Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2013 Feb;24(2):85-91.
doi: 10.1016/j.tem.2012.11.008. Epub 2013 Jan 16.

Glucagon-like peptide 1 and appetite

Megan J Dailey  1 , Timothy H Moran
Affiliations
Review

Glucagon-like peptide 1 and appetite

Megan J Dailey et al. Trends Endocrinol Metab. 2013 Feb.

Abstract

Glucagon-like peptide 1 (GLP-1) and GLP-1 analogs have received much recent attention due to the success of GLP-1 mimetics in treating type II diabetes mellitus (T2DM), but these compounds may also have the potential to treat obesity. The satiety effect of GLP-1 may involve both within-meal enteroenteric reflexes, and across-meal central signaling mechanisms, that mediate changes in appetite and promote satiety. Here, we review data supporting the role of both peripheral and central GLP-1 signaling in the control of gastrointestinal motility and food intake. Understanding the mechanisms underlying the appetite-suppressive effects of GLP-1 may help in developing targeted treatments for obesity.

PubMed Disclaimer

Figures

Figure 1
Figure 1. GLP-1 action in the gut
(A) GLP-1 released from the L cells diffuses into the lamina propria and enters the lymph or capillaries. DPP-IV is expressed in the capillaries and can immediately begin to degrade GLP-1 before it even reaches the hepatic portal vein. GLP-1 released from the L cell can mediate changes in the submucosal (B) and myenteric nerves (C). (D) GLP-1 can have a direct effect on vagal primary afferents. (E) Luminal nutrients in the proximal GI tract may stimulate distal GLP-1 secretion through an enteroendocrine loop that involves vagal and enteric neural connections. Hormones released from the stomach or proximal intestine stimulate vagal pathways that synapse on GRP neurons in the myenteric plexus to cause downstream stimulation of GLP-1 fom the L cell in the mucosal epithelium. Ach: acetylcholine, GRP: gastrin-releasing peptide, DPP-IV: dipeptidyl peptidase-4, GLP-1: Glucagon-like peptide-1.
See this image and copyright information in PMC

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

    1. Mojsov S, et al. Preproglucagon gene expression in pancreas and intestine diversifies at the level of post-translational processing. J Biol Chem. 1986;261:11880–11889. - PubMed
    1. Orskov C, et al. Tissue and plasma concentrations of amidated and glycine-extended glucagon-like peptide I in humans. Diabetes. 1994;43:535–539. - PubMed
    1. Edholm T, et al. Differential incretin effects of GIP and GLP-1 on gastric emptying, appetite, and insulin-glucose homeostasis. Neurogastroenterol Motil. 22:1191–1200. e1315. - PubMed
    1. McIntyre RS, et al. The neuroprotective effects of GLP-1: Possible treatments for cognitive deficits in individuals with mood disorders. Behav Brain Res. 237C:164–171. - PubMed
    1. Drucker DJ, Rosen CF. Glucagon-like peptide-1 (GLP-1) receptor agonists, obesity and psoriasis: diabetes meets dermatology. Diabetologia. 54:2741–2744. - PubMed

MeSH terms

Substances