Skip to main content
. Author manuscript; available in PMC: 2014 Nov 14.
Published in final edited form as: Nat Rev Endocrinol. 2011 Jun 7;7(9):507–516. doi: 10.1038/nrendo.2011.77

Figure 1.

Figure 1

Model of GLP-1 physiology. Nutrient ingestion stimulates intestinal L-cell secretion of glucagon-like peptide 1 (GLP-1), which activates local GLP-1 receptors (GLP1R) to initiate afferent vagal neurotransmission to the hindbrain. These vagal afferent signals, combined with those initiated by gastric distension, may activate hindbrain GLP-1-producing neurons, which in turn activate hindbrain GLP1R, as well as other hindbrain neurons to produce efferent signals leading to decreased meal size. In addition, signaling from hindbrain GLP-1-producing neurons to hypothalamic targets promotes decreased fat mass.