1. Intestinal GLP-1 and satiation: from man to rodents and back.
- Author
-
Steinert RE, Beglinger C, and Langhans W
- Subjects
- Animals, Appetite drug effects, Eating drug effects, Glucagon-Like Peptide 1 metabolism, Humans, Mice, Obesity drug therapy, Obesity metabolism, Rats, Satiation drug effects, Appetite physiology, Eating physiology, Gastrointestinal Motility drug effects, Glucagon-Like Peptide 1 therapeutic use, Glucagon-Like Peptide-1 Receptor antagonists & inhibitors, Obesity physiopathology, Satiation physiology
- Abstract
In response to luminal food stimuli during meals, enteroendocrine cells release gastrointestinal (GI) peptides that have long been known to control secretory and motor functions of the gut, pancreas and liver. Glucagon-like peptide-1 (GLP-1) has emerged as one of the most important GI peptides because of a combination of functions not previously ascribed to any other molecule. GLP-1 potentiates glucose-induced insulin secretion, suppresses glucagon release, slows gastric emptying and may serve as a satiation signal, although the physiological status of the latter function has not been fully established yet. Here we review the available evidence for intestinal GLP-1 to fulfill a number of established empirical criteria for assessing whether a hormone inhibits eating by eliciting physiological satiation in man and rodents.
- Published
- 2016
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