fibers that inhibit the central control system of feeding by CCK acting directly on recently described vagal CCK receptors and/or indirectly through a gastric smooth muscle effect that vagal receptors are sensitive to.",

keywords = "Cholecystokinin, Cholecystokinin receptors, Feeding behavior, Food intake, Gastric emptying, Genetic obesity, Obesity, Satiety, Vagal afferents, Vagal receptors, Vagus",

author = "Smith, {G. P.} and J. Gibbs and C. Jerome and Pi-Sunyer, {F. X.} and Kissileff, {H. R.} and J. Thornton",

note = "Funding Information: Our recent results in men are particularly important for three reasons. First, the main effect of CCK is that men stop eating sooner \[22,36\].T his is what our hypothesis predicts. If CCK is one of the endogenous mechanisms for satiety, then administration of exogenous CCK at the beginning of a meal should produce a concentration of circulating CCK that is 1Supported by grants from NIH (AM 26687, AM 17240), from NIMH (MH 15455) and from Squibb & Co. zSupported by NIMH Research Development Award MH 00149. Send reprint requests to G.P.S. at E.W. Bourne Behavioral Research Laboratory, New York Hospital, 21 Bloomingdale Road, White Plains, NY 10605. aSupported by a fellowship from Irma T. Hirschl Foundation.",

year = "1981",

doi = "10.1016/0196-9781(81)90011-5",

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AU - Smith, G. P.

AU - Gibbs, J.

AU - Jerome, C.

AU - Pi-Sunyer, F. X.

AU - Kissileff, H. R.

AU - Thornton, J.

N1 - Funding Information: Our recent results in men are particularly important for three reasons. First, the main effect of CCK is that men stop eating sooner \[22,36\].T his is what our hypothesis predicts. If CCK is one of the endogenous mechanisms for satiety, then administration of exogenous CCK at the beginning of a meal should produce a concentration of circulating CCK that is 1Supported by grants from NIH (AM 26687, AM 17240), from NIMH (MH 15455) and from Squibb & Co. zSupported by NIMH Research Development Award MH 00149. Send reprint requests to G.P.S. at E.W. Bourne Behavioral Research Laboratory, New York Hospital, 21 Bloomingdale Road, White Plains, NY 10605. aSupported by a fellowship from Irma T. Hirschl Foundation.

PY - 1981

Y1 - 1981

N2 - The satiety effect of cholecystokinin (CCK) that was first observed in rats has now been extended to chickens, rabbits, pigs, sheep, rhesus monkeys, lean mice, genetically obese mice and rats, neurologically obese rats, lean men and women, and obese men. The effect is specific and can be obtained in animals and humans without reports or signs of sickness. The mechanism of the effect is unknown, but the gastric vagal fibers are necessary for the effect. This has led to the hypothesis that the satiety effect is due to activation of vagal afferent fibers that inhibit the central control system of feeding by CCK acting directly on recently described vagal CCK receptors and/or indirectly through a gastric smooth muscle effect that vagal receptors are sensitive to.

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KW - Vagal afferents

KW - Vagal receptors

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The satiety effect of cholecystokinin: A progress report

Abstract

Keywords

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