Interactions between gastric emptying and satiety, with special reference to glucagon-like peptide-1

Physiol Behav. Nov-Dec 2001;74(4-5):735-41. doi: 10.1016/s0031-9384(01)00618-7.

Abstract

The slowing of gastric emptying is an important mechanism for the satiating effect of gut peptide signaling. After food intake, cholecystokinin (CCK), as well as glucagon-like peptide-1 (GLP-1) and glucagon-like peptide-2 (GLP-2), are released from the gastrointestinal tract to mediate satiety. In humans, CCK and the GLP-1 have been found to cause satiety in both normal and obese subjects. This satiating effect may be caused by the peptides circulating as hormones with direct effects in the central nervous system, or indirect effects through signals mediated either via the vagus nerve or by activation of vagal afferent fibers due to slow gastric emptying. These peptides also cause gastric relaxation, considered an additional component in the satiating effect of the peptides. To conclude, after food intake, gut peptides may act in concert as neurohormonal satiety signals acting directly in the brain or indirectly via the vagus nerve, as well as through gastric sensory mechanisms to limit food intake.

Publication types

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

MeSH terms

  • Animals
  • Body Weight / physiology
  • Cholecystokinin / physiology
  • Eating / physiology*
  • Gastric Emptying / physiology*
  • Glucagon / physiology*
  • Glucagon-Like Peptide 1
  • Glucagon-Like Peptide 2
  • Humans
  • Obesity / physiopathology
  • Peptide Fragments / physiology*
  • Peptides / physiology
  • Protein Precursors / physiology*
  • Satiety Response / physiology*
  • Vagus Nerve / physiopathology

Substances

  • Glucagon-Like Peptide 2
  • Peptide Fragments
  • Peptides
  • Protein Precursors
  • Glucagon-Like Peptide 1
  • Glucagon
  • Cholecystokinin