sincalide and litorin

Recent studies have clearly shown powerful control of ingestive behavior by certain peptides known to be present in both brain and gut tissues. These "brain-gut neuropeptides" are thought to constitute endogenous factors responsible for the normal regulation of food intake. This review explores the potential for a role of these peptides in the limitation of ethanol intake, which shares several features with the control of food intake. The putative satiety role of the neuropeptides cholecystokinin and bombesin, and other brain-gut peptides is briefly described. The conclusion that voluntary ethanol intake is partially controlled as a function of the energy ethanol provides, and the rate of its utilization, is illustrated with data from recent studies of rat and hamster ethanol consumption. The possibility of neuropeptide influence on ethanol intake is presented in light of new findings that cholecystokinin and bombesin inhibit ethanol consumption in the rat. If neuropeptides are demonstrated to modulate ethanol intake by eliciting satiety, this information may be useful in the identification and understanding of the endogenous factors which regulate human alcohol intake, and will suggest possible peptide-based therapeutic interventions for control of alcohol abuse and alcoholism.

Topics: Alcohol Drinking; Alcohol Oxidoreductases; Animals; Bombesin; Brain; Cholecystokinin; Cricetinae; Digestive System Physiological Phenomena; Ethanol; Humans; Kinetics; Liver; Mesocricetus; Nerve Tissue Proteins; Oligopeptides; Rats; Satiation; Satiety Response; Sincalide

Topics: Animals; Appetite; Avoidance Learning; Bombesin; Chlorides; Cholecystokinin; Conditioning, Classical; Dose-Response Relationship, Drug; Drinking; Eating; Lithium; Lithium Chloride; Oligopeptides; Rats; Satiation; Sincalide; Taste

Intraperitoneal injections of tetradecapeptide bombesin (BBS) produced large, dose-related suppressions of liquid and solid food intake in rats, with threshold doses of 1--2 micrograms-kg-1. The feeding-associated behaviors of rats receiving BBS by this route at a test meal were normally sequenced, and several other observations suggested that the effect of BBS was specific and not due to malaise. The structurally related amphibian peptide litorin and the structurally related mammalian gastrin-releasing peptide (GRP) produced similar suppressions of food intake. The satiety effect of BBS administered intraperitoneally did not require the accumulation of food in the gut, the presence of intact adrenals, the abdominal vagus, or the release of cholecystokinin. When BBS and cholecystokinin were administered simultaneous, the suppressive effects on food intake were additive. Lateral cerebroventricular injections of BBS also produced large, dose-related suppressions of food intake, with a threshold dose of 100 ng per rat. The effect by this route, however, was not behaviorally specific: BBS produced equivalent inhibitions of food and water intake at every point on the dose-response curve, and produced a marked increase in grooming which dominated the behavioral display. Thus, (1) peripheral BBS is a putative satiety signal in the rat; (2) the class (endocrine, paracrine, or neural) and mechanism of this satiety action is not established; and (3) the differences in specificity and behavior following intraperitoneal and cerebroventricular routes indicate that peripheral BBS does not act solely via the cerebrospinal fluid to elicity satiety.

Topics: Adrenalectomy; Animals; Bombesin; Cholecystokinin; Dose-Response Relationship, Drug; Eating; Feeding Behavior; Gastrin-Releasing Peptide; Gastrointestinal Hormones; Injections, Intraventricular; Oligopeptides; Peptide Fragments; Peptides; Rats; Satiation; Sincalide; Vagotomy