Intestinal GLP-1 and satiation: from man to rodents and back

Int J Obes (Lond). 2016 Feb;40(2):198-205. doi: 10.1038/ijo.2015.172. Epub 2015 Aug 28.

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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Appetite / drug effects
  • Appetite / physiology*
  • Eating / drug effects
  • Eating / physiology*
  • Gastrointestinal Motility / drug effects*
  • Glucagon-Like Peptide 1 / metabolism
  • Glucagon-Like Peptide 1 / therapeutic use*
  • Glucagon-Like Peptide-1 Receptor / antagonists & inhibitors*
  • Humans
  • Mice
  • Obesity / drug therapy
  • Obesity / metabolism
  • Obesity / physiopathology*
  • Rats
  • Satiation / drug effects
  • Satiation / physiology*

Substances

  • Glucagon-Like Peptide-1 Receptor
  • Glucagon-Like Peptide 1