1. Pancreas and Not Gut Mediates the GLP-1-Induced Glucoincretin Effect
Joel F. Habener, Violeta Stanojevic 
Cell Metabolism 
Volume 25, Issue 4, Pages (April 2017)
DOI: /j.cmet
Copyright © 2017 Elsevier Inc. Terms and Conditions

2. Figure 1
A Model Proposes Local Paracrine Action of the GLP-1/GLP-1R Axis in Both the Pancreas and the Gut
In the pancreatic islets, GLP-1 is produced by α cells and acts on GLP-1 receptors on adjacent juxtaposed β cells that induce GSIS. In the gut, GLP-1 secreted locally from enteroendocrine L-cells acts on GLP-1 receptors located on vagal afferent nerve terminals juxtaposed to the L-cells, sending neural pathway signals to the solitary nucleus in the hindbrain. Efferent vagal nerve output is sent to the hypothalamus, stomach, and liver to control food intake, gastric emptying, and hepatic glucose production, respectively. Vagal efferent signaling to the liver is shown as an example. The model further illustrates the presence of the N-terminal diamino-peptidase, Dpp4, which cleaves and inactivates GLP-1, present locally within the tissues at the sites of paracrine GLP-1/GLP-1R signaling in both the pancreatic islets and in the gut. The cleavage of active GLP-1, GLP-1(7-36)amide, results in the production of the receptor-inactive metabolite GLP-1(9-36)amide (GLP-1m), which is secreted into the circulation.
Cell Metabolism  , DOI: ( /j.cmet )
Copyright © 2017 Elsevier Inc. Terms and Conditions