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Printed in U.S.A. Copyright © 1999 by The Endocrine Society Physiological Role of Cholecystokinin B/Gastrin

By Receptor In Leptin Secretion, Yannick Le Marchand-brustel, J. M. Miguel Lewin and André Bado

Abstract

THE GASTROINTESTINAL polypeptide hormones gastrin and cholecystokinin (CCK) are related peptides that share the same C-terminal sequence that carries the biological message. Eating a meal stimulates gastrin secretion from G cells in the antral part of the stomach (1) and CCK secretion from duodenal I cells (2–5). Both peptides activate the gastrin/CCK-B receptor, whereas only CCK activates the CCK-A receptor (6). In 1973, Gibbs and co-workers first reported that CCK, a brain-gut peptide (7, 8), suppressed food intake in rats, with the animals exhibiting the entire normal behavioral sequence of satiety (9). Further studies were also consistent with a physiological role for peripheral CCK in short term regulation of food intake (for review, see. Ref. 10). The effect is initiated by feeding, triggered by signals originating from the gastrointestinal tract and mediated by the vagus nerve (11, 12). Leptin, the product of the ob gene, was identified as an adipocyte-secreted protein (13). It is secreted into the blood by fat tissue to inform the brain about the adipocyte mass and thereby control appetite and body weight homeostasis (14–16). In contrast to that of CCK, the satiety effect induced by circulating leptin is only effective in the long term. This effect requires leptin cross the blood-brain barrier (17) to reach specific hypothalamic receptors (18, 19), which, in turn, modulate the actio

Year: 1999
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